Headache PDF

Headache Headache -All age groups -1% to 2% of emergency department -4% of medical office visits -Headache requires thorough and systematic evaluation. Pain-Sensitive Structures A. Pain-Sensitive Structures Within the Cranial Vault -Venous sinuses (eg, sagittal sinus) -Anterior and middle mening...

Headache Headache -All age groups -1% to 2% of emergency department -4% of medical office visits -Headache requires thorough and systematic evaluation. Pain-Sensitive Structures A. Pain-Sensitive Structures Within the Cranial Vault -Venous sinuses (eg, sagittal sinus) -Anterior and middle meningeal arteries -Dura at the base of the skull -Trigeminal (V) -Glossopharyngeal (IX) -Vagus (X) nerves -Proximal portions of the internal carotid artery and its branches near the circle of Willis -Brainstem peri aqueductal gray matter -Sensory nuclei of the thalamus B. Extracranial Pain-Sensitive Structures -Periosteum of the skull -Skin -Subcutaneous tissues -Muscles, and arteries; neck muscles; second (C2) and third (C3) cervical nerves -Eyes, ears, teeth, sinuses, and oropharynx; and mucous membranes of the nasal cavity. Causes of headache A. Acute B. Subacute C. Chronic A-Acute Headache 1-Subarachnoid hemorrhage 2-CNS infection 3- Glucoma 4-Coitus 5-Seizure 6- Hypertensive encephalopathy B-Subacute Headache 1-Giant cell (temporal) arteritis 2-Intracranial mass (tumor, subdural hematoma, abscess) 3-Pseudotumor cerebri (idiopathic intracranial hypertension) 4-Trigeminal neuralgia (tic douloureux) 5-Glossopharyngeal neuralgia 6-Postherpetic neuralgia 7-Persistent idiopathic facial pain C- Chronic Headache 1-Migraine 2-Medication overuse headache 3-Cluster headache and trigeminal autonomic cephalalgias 4-Tension-type headache 5-Icepick-like pain 6-Cervical spine disease 7-Sinusitis 8-Dental disease Primary Headache: migraine , tension, cluster and others. Secondary headache to increase intracranial pressure like: brain tumor , peudotumor cerebri and idiopathic intracainial hypertention(IIH) Migraine Migraine -Second most common cause of headache -The most common headache-related, and indeed neurologic, cause of disability in the world. -Afflict 15% o women and 6% o men over a 1-year period. -Episodic headache -Associated with certain features such as sensitivity to light, sound, or movement; nausea and vomiting often accompany the headache. Pathogenesis of Migraine -Sensory sensitivity that is characteristic of migraine due to dysfunction of monoaminergic sensory control systems located in the brainstem and hypothalamus. Activation of cells in the trigeminal nucleus results in the release of vasoactive neuropeptides, particularly calcitonin gene–related peptide (CGRP), at vascular terminations of the trigeminal nerve and within the trigeminal nucleus. -CGRP receptor antagonists, gepants effective in the acute treatment and prevention of migraine, and monoclonal antibodies to CGRP have been shown effective in multiple phase II clinical trials. -Despite there is a genetic theory and vascular theory lead to vasodilatation but now the immune theory is most acceptable one. Clinical criteria of Migraine 1-Migraine without aura(common type) 2-Migraine with aura (classical type) 1-Migraine without aura(common type) At least 5 episodic attacks of headache each one lasting from4- 72 hours+ 2 Of The Following: 1-Unilat. 2-Throbbing 3-Moderate to severe 4-Interfere with daily activity and activated by movement And 1 Of The Following 1-Nausea and or vomiting 2-Photophobia and phonophobia Migraine with aura (classical type) -30% of migraine patients -Headache is preceded by transient neurologic symptoms (aura) lasting less than one hour. -Auras may be visual, sensory (affecting limb, face, or tongue), vertebrobasilar, or motor. -The most common auras are visual alterations, particularly hemianopic field defects and scotomas (blind spots) -Migrainous aura occasionally produces neurologic deficits that persist into or beyond the pain phase (eg,hemiplegic migraine) and may rarely cause stroke. -Motor manifestations of migraine can be distinguished from stroke by both the gradual onset (“migrainous march”) and spontaneous resolution of symptoms. Especially after 50 years of age, the aura may occur without headache (late-life migraine equivalents). Symptoms include visual disturbance, hemiparesis, hemisensory loss. so migraine with aura is the same criteria of without aura but occurs with aura. Other migraine subtypes include retinal migraine (headache with monocular scotoma), vestibular migraine, and menstrual migraine. Associations: 1-Nausea 2-Photophobia 3-Lightheadedness 4-Scalp tenderness 5-Vomiting 6-Visual disturbances 7-Paresthesias 8-Vertigo 9-Photopsia 10-Alteration of consciousness 11-Diarrhea 12-Syncope 13-Seizure 14-Confusional state Treatment 1-Abortive treatment Nonsteroidal anti inflammatory drugs like : naproxen ,ibuprofen, aspirin, combination of acetaminophen and aspirin and caffeine , or acetaminophen and codeine , or ibuprofen and acetaminophen and caffeine , meperidine. Antiemetics like : metochlopramide , prochlorperazine , promethazine 2- Triptans Sumatriptans : orally or s.c injection Zolmitriptan orally or intranasaly Other triptans like nara , riza and frovatriptans Ergotamin and dihydroergotamine Prophylaxis --Antiepileptic like Topiramate, valproate, gabapentine --Beta blocker like propranalol, metoprolol --Tricyclic anti depressant like amitriptyline , nortiptyline ,venlafaxine --Ca channel blocker like verapamil , flunarizine --Other agents like Riboflavine, bottox , candesartan Cluster Headache Cluster headache -Repetitive episodes (clusters) of brief (15-180 minutes), very severe, unilateral, constant, nonthrobbing headaches. -Episodes may be precipitated by alcohol or vasodilating drugs, especially if used during acluster siege. -The headache may begin as a burning sensation over the lateral aspect of the nose or as pressure behind the eye. -The headache is associated with ipsilateral conjunctival injection, lacrimation, nasal stuffiness, or Horner syndrome. -Cluster headaches are always unilateral and usually recur on the same side in a given patient. -They occur most often at night, awakening the patient from sleep. -Cluster headache occurs much more frequently in men than in women (3:1) -Typically begins at a somewhat later age than migraine (mean onset at 25 years). - There is occasionally a family history. Treatment Abortive 1-Oxygen high conc. 7-12 L FOR 15 – 20 min.(100%) 2- Subcut. Triptans , intranasal , oral 3- I.M or Subcut. Or Oral ergot or dehydroergotamine 4- Subcut. Octreotide 5- Intranasal lidocaine Prophylaxis 1-Verapamil 80 mg 1*3 or sustained release tab 270 mg per day 2- Topiramate 50- 200 mg per day 3-Valproic acid 4- gabapentine 5-Melatonine 6- Occipital nerve stimulation 7- No role of botox Paroxysmal Hemicrainia Paroxysmal Hemicrania -It is type of autonomic cephlagia headache like cluster headache. -it is 1ry headache -Occurs in bouts lasting 2-5 minutes several times about 10 – 20 times per day -Associated with redness of eye , lacrimation, nasal stiffness -Affect one side only not transfer to the other side. - Treated by indomethacine 25 mg 3 times daily for days for acute attack and for prevention , topiramate has good role for it.  Sunct And Suna Sunct And Suna -It is also 1ry headache -Sometimes occurs 2ndry to pituitary tumor but rarly -Occurs in bouts 100 times per day lasting seconds to less than 2 min. -Associated also with autonomic cephalgia. -Treated by indomethacine as abortive therapy and for prophlaxis lamotrigen (25- 150 mg). SUNCT (Short-lasting Unilateral Neuralgiform headache with Conjunctival injection and Tearing). SUNA (Short-lasting Unilateral Neuralgiform headache with Autonomic sympto Tension Headache Tension Headache -chronic or recurrent headache of unapparent cause that lacks features of migraine or other headache syndromes. -The underlying pathophysiologic mechanism is unknown. -Tension-type headache is a chronic disorder that begins after age 20 years. -It is characterized by attacks of nonthrobbing, bilateral occipital head pain that is not associated with nausea, vomiting, or prodromal visual disturbance. -Headache duration is from hours to days. -The pain is sometimes likened to a tight band around the head. -Women are more commonly affected than men. Treatment -Acute attacks may respond to aspirin, other nonsteroidal anti-inflammatory drugs, or acetaminophen. -Tension-type headache in migraineurs may respond to triptans. -For prophylactic treatment, amitriptyline, nortriptyline or imipramine is often effective. -Trials of botulinum toxin mostly show that it is unhelpful. -Massage, physical therapy, and relaxation techniques can provide additional benefit in selected cases. Coital Headache Coital Headache -Most coital headaches are benign. -Men are more often affected than women. -The pain may be either a dull, bilateral pain occurring during sexual excitement or a severe, sudden headache occurring at the time of orgasm, presumably caused by a marked increase in systemic blood pressure. - Persistent headache after orgasm—worse in the upright posture. -Patients reporting severe headache in association with orgasm should be evaluated for possible subarachnoid hemorrhage. - prophylactic treatment with indomethacin, 50 to 100 mg orally 30 to 60 minutes prior to intercourse, may be effective. Trigeminal Neuralgia Trigeminal Neuralgia -Trigeminal neuralgia (tic douloureux) is a facial pain syndrome that develops in middle to late life and is more common in women than men. -Pain is unilateral and typically confined to the area supplied by the second (V2) and third (V3) divisions of the trigeminal (V) nerve ,.Involvement of the first division or bilateral disease occurs in less than 5% of cases. -Pain occurs as lightning-like, momentary (>1 second to approximately 2 minutes) jabs of excruciating pain that spontaneously abate, and attacks are stereotypic in a given patient. -Occurrence during sleep is uncommon. -Pain-free intervals may last for minutes to weeks, but long- term spontaneous remission is rare. -Stimulation of trigger zones about the cheek, nose, or mouth by touch, cold, wind, talking, or chewing can precipitate the pain. -In classical trigeminal neuralgia, physical examination discloses no abnormalities trigeminal sensory deficits or abnormal trigeminal (eg, corneal or jaw jerk) reflexes exclude an idiopathic diagnosis. - Rarely, similar pain may occur in multiple sclerosis or with brainstem tumors, which should be considered in young patients, in those with ophthalmic; division pain, and in all patients who show neurologic abnormalities on examination or who experience bilateral symptoms. CT scan, conventional MRI, and arteriography are normal. Although high-resolution MRI techniques may show microvascular nerve compression. Treatment of T.N 1-Carbemazapin 400mg -1200mg orally 2-Oxycarbamazapin 3-Lamotrigen 4-Baclofen 5-Acute attack iv phenytoin 250mg followed by oral 100- 300mg 6- if not responding to medical so surgical decompression of trigeminal nerve from sup. Cerebella aretery , other option Gamma knife.  Glossopharyngeal Neuralgia -Glossopharyngeal neuralgia is a rare syndrome mainly characterized by unilateral pain localized to the oropharynx, tonsillar pillars, base of the tongue, or auditory meatus. -Pain may be paroxysmal, resembling that described for trigeminal neuralgia, or more continuous and burning or aching in quality. -Rarely, cardiac syncopedue to bradyarrhythmia may occur. symptoms are initiated by swallowing or talking. Paroxysms of pain can occur many times daily. -Women are affected more frequently than men. -Symptoms begin at a somewhat younger age than in trigeminal neuralgia. -The diagnosis is established by the history and by reproducing pain through stimulation of peritonsillar trigger zones. -There are no abnormal neurologic signs. - -Bilateral symptoms, abnormal signs, or other atypical - features should prompt a search for disorders that can mimic glossopharyngeal neuralgia, such as multiple sclerosis, cerebellopontine angle tumor, and nasopharyngeal carcinoma. -As in trigeminal neuralgia, conventional imaging techniques show no abnormalities, but high- resolution MRI techniques may reveal microvascular or space occupying lesions compressing the glossopharyngeal (IX) nerve. -Carbamazepine or phenytoin (as described earlier for trigeminal neuralgia) usually produces dramatic relief; microvascular decompression has been used in drug resistant. Herpetic & Postherpetic Neuralgia Herpetic & Postherpetic Neuralgia -Varicella-zoster virus infection produces a febrile illness with a disseminated vesicular rash (chickenpox). -After the primary infection, the virus remains dormant in sensory ganglia but may reactivate, particularly with age or immunosuppression resulting in a unilateral vesicular eruptiontermed shingles. -These eruptions, which occur in a dermatomal distribution (most commonly thoracic, 50%; ophthalmic distribution of the trigeminal nerve, 25%), are associated with sharp, lancinating, localized radicular pain with dysesthesia. In patients over 50, pain may persist beyond six weeks. -Postherpetic neuralgia is characterized by constant, severe, stabbing or burning, dysesthetic pain. -In the head, the first division (V1) of the trigeminal (V) nerve is most commonly affected, so pain localized to the forehead on one side is usually the presenting feature -Scarring, resulting from healing of the vesicular rash, may be present in the distribution of pain. -Careful testing of the painful area reveals decreased cutaneous sensitivity to pinprick. -The other major complication of herpes zoster in the trigeminal distribution is decreased corneal sensation with impaired blink reflex, which can lead to corneal abrasion, scarring, and ultimately loss of vision. Persistent Idiopathic Facial Pain Persistent Idiopathic Facial Pain -Constant, boring, mainly unilateral, lower facial pain for which no cause can be found is referred to as persistent idiopathic or atypical facial pain. -Unlike trigeminal neuralgia, it is not confined to the trigeminal nerve distribution and is not paroxysmal. -Neurologic and neuroradiographic examinations are normal. -This idiopathic disorder must be distinguished from similar pain syndromes related to nasopharyngeal carcinoma, intracranial extension of squamous cell carcinoma of the face, or infection at the site of a tooth extraction. - Treatment is with amitriptyline 20 to 250 mg/d orally, alone or in combination with phenelzinen30 to 75 mg/d orally. Phenytoin can be an effective alternative especially if a tricyclic antidepressant is poorly tolerated.  Headache Primary stabbing headache Primary headache- Repeated attack of stabbing pain- occurs on di7erent area of head like temporal - region , parietal and behind the eye unilateral- Changing the site- lasting seconds-. occurs one to several times per day - treated by indomethacin - Giant Cell Arteritis -also known as temporal arteritis -systemic vasculitis -a7ects medium-sized and large arteries, especially branches of the external carotid artery. -It is characterized pathologically by subacute granulomatous inBammation (consisting of lymphocytes, neutrophils, and giant cells). - InBammation of the pain-sensitive arterial wall produces headache, and arterial stenosis leads to ischemia. -a7ects Caucasians most often, women twice as frequently as men, and is uncommon before 60 years of age. - It is frequently associated with malaise, myalgia, weight loss, arthralgia, and fever (polymyalgia rheumatica complex) due to periarticular InBammation. The most common symptom -new, nonspeciHc headache -can be unilateral or bilateral -often fairly severe and boring in quality -characteristically localized to the scalp, especially over the temporal arteries. Scalp tenderness may be especially apparent when lying with the head on a pillow or brushing the hair. -Pain or sti7ness in the jaw during chewing (jaw claudication) is highly suggestive of giant cell arteritis and is due to arterial ischemia in the muscles of mastication (the tongue may also be a7ected). Ocular involvement can manifest as transient visual obscurations in one or both eyes lasting minutes to a few hours. Diplopia from ischemia to cranial nerves or extra ocular muscles may be a presenting feature. Anterior ischemic optic neuropathy, characterized by optic disc odema in one eye , visual Held defect and primary optic atrophy results in permanent visual loss. Involvement of the ophthalmic artery may lead to sudden visual loss. Diagnosis: clinically + high ESR + positive C-reactive protein + histopathology of superHcial temporal artery. Teatment: by oral steroid for several years may be lifelong and cytotoxic drugs. Intracranial Mass Headaches associated with brain tumors are most often nonspeciHc in character, mild to moderate in severity, dull and steady in nature, and intermittent. The pain is characteristically bifrontal, worse ipsilaterally, and aggravated by a change in position or by maneuvers that increase intracranial pressure, such as coughing, sneezing, and straining. Headache is worse with bending over. Both tension or migraine type features may be found. Evidence of lateralized features on exam are most suggestive of a mass. The classic brain tumor headache (severe, early morning, and associated with nausea and vomiting) is uncommon; nausea and vomiting occur in less than half of brain tumor patients. The occurrence of headaches in brain tumor isproportional to tumor size and midline shift. Idiopathic Intracranial Hypertension It is the result of a di7use increase in intracranial pressure that can cause headache of di7use but variable character papilledema, pulsatile tinnitus, visual loss, and diplopia (from abducens [VI] nerve palsy). Impaired CSF absorption due to venous outBow obstruction may be involved in pathogenesis. Women are a7ected much more commonly than men, with a peak incidence in the third decade. Most patients are obese. Di7use headache is almost always a presenting symptom. The headaches are daily in occurrence, pulsatile or pressing, moderate in intensity, and aggravated by.coughing or straining Transient (seconds-long) visual obscurations and visual.blurring also occur in most cases Visual acuity is normal in most patients at presentation, but moderate to severe papilledema is seen in almost.all visual loss can develop from increased intracranial.pressure, which leads to optic (II) nerve atrophy Symptoms of idiopathic intracranial hypertension are generally self-limited over several months and papilledema may disappear, but CSF pressure remains elevated for years, and recurrent symptomatic episodes.occur in 10% Normal disc Papilloedema Diagnosis: 1-CT – SCAN and MRI brain showing small (“slit-like”) ventricles and demonstrate an empty sella turcica in 70% of instances. The optic nerve sheath is characteristically dilated, and the back of the globe is Battened. 2-CSF pressure is high by lumbar puncture --Elevated intracranial pressure (CSF opening pressure >250 mm H2O) is documented by lumbar puncture, and removal of 20 to 40 mL of CSF may transiently relieve headache. Cells, glucose, and protein content of the CSF are normal. 3- Investigation if there is 2ry cause (pseudotumor cerbri) like metabolic and endocrine screen , connective tissue screen , neoplastic metastatic screen, MRV for cerebral venous thrombosis Small Ventricles + E7acement of Groves Treatment 1-If pseudo tumor cerebri treat the underlying cause 2-medical therapy --acetazolamide (1000-1250 mg/d) Topiramate (50- 100 mg /d) 3- Repeated LP specially in pregnant 4-Surgical therapy by optic nerve sheath fenestration and ventriculoperitonial shunt and lumboperitonial shunt if not responding to medical therapy 5- Wt. loss 6- Corticosteroids are e7ective, but have untoward side e7ects, and papilleodema tends to rebound when they are discontinued. Intracranial hypotension Post-lumbar-puncture headache is diagnosed by a history of a dural puncture (eg, spinal tap, spinal anesthesia) and is characteristically a postural headache, with marked increase in pain in the upright position and relief with recumbency. The pain is typically occipital, comes on within 48 to 72 hours after the procedure, and lasts 1 to 2 days. Nausea and vomiting may occur. Headache is caused by persistent leak of CSF from the spinal subarachnoid space, with resultant traction on pain-sensitive structures at the base of the brain. The risk of this complication can be reduced by using a small-gauge needle (22 gauge or smaller) for the puncture. Lying Bat afterward, for any length of time, does not lessen the risk. Low-pressure headache syndromes are usually self limited. they may respond to the administration of ca7eine sodium benzoate, 500 mg intravenously, which can be repeated after 45 minutes if headache persists or recurs upon standing. In persistent cases, the subarachnoid rent can be sealed by injection of autologous blood into the epidural space at the site of the puncture; this requires an experienced anesthesiologist.  Spontaneous intracranial hypotension can produce headache similar in character to.that caused by lumbar puncture T1-weighted, gadolinium-enhanced MRI may show smooth enhancement of the pachymeninges and a“sagging brain”, the enhancement may be confused with that.associated with meningitis Low CSF pressure can produce the same MRI.picture in the absence of headache Autologous blood patch injection may produce.immediate relief Thunderclap headache Sudden and severe headache reaching maximum intensity within seconds Causes 1-subarachnoid hemorrhage 2-cerebral venous thrombosis 3-viral encephalitis 4- crash migraine