PostConcussion Headaches Charles Clarke MD Assistant Professor of

Post-Concussion Headaches Charles Clarke, MD Assistant Professor of Neurology Vanderbilt Williamson Neurology

History of Concussion • Initially brought to the interest of the medical community by Dr. Joseph Babinski. Due to blast injuries of WWI soldiers. • Now appropriately at the forefront of popular culture due to prominent athletes being concussed and its relationship to chronic traumatic encephalopathy.

Definitions of Concussion • The latin meaning for concuss literally means to “shake violently” or “dash [strike] together” • Clinically, though it is a “syndrome of neurocognitive and behavioral dysfunction due to alteration in brain physiology due to a mechanical injury. ” • Often used synonymously with mild TBI • Mild TBI is a GCS of 13 -15

Objectives • Discuss the epidemiology of post-concussion headaches • Discuss the evaluation of post-concussion headaches. • Explain the management of post-concussion headaches.

Epidemiology • There is a widely variable incidence of postconcussion headaches between 25%-78% of patients with mild TBI. • Post-concussion headaches are unexpectedly more prevalent, greater in severity, and greater in duration after mild TBI than more severe TBI.

Headache Type • Post-traumatic headaches according to the International Headache Society (HIS) can be classified as migraine and/or tension headaches most commonly. • Other headache types include: occipital neuralgia, vascular dissections, trigeminal neuralgia, low CSF pressure headaches, hemicranias continua, etc. • Many patients with have more than one headache type.

Tension Headache • Typically this pain is a dull pressure or sensation of tightness. • This is classically described as band-like wrapping around the head, but can be located essentially anywhere. • Patient is able to remain active typically • No other associated symptoms • Can be acute or chronic

Tension Headache Treatment • NSAIDS are the mainstay of acute tension headache treatment, butalbital/caffeine/APAP preparations can be used as well in moderation. • Tricyclic antidepressants are often used for prevention of chronic tension headaches. • Due to short acting pain medication use co-morbid medication overuse headache or rebound headache is commonly associated with this.

Rebound Headache • Highest risk ▫ Opiods ▫ Butalbital compounds ▫ ASA/acetaminophen/caffeine combos • Lower risk ▫ -triptans/ergots ▫ NSAIDS

Rebound Headache • Paramount in treatment is the withdrawal of the offending medication for at least 2 weeks ▫ Taper opiods or use clonidine patch ▫ Butalbital withdraw 100 mg of butalbital = 30 mg of phenobarb OR 30 mg phenobarb BID x 2 wks then 15 mg BID x 2 wks ▫ You can abruptly stop other offending medications

Rebound Headache • Use a bridge therapy ▫ Long acting NSAIDS ▫ Tizanidine ▫ Steroids • 2 weeks of treatment with naproxen and tizanidine has been shown to be helpful for headache management during the withdrawal period. • Start prophylactic medication for primary headache condition

Migraine • In general there is a cumulative lifetime prevalence of ▫ 43% in women ▫ 18% in men • Estrogen’s role in migraine is thought to be due to it increasing NO synthase activity.

Migraine • Most often a lateralized, moderate to severe, throbbing head pain • Associated with additional features such as nausea, vomiting, photophobia, phonophobia, and/or aura • Can be episodic or chronic

Migraine • Where does the pain originate? ▫ Trigeminovascular system: dura, arteries, venous sinuses, CNs, cranial musculoskeletal components, and nasal sinuses. • What causes aura? ▫ Cortical spreading depression of depolarization partially under the influence of NO

Migraine Treatment • Acute migraine can be treated with NSAIDS, various –triptans, and less commonly DHE preparations. • Migraine preventatives ▫ Class A evidence: Beta blockers, topiramate, valproic acid ▫ Others: TCAs, venlafaxine, verapamil, ACEinhibitors

Acute Migraine Treatment • Non-specific acute treatments ▫ NSAIDs ▫ Dopamine antagonists Prochlorperazine Metaclopramide ▫ Antihistamine Promethazine ▫ Serotonin antagonist Ondancetron ▫ Corticosteroids

Acute Migraine Treatment • Specific acute treatments ▫ Triptans Mechanism Vasoconstriction via 5 HT receptor modulation Peripheral neuronal inhibition Dorsal horn stimulation causing 2 nd order brain stem inhibition ▫ Ergots Less specific than triptans, but similar mechanisms

Emergency Rescue Treatment • “Migraine cocktail” ▫ ▫ ▫ Sumatriptan sub. Q Anti-emetic IM NSAID (ketorolac) Magnesium IV IV valproic acid Consider Corticosteroids Opiates

Migraine Prevention • Best data (Level A) ▫ Beta blockers (propranolol, timolol, and metoprolol) ▫ Valproic acid ▫ Topiramate • Next best (Level B) ▫ Amitriptyline ▫ Venlafaxine

Migraine Prevention • Others commonly used ▫ ▫ ▫ Nortriptyline Verapamil Gabapentin Pregabalin Ace-inhibitors

Alternative Migraine Treatments • • Coenzyme Q 10 Riboflavin Magnesium Butterbur ▫ Can be carcinogenic, teratogenic, and hepatoxic • Feverfew • • ▫ Migrelief B-complex vitamins Acupuncture Trigger avoidance Cognitive behavioral therapy

Chronic Intractable Migraine • Defined as >=15 headache days per month lasting >=4 hours with the failure of 2 or more preventative medications from separate classes. • Current mainstay of treatment is onabotulinum toxin A injection. ▫ 155 un divided equally over 31 sites ▫ Injected every 12 weeks

Hemicrania Continua • The location is frontal, retro-orbital, or temporal • Pain is widely variable in severity and nature, but is usually unrelenting • Often associated with cranial autonomic symptoms • Response to indomethacin is required by strict diagnostic definition

Hemicrania Continua Treatment • Indomethacin is the mainstay of treatment ▫ Dosing 25 -75 mg every 8 hours is typical (doses up to 200 mg per day are used) ▫ Often limited by GI side effects ▫ Other oral alternatives: COX-2 inhibitors, topiramate, verapamil, melatonin, and gabapentin ▫ Rare invasive treatments include onabotulinum toxin A injection, vagus nerve stimulation, and occipital nerve stimulation

Occipital Neuralgia • Occipital head pain or dysesthesias that are caused by irritation or damage to the occipital or upper cervical nerves. • Greater occipital nerve originates from the 2 nd cervical nerve and perforates the semispinalis capitus and trapezius muscles. • Can be unilateral or bilateral

Occipital Neuralgia • Diagnosis ▫ ▫ Paroxyms of pain in the correct distribution Dysesthesia or allodynia to the area Occipital tender points Pain improved by occipital nerve block

Occipital Neuralgia • Conservative management ▫ Heat or cold compresses • Occipital nerve block • Medical management ▫ TCAs, Carbemazepine, or gabapentin • Rarely, occipital nerve stimulation

Occipital Nerve Block Lesser occipital nerve

Other Associated Head Pain • Trigeminal neuralgia • Low pressure headache • Traumatic vascular dissections • Cluster headaches

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