170
January 2014
authorizing use of Botox. Patients are exposed to potential systemic side effects to drugs that are not FDA approved for CM. Delaying the use of Botox with unproven, non-FDA-approved therapies only increases the risk of refractory chronification of CM.5 4. Botox should be utilized for the treatment of CM without first requiring treatment with non-FDAapproved drug treatments. James A. Charles, MD Department of Neurosciences, New Jersey Medical School, Bayonne, NJ, USA
REFERENCES 1. https://www.unitedhealthcareonline.com/ccmcontent/ ProviderII/UHC/en-US/Assets/ProviderStatic Files/ProviderStaticFilesPdf/Tools%2520and%2520 Resources/Policies%2520and%2520Protocols/Medical %2520Policies/Drug%2520Policies/Botulinum_toxin _policy.pdf. 2. http://www.cigna.com/health/provider/medical/forms/ Botox-041310.pdf. 3. https://services3.horizon-bcbsnj.com/hcm/MedPol2.nsf. 4. https://www.oxhp.com/secure/policy/botox _commercial_711.html. 5. Scher AI, Lipton RB, Stewart W. Risk factors for chronic daily headache. Curr Pain Headache Rep. 2002;6:486-491.
Vagus Nerve Stimulation for Refractory Cluster Headaches Tepper and Stillman provide an excellent overview of treatment options in refractory cluster headache patients.1 While they mention noninvasive vagus nerve stimulation (VNS), they fail to discuss a possibly more effective option, from which the idea for noninvasive VNS was derived. This option is VNS using an implanted electrode that provided very good relief in both patients with refractory cluster headaches in whom it was tried.2 VNS is approved by the Food and Drug Administration for refractory epilepsy and depression, and considering that anticonvulsants and antidepressants are effective in the treatment of headaches, it is likely that VNS will work for headache patients as well. Alexander Mauskop, MD, FAAN Neurology, New York Headache Center, New York, NY, USA
REFERENCES 1. Tepper SJ, Stillman MJ. Cluster headache: Potential options for medically refractory patients (when all else fails). Headache. 2013;53:1183-1190. 2. Mauskop A. Vagus nerve stimulation relieves chronic refractory migraine and cluster headaches. Cephalalgia. 2005;25:82-86.
Classification Challenge in Migrainous Infarction The International Classification of Headache Disorders, 3rd Edition (ICHD-3) beta version defines migrainous infarction as 1 or more otherwise typical aura symptoms that persist beyond 1 hour with neuroimaging confirmation of an ischemic infarction in the affected territory.1 Here we describe a woman with migraine with brainstem aura, who experienced acute-onset left sensorimotor deficits in addition to her typical aura symptoms in the midst of a prolonged, but otherwise typical attack. Magnetic resonance imaging (MRI) of the brain revealed a pontine lesion consistent with an ischemic stroke. Our case illustrates potential limitations of the ICHD-3 beta definition of migrainous infarction. Our patient developed episodic headaches that fulfilled ICHD-3 beta criteria for episodic migraine without aura in her adolescence.1 At the age of 30, she began to experience episodes of transient neurological symptoms antecedent to her typical headache attacks. The symptoms included vertigo, tinnitus, hypacusis, gait unsteadiness, disorientation, and severe nausea and vomiting slowly evolving over hours, lasting 1-5 days prior to the onset of headache and usually continuing throughout the duration of a headache attack. On occasion, she would experience the symptom complex without associated headache. Postictal neurologic examination and brain MRI at that time were unremarkable. At the age of 42, she developed the typical constellation of aura symptoms followed by a 2-week period of status migrainosus. Several days into the headache phase, she experienced acute, maximal-at-onset dysarthria and left face, Conflicts of Interest: Dr.Vollbracht has received honoraria from the American Headache Society. Dr. Robbins has received honoraria from Medlink Neurology and book royalties from Headache (Neurology in Practice Series). Dr. Kister reports no disclosures. Study Funding: None.
Headache arm, and leg numbness and weakness.These symptoms minimally improved over several weeks, leaving her with mild residual left-sided sensorimotor deficits and dysarthria. At the time of the event, the patient took eletriptan 40 mg once or twice daily as well as an estrogen-containing oral contraceptive, fluoxetine, pseudoephedrine, alprazolam, and synthroid. Fourteen months later, she underwent MRI of the brain, which revealed non-enhancing T2-weighted/FLAIR hyperintensities predominantly in the right pontine tegmentum. The lesion was slightly hypointense on T1-weighted sequence. No other abnormalities were noted. Medical history included Hashimoto’s thyroiditis, depression, anxiety, and osteopenia, but not spontaneous abortions or coagulopathy. Both her paternal grandmother and father suffered from migraine, and her father died suddenly at 49 from a suspected stroke. There was no family history of seizures, early onset dementia, or thrombophilia. The patient denied tobacco, alcohol, or illicit drug use. Neurologic examination in our clinic 2 years after the acute event was significant for hypometric horizontal saccades in both directions, decreased sensation in the left trigeminal distribution, incomplete left ptosis without anisocoria, and partial left lower facial weakness. Fine finger movements in the left hand were decreased, and there was cupping of the left hand on extension, but no weakness was detected on confrontation testing. Sensation was decreased to all modalities in the left arm and leg. There was moderate dysmetria and dysdiadochokinesia on the left hand and postural tremor bilaterally. Gait was mildly spastic. Aside from elevated thyroid peroxidase antibody titers, an extensive hypercoagulable and rheumatological work-up, as well as genetic testing for cerebral autosomal dominant arteriopathy with subcortical infarcts and leukoencephalopathy and serum lactic acid and pyruvate, was unrevealing. Cerebrospinal fluid examination was unremarkable, including IgG index, cytology, Lyme antibody, and absent oligoclonal bands. Magnetic resonance angiogram of the head without contrast revealed fenestration of the proximal basilar artery. MRI of the cervical cord without contrast, electroencephalogram, optical coherence tomography, electromyelogram, nerve conduction studies, carotid ultrasound, and transthoracic echocardiogram were normal. Triptans were immediately discontinued, and topiramate and magnesium oxide were initiated as prophylactic therapy with dramatic reduction in headache frequency and severity. No new symptoms developed during the 4-year observation period. A follow-up MRI of the brain was unchanged.
171 Our patient with no traditional vascular risk factors or coagulopathy experienced brainstem stroke during status migrainosus with her typical brainstem aura. It is plausible that migraine was a contributing factor to the stroke, especially in view of evidence that brain hypoperfusion2 and basilar artery narrowing, and even occlusion,3 occur during migraine with brainstem aura. Other potential contributory factors included repetitive triptan use, treatment with estrogen-containing oral contraceptive, pseudoephedrinecontaining compound, selective serotonin reuptake inhibitor use, and basilar artery fenestration. Despite compelling arguments for a link between migraine and stroke in our patient and others,3 the patient would not be diagnosed with migrainous infarction according to the ICHD-3 beta criteria because her stroke symptoms were not part of her typical aura syndrome. By excluding patients with “extra-aural” symptoms at the time of infarction, ICHD-3 beta likely improves specificity of migrainous infarction criteria at the expense of sensitivity. This may lead to an underestimation of the role of migraine in stroke etiology. We would like to argue that a less restrictive category – “probable migrainous infarction” or “migraine-associated stroke” – could be introduced in the appendix to the final ICHD-3 to account for such patients who experience additional non-aura stroke symptoms during an otherwise typical migraine with aura attack, as we believe such cases truly are complications of migraine. Sarah Vollbracht, MD; Matthew S. Robbins, MD; Ilya Kister, MD From the Montefiore Headache Center, Saul R. Korey Department of Neurology, Albert Einstein College of Medicine, Bronx, NY, USA (S. Vollbracht and M.S. Robbins); Department of Neurology, NYU–Multiple Sclerosis Center, New York University School of Medicine, New York, NY, USA (I. Kister).
REFERENCES 1. Headache Classification Committee of the International Headache Society (IHS). The international classification of headache disorders, 3rd edition (beta version). Cephalalgia. 2013;33:629-808. 2. Seto H, Shimizu M, Futatsuya R, et al. Basilar artery migraine reversible ischemia demonstrated by Tc-99m HMPAO brain SPECT. Clin Nucl Med. 1994;19:215-218. 3. Caplan LR. Migraine and vertebrobasilar ischemia. Neurology. 1991;41:55-61.
January 2014
authorizing use of Botox. Patients are exposed to potential systemic side effects to drugs that are not FDA approved for CM. Delaying the use of Botox with unproven, non-FDA-approved therapies only increases the risk of refractory chronification of CM.5 4. Botox should be utilized for the treatment of CM without first requiring treatment with non-FDAapproved drug treatments. James A. Charles, MD Department of Neurosciences, New Jersey Medical School, Bayonne, NJ, USA
REFERENCES 1. https://www.unitedhealthcareonline.com/ccmcontent/ ProviderII/UHC/en-US/Assets/ProviderStatic Files/ProviderStaticFilesPdf/Tools%2520and%2520 Resources/Policies%2520and%2520Protocols/Medical %2520Policies/Drug%2520Policies/Botulinum_toxin _policy.pdf. 2. http://www.cigna.com/health/provider/medical/forms/ Botox-041310.pdf. 3. https://services3.horizon-bcbsnj.com/hcm/MedPol2.nsf. 4. https://www.oxhp.com/secure/policy/botox _commercial_711.html. 5. Scher AI, Lipton RB, Stewart W. Risk factors for chronic daily headache. Curr Pain Headache Rep. 2002;6:486-491.
Vagus Nerve Stimulation for Refractory Cluster Headaches Tepper and Stillman provide an excellent overview of treatment options in refractory cluster headache patients.1 While they mention noninvasive vagus nerve stimulation (VNS), they fail to discuss a possibly more effective option, from which the idea for noninvasive VNS was derived. This option is VNS using an implanted electrode that provided very good relief in both patients with refractory cluster headaches in whom it was tried.2 VNS is approved by the Food and Drug Administration for refractory epilepsy and depression, and considering that anticonvulsants and antidepressants are effective in the treatment of headaches, it is likely that VNS will work for headache patients as well. Alexander Mauskop, MD, FAAN Neurology, New York Headache Center, New York, NY, USA
REFERENCES 1. Tepper SJ, Stillman MJ. Cluster headache: Potential options for medically refractory patients (when all else fails). Headache. 2013;53:1183-1190. 2. Mauskop A. Vagus nerve stimulation relieves chronic refractory migraine and cluster headaches. Cephalalgia. 2005;25:82-86.
Classification Challenge in Migrainous Infarction The International Classification of Headache Disorders, 3rd Edition (ICHD-3) beta version defines migrainous infarction as 1 or more otherwise typical aura symptoms that persist beyond 1 hour with neuroimaging confirmation of an ischemic infarction in the affected territory.1 Here we describe a woman with migraine with brainstem aura, who experienced acute-onset left sensorimotor deficits in addition to her typical aura symptoms in the midst of a prolonged, but otherwise typical attack. Magnetic resonance imaging (MRI) of the brain revealed a pontine lesion consistent with an ischemic stroke. Our case illustrates potential limitations of the ICHD-3 beta definition of migrainous infarction. Our patient developed episodic headaches that fulfilled ICHD-3 beta criteria for episodic migraine without aura in her adolescence.1 At the age of 30, she began to experience episodes of transient neurological symptoms antecedent to her typical headache attacks. The symptoms included vertigo, tinnitus, hypacusis, gait unsteadiness, disorientation, and severe nausea and vomiting slowly evolving over hours, lasting 1-5 days prior to the onset of headache and usually continuing throughout the duration of a headache attack. On occasion, she would experience the symptom complex without associated headache. Postictal neurologic examination and brain MRI at that time were unremarkable. At the age of 42, she developed the typical constellation of aura symptoms followed by a 2-week period of status migrainosus. Several days into the headache phase, she experienced acute, maximal-at-onset dysarthria and left face, Conflicts of Interest: Dr.Vollbracht has received honoraria from the American Headache Society. Dr. Robbins has received honoraria from Medlink Neurology and book royalties from Headache (Neurology in Practice Series). Dr. Kister reports no disclosures. Study Funding: None.
Headache arm, and leg numbness and weakness.These symptoms minimally improved over several weeks, leaving her with mild residual left-sided sensorimotor deficits and dysarthria. At the time of the event, the patient took eletriptan 40 mg once or twice daily as well as an estrogen-containing oral contraceptive, fluoxetine, pseudoephedrine, alprazolam, and synthroid. Fourteen months later, she underwent MRI of the brain, which revealed non-enhancing T2-weighted/FLAIR hyperintensities predominantly in the right pontine tegmentum. The lesion was slightly hypointense on T1-weighted sequence. No other abnormalities were noted. Medical history included Hashimoto’s thyroiditis, depression, anxiety, and osteopenia, but not spontaneous abortions or coagulopathy. Both her paternal grandmother and father suffered from migraine, and her father died suddenly at 49 from a suspected stroke. There was no family history of seizures, early onset dementia, or thrombophilia. The patient denied tobacco, alcohol, or illicit drug use. Neurologic examination in our clinic 2 years after the acute event was significant for hypometric horizontal saccades in both directions, decreased sensation in the left trigeminal distribution, incomplete left ptosis without anisocoria, and partial left lower facial weakness. Fine finger movements in the left hand were decreased, and there was cupping of the left hand on extension, but no weakness was detected on confrontation testing. Sensation was decreased to all modalities in the left arm and leg. There was moderate dysmetria and dysdiadochokinesia on the left hand and postural tremor bilaterally. Gait was mildly spastic. Aside from elevated thyroid peroxidase antibody titers, an extensive hypercoagulable and rheumatological work-up, as well as genetic testing for cerebral autosomal dominant arteriopathy with subcortical infarcts and leukoencephalopathy and serum lactic acid and pyruvate, was unrevealing. Cerebrospinal fluid examination was unremarkable, including IgG index, cytology, Lyme antibody, and absent oligoclonal bands. Magnetic resonance angiogram of the head without contrast revealed fenestration of the proximal basilar artery. MRI of the cervical cord without contrast, electroencephalogram, optical coherence tomography, electromyelogram, nerve conduction studies, carotid ultrasound, and transthoracic echocardiogram were normal. Triptans were immediately discontinued, and topiramate and magnesium oxide were initiated as prophylactic therapy with dramatic reduction in headache frequency and severity. No new symptoms developed during the 4-year observation period. A follow-up MRI of the brain was unchanged.
171 Our patient with no traditional vascular risk factors or coagulopathy experienced brainstem stroke during status migrainosus with her typical brainstem aura. It is plausible that migraine was a contributing factor to the stroke, especially in view of evidence that brain hypoperfusion2 and basilar artery narrowing, and even occlusion,3 occur during migraine with brainstem aura. Other potential contributory factors included repetitive triptan use, treatment with estrogen-containing oral contraceptive, pseudoephedrinecontaining compound, selective serotonin reuptake inhibitor use, and basilar artery fenestration. Despite compelling arguments for a link between migraine and stroke in our patient and others,3 the patient would not be diagnosed with migrainous infarction according to the ICHD-3 beta criteria because her stroke symptoms were not part of her typical aura syndrome. By excluding patients with “extra-aural” symptoms at the time of infarction, ICHD-3 beta likely improves specificity of migrainous infarction criteria at the expense of sensitivity. This may lead to an underestimation of the role of migraine in stroke etiology. We would like to argue that a less restrictive category – “probable migrainous infarction” or “migraine-associated stroke” – could be introduced in the appendix to the final ICHD-3 to account for such patients who experience additional non-aura stroke symptoms during an otherwise typical migraine with aura attack, as we believe such cases truly are complications of migraine. Sarah Vollbracht, MD; Matthew S. Robbins, MD; Ilya Kister, MD From the Montefiore Headache Center, Saul R. Korey Department of Neurology, Albert Einstein College of Medicine, Bronx, NY, USA (S. Vollbracht and M.S. Robbins); Department of Neurology, NYU–Multiple Sclerosis Center, New York University School of Medicine, New York, NY, USA (I. Kister).
REFERENCES 1. Headache Classification Committee of the International Headache Society (IHS). The international classification of headache disorders, 3rd edition (beta version). Cephalalgia. 2013;33:629-808. 2. Seto H, Shimizu M, Futatsuya R, et al. Basilar artery migraine reversible ischemia demonstrated by Tc-99m HMPAO brain SPECT. Clin Nucl Med. 1994;19:215-218. 3. Caplan LR. Migraine and vertebrobasilar ischemia. Neurology. 1991;41:55-61.
