Headache & Facial Pain

Headache & Facial Pain: Definition; Headache: Pain in the head: From the orbit back to the sub- occipital region. Facial pain: Pain elsewhere in the face.  Mechanism; Traction or distention of pain sensitive structures  Pain sensitive structures  Dura of skull base  Cerebral arteries  Venous sinuses  Nerves Cranial nerves; 5, 9, 10 Cervical nerves; C2,3

Background Headache is the 4th most common symptom of outpatient visits Headache is the 4th most common symptom of outpatient visits 99% of women and 93% of men have had headache during their lifetime 99% of women and 93% of men have had headache during their lifetime 12.6 % prevalence (18% women, 6.5% men) 12.6 % prevalence (18% women, 6.5% men) Prevalence is highest between age 25 – 55 years Prevalence is highest between age 25 – 55 years 25% of women and 8% of men have had migraine headache 25% of women and 8% of men have had migraine headache Approximately 50% remain undiagnosed Approximately 50% remain undiagnosed

Headaches: Pathophysiology Where does the pain arise from? Where does the pain arise from? Scalp Scalp Dura mater Dura mater Blood vessels Blood vessels Cervical & cranial nerves Cervical & cranial nerves Blood vessels Blood vessels Dilate Dilate Become congested  Pain Become congested  Pain

Headache Classification IHS Classification Primary Headaches ( The headache is the disease ) Benign Headache disorders  Migraine (with or without aura)  Tension-type headaches  Cluster headaches  Drug rebound headaches-Medication overuse headache  Chronic daily headache Secondary Headaches Headaches that are symptoms of organic disease

Characters of Primary Headache Benign, Recurrent Benign, Recurrent NOT associated with underlying pathology NOT associated with underlying pathology The headache is the disease The headache is the disease Recurrent attacks Recurrent attacks Symptoms free between the attacks Symptoms free between the attacks Clinical syndromes Clinical syndromes Normal physical examination Normal physical examination No organic causes No organic causes Exception: drug-abuse headache Exception: drug-abuse headache Diagnosis is based on exclusion Diagnosis is based on exclusion

Characters of Secondary Headache Sudden, progressive Course Sudden, progressive Course Symptoms persist Symptoms persist Pain select to anatomical lesions Pain select to anatomical lesions Physical examination usually abnormal Physical examination usually abnormal Associated with pathology Associated with pathology May require immediate action May require immediate action

Secondary Headache SAH SAH Meningitis Meningitis Stroke Stroke SOL SOL Trigeminal Neuralgia Trigeminal Neuralgia Temporal Arteritis Temporal Arteritis Hypertension Hypertension Benign Intracranial Hypertension Benign Intracranial Hypertension Lumbar Puncture Headache Lumbar Puncture Headache Sinus Headache Sinus Headache

Secondary Headache Warning Signs and Signals Secondary Headache Warning Signs and Signals Sudden onset Sudden onset Onset after age 50 years Onset after age 50 years Systemic signs (fever, myalgias, weight loss) Systemic signs (fever, myalgias, weight loss) Systemic disease (Malignancy, AIDS) Systemic disease (Malignancy, AIDS) Change in headache pattern Change in headache pattern Progressive headache with loss of headache-free periods Progressive headache with loss of headache-free periods Change in frequency or severity Change in frequency or severity Neurologic symptoms or abnormal physical findings Neurologic symptoms or abnormal physical findings Cognitive changes Cognitive changes Asymmetry Asymmetry

Secondary Headache Paracranial Structure Areas responsible for pain: Sinus, Eye, Dental, Ear, Skull and base of skull, Vascular, Soft tissue of head and neck Character of headache Character of headache 1. Small focal area of referred pain 2. Localized tenderness 3. Local symptoms of the affected organ 4. Persistent pain

History of Presenting Complaint How recent in onset? How recent in onset? Abrupt onset? Abrupt onset? How frequent? How frequent? Episodic or constant? Episodic or constant? How long lasting? How long lasting? Intensity of pain? Intensity of pain? Quality of pain? Quality of pain? Site of pain? Site of pain? Radiation? Radiation? Eye pain? Eye pain? Aura? Aura? Photophobia? Photophobia? Phonophobia? Associated vomiting? Diurnal variation? Snoring? Neck stiffness? Trigger factors? Aggravating factors? Relieving factors? Family history? What does the patient do during headache? What medication used?

Physical Examination Fever? Fever? Pulse/BP Pulse/BP Neck stiffness? Neck stiffness? Purpuric rash? Purpuric rash? Pupils? Pupils? Neurologic exam Neurologic exam GCS score GCS score Scalp tenderness? Scalp tenderness? Examine ear drum Examine ear drum Thickened temporal arteries? Fundoscopy – papilloedema? Sinus tenderness? Cervical tenderness Obese? Facial plethora?

Localization & Characterization of HA Location: Unilateral or Bilateral Location: Unilateral or Bilateral Characteristics Characteristics Pulsating, Tightness, Dull & Steady, Sharp/Lancinating, Ice Pick Pulsating, Tightness, Dull & Steady, Sharp/Lancinating, Ice Pick Associated Symptoms Associated Symptoms Weight Loss Weight Loss Fever/Chills Fever/Chills Dyspnea Dyspnea Visual Disturbances Visual Disturbances Nausea/Vomiting Nausea/Vomiting Photophobia Photophobia

Location of pain Forehead : Primary > Secondary Forehead : Primary > Secondary Occipital area : Primary > Secondary Occipital area : Primary > Secondary Face : Secondary > Primary Face : Secondary > Primary Neck : primary = Secondary Neck : primary = Secondary Unilateral pain: Unilateral pain: - Large area  intracranial structure ( Diffuse ) - Meningeal pain - Increased intracranial pressure - Low intracranial pressure - Toxic vascular headache

In Summary…. To what extend should each patient be evaluated? Absolute clinical indications Worst headache ever Onset associated with exertion Depressed cognition or neurologic deficit on exam Nuchal signs Deterioration during observation Conservative approach acceptable in patients Lack the above findings with normal VS Improvement during observation

When to consider Imaging Studies: Recent dramatic increase in frequency or severity of HA Recent dramatic increase in frequency or severity of HA Onset of HA after 50 Onset of HA after 50 Abnormal neurologic exam or persistent neurologic deficits after HA Abnormal neurologic exam or persistent neurologic deficits after HA HA after trauma HA after trauma Transient neurologic deficits without succeeding HA First bout of basilar or ophthalmoplegic migraine Orbital or intracranial bruits

Investigations FBC FBC ESR ESR Blood glucose Blood glucose Plasma Alkaline phosphatase Plasma Alkaline phosphatase Arterial blood gas Arterial blood gas Skull radiograph Skull radiograph Cervical spine radiographs Cervical spine radiographs CT Brain CT Brain Lumbar puncture Lumbar puncture CSF manometry CSF manometry MR angiogram MR angiogram Temporal artery biopsy Temporal artery biopsy Sinus radiographs Sinus radiographs Sleep studies Sleep studies

Differential Diagnosis Tension headache Tension headache Cluster headache Cluster headache Trauma Trauma Vascular VascularMigraine Subarachnoid haemorrhage Subdural haematoma Hypertensive encephalopathy Temporal arteritis Skull disease Skull diseaseSinusitis Skull fracture Mastoiditis Paget’s disease of bone Acute mountain sickness Acute mountain sickness Medications Nitrates Sildenafil OCP Metabolic Sepsis CO 2 retention Hypoxia Obstructive sleep apnoea Hypoglycaemia Alcohol withdrawal Raised intracranial pressure Cerebral tumour Meningitis Otitis media Acute angle-closure glaucoma Hyperviscosity

Tension-Type Headache Most common headache syndrome Most common headache syndrome Episodic < 15 days per month Episodic < 15 days per month Chronic > 15 days per month (2% of population) Chronic > 15 days per month (2% of population) Lifetime prevalence of 88% (F) and 69% (M) Lifetime prevalence of 88% (F) and 69% (M) Highest prevalence in women, age 30-39, with higher education Highest prevalence in women, age 30-39, with higher education

TTH - Characteristics Often occur during or after stress Often occur during or after stress Skeletal muscle overcontraction, depression, and nausea may accompany HA Skeletal muscle overcontraction, depression, and nausea may accompany HA No prodrome No prodrome 30 minutes to 7 days 30 minutes to 7 days Dull, persistent HA ( Pressing or tightening ) Dull, persistent HA ( Pressing or tightening ) Mild to moderate pain (Usually NOT debilitating and intensity may fluctuate throughout the day ) Mild to moderate pain (Usually NOT debilitating and intensity may fluctuate throughout the day ) Variable location, often bilateral Variable location, often bilateral Nausea and vomiting rare Nausea and vomiting rare

TTH - Treatment Stress management Stress management Biofeedback Biofeedback Stress reduction Stress reduction Posture correction Posture correction Medication rarely needed Medication rarely needed Benzodiazepines Benzodiazepines amitriptyline amitriptyline CTTH Abortive NSAIDs ASA-caffeine Paracetamol Preventative Antidepressants Muscle relaxants NSAIDs

Migraine 17% of females, 6% of males ( F > M ) 17% of females, 6% of males ( F > M ) Moderate to severe pain Moderate to severe pain 4 to 72 hours 4 to 72 hours Typically - Unilateral (may be bilateral), pulsating (progresses from dull ache to pulsating pain) Typically - Unilateral (may be bilateral), pulsating (progresses from dull ache to pulsating pain) Moderate or severe intensity, aggravated by routine physical activity and associated w/ nausea, photo & phonophobia Moderate or severe intensity, aggravated by routine physical activity and associated w/ nausea, photo & phonophobia Sub classified to Aura or No Aura Sub classified to Aura or No Aura

Migraines - Causation Sterile inflammation of intracranial vessels - trigeminovascular system Sterile inflammation of intracranial vessels - trigeminovascular system Serotonin (5- hydroxytryptamine) receptors Serotonin (5- hydroxytryptamine) receptors Triggering factors Stress Menses OCP Infection Trauma Vasodilators Aged cheeses

Aura Occurs with Migraine in about 30% of cases Occurs with Migraine in about 30% of cases Complex of focal neurologic symptoms Complex of focal neurologic symptoms alterations in vision or sensation alterations in vision or sensation Usually begin 10 minutes to 1 hr prior to onset of head pain Usually begin 10 minutes to 1 hr prior to onset of head pain Light headedness and photophopsia (unformed flashes of light) Light headedness and photophopsia (unformed flashes of light) Scotoma- Isolated area within the visual field where vision is absent (30% of cases) Scotoma- Isolated area within the visual field where vision is absent (30% of cases) Scintillating scotoma Scintillating scotoma

Migraine - Treatment Abortive Abortive 5- hydroxytryptamin e receptor agonists 5- hydroxytryptamin e receptor agonists Imitrex (Oral, SQ, nasal spray ) Imitrex (Oral, SQ, nasal spray ) Maxalt Maxalt Zomig Zomig Amerge Amerge Symptomatic Ergotamine Chlorpromazine Haloperidol Lorazepam NSAIDs Lidocaine Preventative Preventative Antidepressa nts Antidepressa nts Bellergal (ergotamine) Bellergal (ergotamine) NSAIDs NSAIDs  -blockers  -blockers Calcium channel blockers Calcium channel blockers

Cluster Headache

Cluster Headaches (HA) M>F (5:1), usually years old M>F (5:1), usually years old Recurrent HA separated by periods of remission (months to years) Recurrent HA separated by periods of remission (months to years) During the “cluster”time -HA occur >1/day During the “cluster”time -HA occur >1/day Unilateral, occurs behind eye, reaches maximal intensity over few minutes, lasts for <3hrs Unilateral, occurs behind eye, reaches maximal intensity over few minutes, lasts for <3hrs Unilateral lacrimation, rhinorrhea, and facial flushing may accompany cluster Unilateral lacrimation, rhinorrhea, and facial flushing may accompany cluster HA is commonly precipitated by alcohol, stress, missed meals and vasodilating drugs - (Avoid during cluster period) HA is commonly precipitated by alcohol, stress, missed meals and vasodilating drugs - (Avoid during cluster period) No Aura No Aura

Cluster Headache Intensely severe pain Intensely severe pain Unilateral Unilateral Periorbital Periorbital 15 to 180 minutes 15 to 180 minutes Nausea and vomiting uncommon Nausea and vomiting uncommon No aura No aura Alcohol intolerance Male predominance Autonomic hyperactivity Conjunctival injection Lacrimation Nasal congestion Ptosis

Cluster Headache - Treatment Preventative Preventative Calcium channel blockers Calcium channel blockers Lithium Lithium Methysergide Methysergide Steroids Steroids Valproate Valproate Antihistamines Antihistamines Abortive Oxygen 5-HT receptor agonists Intranasal lidocaine

Chronic Headaches Analgesic/Caffeine Withdrawal Headaches Analgesic/Caffeine Withdrawal Headaches Associated with intake of high doses of caffeine and/or analgesics Associated with intake of high doses of caffeine and/or analgesics Pathophysiology Pathophysiology Serum level drop Serum level drop Clinical Presentation Clinical Presentation Constant Constant Atypical Atypical After noon After noon History is the key History is the key

Acute Headache (HA) May be symptomatic of May be symptomatic of Subarachnoid hemorrhage (SAH), stroke, Meningitis, Intracranial mass lesion (e.g. brain tumor, hematoma, abscess) Subarachnoid hemorrhage (SAH), stroke, Meningitis, Intracranial mass lesion (e.g. brain tumor, hematoma, abscess) SAH headache - “worst HA of my life”, may also see alteration in mental status and focal neurologic signs SAH headache - “worst HA of my life”, may also see alteration in mental status and focal neurologic signs Meningitis HA - usually bilateral, develops over hrs to days, may also see fever, photophobia, positive meningeal signs (Kernigs’s Brudzinski) Meningitis HA - usually bilateral, develops over hrs to days, may also see fever, photophobia, positive meningeal signs (Kernigs’s Brudzinski)

Headaches of Acute Onset Subarachnoid Hemorrhage (SAH) Subarachnoid Hemorrhage (SAH) Background Background Aneurysms & AVM’s Aneurysms & AVM’s Clinical Presentation Clinical Presentation Signs & Symptoms Signs & Symptoms NEW, Sudden onset, LOC frequent, Vomiting & stiff neck NEW, Sudden onset, LOC frequent, Vomiting & stiff neck Lab Findings Lab Findings CT & Lumbar Puncture CT & Lumbar Puncture Complications Complications Reoccurnance doubles mortality rate Reoccurnance doubles mortality rate Prognosis Prognosis 20% DOA 20% DOA 25% die from initial bleed; 20% from reoccurance 25% die from initial bleed; 20% from reoccurance Survival Survival

Headaches of Acute Onset Infectious Headaches Infectious Headaches Background Background Meningitis and Encephalitis Meningitis and Encephalitis Clinical Presentation Clinical Presentation Classic: HA, Fever, Stiff Neck, & Altered Level of Consciousness Classic: HA, Fever, Stiff Neck, & Altered Level of Consciousness S/S can vary depending on age S/S can vary depending on age Neonate, Children & Adults, Adults, Older generation Neonate, Children & Adults, Adults, Older generation Headache Presentation Headache Presentation Diagnosis & Management: Diagnosis & Management: CSF analysis CSF analysis Neurologist Neurologist

Headaches of Acute Onset Headaches Following Lumbar Puncture Headaches Following Lumbar Puncture Background Background Low Pressure Headache Low Pressure Headache MC is lumbar puncture MC is lumbar puncture Headache Presentation Headache Presentation Clinical Pearl: Clinical Pearl: Worse with sitting or standing Worse with sitting or standing Vertex or occipital, pulling, steady Vertex or occipital, pulling, steady Usually resolve spontaneously (Blood patch for resistant cases ) Usually resolve spontaneously (Blood patch for resistant cases ) The more severe the HA, the more frequent it is assoc. w/ vertigo, nausea/vomiting, & tinnitus The more severe the HA, the more frequent it is assoc. w/ vertigo, nausea/vomiting, & tinnitus The longer the pt is upright, the longer it takes for the HA to subside The longer the pt is upright, the longer it takes for the HA to subside

Subacute Headache (HA) May be symptomatic of May be symptomatic of Increased intracranial pressure Increased intracranial pressure Intracranial mass lesion Intracranial mass lesion Temporal arteritis Temporal arteritis Sinusitis Sinusitis Trigeminal neuralgia Trigeminal neuralgia

Temporal Arteritis = Giant Cell Arteritis Classic presentation is a 50 plus year old female with unilateral HA that is causing unilateral visual disturbance. Intensity is moderate to severe and will be insidious in onset. Classic presentation is a 50 plus year old female with unilateral HA that is causing unilateral visual disturbance. Intensity is moderate to severe and will be insidious in onset. Moderate to severe, unilateral pain Moderate to severe, unilateral pain Patients over 65 Patients over 65 Tortuous scalp vessels Tortuous scalp vessels ESR elevated ESR elevated Biopsy for definitive diagnosis Biopsy for definitive diagnosis Treat with steroids Treat with steroids Untreated complicated by vision loss Untreated complicated by vision loss Other findings: Other findings: Jaw claudication Jaw claudication Bruits over temporal artery Bruits over temporal artery Blindness Blindness May be accompanied by polymyalgia rheumatica. May be accompanied by polymyalgia rheumatica.

Trigeminal Neuralgia= Tic Douloureux Paroxysmal pain – seconds to < 2 min Paroxysmal pain – seconds to < 2 min Distributed along 5 th cranial nerve ( V2 & V3 ) Distributed along 5 th cranial nerve ( V2 & V3 ) Asymptomatic between attacks Asymptomatic between attacks Trigger points ( triggered by talking, chewing, shaving) Trigger points ( triggered by talking, chewing, shaving) Intense burning Intense burning Face may distort = tic Face may distort = tic >40, F>M, >40, F>M, Characterized by sudden intense pain that recurs paroxysmally, occurs along the second or third division of trigeminal nerve and lasts only moments, Characterized by sudden intense pain that recurs paroxysmally, occurs along the second or third division of trigeminal nerve and lasts only moments,

Trigeminal Neuralgia - Treatment Carbamazepine Carbamazepine Gabapentin Gabapentin Baclofen Baclofen Phenytoin Phenytoin Valproate Valproate Chlorphenesin Chlorphenesin Adjuvant TCAs NSAIDs Surgery for refractory cases

Herpes zoster Facial pain Herpetic eruption in territory of nerve in distribution of nerve (10 – 15% the trigeminal ganglion and 80% the ophthalmic division) Herpetic eruption in territory of nerve in distribution of nerve (10 – 15% the trigeminal ganglion and 80% the ophthalmic division) Geniculate ganglion causes eruption in the EAM. Geniculate ganglion causes eruption in the EAM. Upper cervical nerve roots affects soft palate. Upper cervical nerve roots affects soft palate. Pain precedes herpetic eruption by <7 days Pain precedes herpetic eruption by <7 days Pain resolves within 3 months Pain resolves within 3 months Postherpetic Neuralgia Postherpetic Neuralgia Neuralgia of the trigeminal nerve following herpes infection. Neuralgia of the trigeminal nerve following herpes infection. Most commonly affects V1 as well as V2 & V3 Most commonly affects V1 as well as V2 & V3 This is the KEY difference between post-herpetic and trigeminal neuralgia. This is the KEY difference between post-herpetic and trigeminal neuralgia.

Post-Herpetic Neuralgia Persistent neuritic pain for > 2 months after acute eruption Persistent neuritic pain for > 2 months after acute eruption Treatment Treatment Anticonvulsants Anticonvulsants TCAs TCAs Baclofen Baclofen

Glossopharyngeal Neuralgia Severe (Unilateral pain ) Severe (Unilateral pain ) Transient stabbing pain in the ear, base of tongue, tonsillar fossa, or beneath the angle of the jaw. (auricular and pharyngeal branches of the vagus nerve and glossopharyngeal nerve) Transient stabbing pain in the ear, base of tongue, tonsillar fossa, or beneath the angle of the jaw. (auricular and pharyngeal branches of the vagus nerve and glossopharyngeal nerve) Evoked by swallowing, talking, or coughing Evoked by swallowing, talking, or coughing Treatment as for Trigeminal Neuralgia Treatment as for Trigeminal Neuralgia

Occipital Neuralgia Paroxysmal jabbing pain in the distribution of the greater and lesser occipital nerves or the third occipital nerve Paroxysmal jabbing pain in the distribution of the greater and lesser occipital nerves or the third occipital nerve Sometimes diminished sensation Sometimes diminished sensation Pain is eased by local anaesthetic block Pain is eased by local anaesthetic block Must be distinguished from occipital referral of pain from the atlantoaxial or upper zygoapophyseal joint or trigger points in suboccipital muscles Must be distinguished from occipital referral of pain from the atlantoaxial or upper zygoapophyseal joint or trigger points in suboccipital muscles

Posttraumatic Headache(PTHA) Estimated that 30-50% of 2 million closed head injuries per year develop headache. Estimated that 30-50% of 2 million closed head injuries per year develop headache. Associated with dizziness, fatigue, insomnia, irritability, memory loss, and difficulty with concentration. Associated with dizziness, fatigue, insomnia, irritability, memory loss, and difficulty with concentration. Acute PTHA develops hours to days after injury and may last up to 8 weeks. Acute PTHA develops hours to days after injury and may last up to 8 weeks. Chronic PTHA may last from several months to years. Patients have normal neurological examination and imaging Treatment for acute PTHA is symptomatic while for chronic PTHA, adjunct therapies include beta- blockers and antidepressants.

Atypical Facial Pain Diagnosis of exclusion Diagnosis of exclusion ? Psychogenic facial pain ? Psychogenic facial pain Location and description inconsistent Location and description inconsistent Women, 30 – 50 years old Women, 30 – 50 years old Usually accompanies psychiatric diagnosis Usually accompanies psychiatric diagnosis Treat with antidepressants Treat with antidepressants

Temporomandibular Disorders Symptoms Symptoms Temporal headache Temporal headache Earache Earache Facial pain Facial pain Trismus Trismus Joint noise Joint noise 60% spontaneous 60% spontaneous Tenderness to palpation Tenderness to palpation Pain with movement Pain with movement Audible click Audible click

Myofascial Pain Most common 60% - 70% Most common 60% - 70% Muscle pain dominates Muscle pain dominates Tenderness to palpation of masticatory muscles Tenderness to palpation of masticatory muscles

TMD - Treatment NSAIDs NSAIDs Physical therapy Physical therapy Biofeedback Biofeedback Trigger point injection Trigger point injection Benzodiazepines Benzodiazepines TCAs or SSRIs for chronic muscle pain TCAs or SSRIs for chronic muscle pain

Pseudotumor Cerebri Intermittent headache Intermittent headache Variable intensity Variable intensity Normal exam except papilledema Normal exam except papilledema Normal imaging Normal imaging CSF pressures > 200 cm H 2 O CSF pressures > 200 cm H 2 O

Pseudotumor Cerebri - Associated History Mastoid or ear infection Mastoid or ear infection Menstrual irregularity Menstrual irregularity Steroid exposure Steroid exposure Retro-orbital or vertex headache Retro-orbital or vertex headache Vision fluctuation Unilateral or bilateral tinnitus Constriction of visual fields Weight gain

Idiopathic Intracranial Hypertension(IIP) Treatment Treatment -Stop offending med -Lower CSF production with acetazolomide and furosemide. -Steroids -Repeat LPs -Ventricular shunt if with impending visual loss. Diagnostic Criteria for IIP Increased intracranial pressure(>200mmHg) measured by lumbar puncture Signs and symptoms of increased ICP, without localizing signs No mass lesions or hydrocephalus on imaging Normal or low CSF protein No clinical or neuroimaging suspicion of venous sinus thrombosis

Mass Lesion - Brain Tumor Children - 75% Infratentorial Children - 75% Infratentorial Adults - 75% Supratentorial Adults - 75% Supratentorial Metastatic tumor most common mid-life Metastatic tumor most common mid-life Symptoms due to increased intracerebral pressure, tissue destruction, irritation Symptoms due to increased intracerebral pressure, tissue destruction, irritation Depends on growth rate and location Depends on growth rate and location Headache ( 30 % ) - steady, non-throbbing, dull, worse in AM. May be intermittent initially. Headache ( 30 % ) - steady, non-throbbing, dull, worse in AM. May be intermittent initially. Headache worse with bending over, Valsalva maneuvers Headache worse with bending over, Valsalva maneuvers Hx of IV drug abuse - abscess Hx of IV drug abuse - abscess

Hypertension Usually with diastolic pressures > 115 mm Hg Usually with diastolic pressures > 115 mm Hg Throbbing Throbbing Nausea Nausea

Sinus Headache Acute sinusitis accepted Acute sinusitis accepted Chronic sinusitis controversial Chronic sinusitis controversial Constant, dull, aching Constant, dull, aching Worsened with stooping or leaning forward Worsened with stooping or leaning forward Referred pain possible Referred pain possible

“ RED FLAG “ Headaches Headache with altered mental status Headache with altered mental status Headache with focal neurological findings Headache with focal neurological findings Headache with papillidema Headache with papillidema Headache with meningeal signs Headache with meningeal signs The “worst headache of life” The “worst headache of life” Headache in the patient with AIDS Headache in the patient with AIDS

Conclusion Headache & facial pain are common complaints Headache & facial pain are common complaints History most important in making accurate diagnosis History most important in making accurate diagnosis Recognize psychological aspects of pain Recognize psychological aspects of pain