Headache position statement states that MTSDS supporting data are not convincing, may produce side effects that are not reversible, and can be extremely expensive.7 Similar sentiments are expressed in “Choosing wisely in headache medicine: the American Headache Society’s list of five things physicians and patients should question,” which was an initiative of the American Board of Internal Medicine Foundation.8 In conclusion, MTSDS are a set of procedures that may be effective for the treatment of headaches in a certain patient subpopulation, but further studies need to be performed to determine the screening tests that may better clarify which patients may potentially benefit from these procedures with an acceptable risk of side effects. Future surgical procedures should only be performed in the setting of a clinical trial after evaluation by a headache specialist, and imaging studies have demonstrated a clear surgical target involving compression. Paul G. Mathew, MD, FAHS From the Department of Neurology, John R. Graham Headache Center, Brigham and Women’s Hospital, Boston, MA, USA; Division of Neurology, Cambridge Health Alliance, Cambridge, MA, USA; Harvard Medical School, Boston, MA, USA
1233 2. Mathew PG. A critical evaluation of migraine trigger site deactivation surgery. Headache. 2014;54:142-152. 3. Guyuron B, Kriegler JS, Davis J, Amini SB. Five year outcome of surgical treatment of migraine headaches. Plast Reconstr Surg. 2011;127:603-608. 4. Guyuron B, Reed D, Kriegler JS, Davis J, Pashmini N, Amini S. A placebo-controlled surgical trial of the treatment of migraine headaches. Plast Reconstr Surg. 2009;124:461-468. 5. Diener HC, Dodick DW, Aurora SK, et al. PREEMPT 2 chronic migraine study group. OnabotulinumtoxinA for treatment of chronic migraine: Results from the double-blind, randomized, placebo-controlled phase of the PREEMPT 2 trial. Cephalalgia. 2010;30:804-814. 6. Lipscombe SL, Prior T. Is there any relationship between handedness and unilateral headache in migraine? Cephalalgia. 2002;22:146-148. 7. American Headache Society. http://www .americanheadachesociety.org/american_headache _society_urges_caution_in_using_any_surgical _intervention_in_migraine_treatment/. 8. Loder E, Weizenbaum E, Frishberg B, Silberstein S. American headache society choosing wisely task force. Choosing wisely in headache medicine: The American Headache Society’s list of five things physicians and patients should question. Headache. 2013;53:1651-1659.
REFERENCES 1. Guyuron B. A discussion of “critical evaluation of migraine trigger site decompression surgery.” Headache. 2014;54:1065-1072.
Transient Global Amnesia as a Presenting Aura or Epilepsy? We read with great interest the paper by Dalla Volta and colleagues, reporting a 70-year-old patient presenting with recurrent episodes of transient amnesia followed by headache.1 The authors postulated that transient global amnesia (TGA) could be the presenting aura of a migraine attack.1
The temporal association between TGA and migraine has been sporadically observed.2,3 Several
*These authors share the same contribution. Conflict of Interest: None.
1234 investigations also demonstrated a common pathophysiology between these conditions. Similar to the “cortical spreading depression model” of migraine aura, transient hypoperfusion in memory-eloquent brain structures, such as the mesial temporal lobe structures, has been proposed to be the causative mechanism of TGA.4 Acute confusional migraine (ACM) is an uncommon condition characterized by a sudden onset of amnesia, disorientation, variable degree of agitation, followed or accompanied by typical migraine headache, usually occurring in children and adolescents.5,6 Currently, it is still debated if it could be considered as a complex migraine variant; therefore, it is not yet mentioned in the International Classification of Headache Disorders, 2nd edition as a distinct entity.7 Diagnosis of ACM may be challenging, and it is often based on the exclusion of alternative diagnoses such as epilepsy, stroke, neoplasm, intoxication, and encephalitis by mean of accurate anamnesis, clinical examination, laboratory, radiological, and electroencephalogram (EEG) findings. Headache may also occur after an epileptic seizure, and occasionally can be the only ictal symptom.8,9 The difficulty of a correct diagnostic assessment, and consequently the frequent misdiagnosis between periictal headache and complex migraine variants, has been debated in our previous papers.9,10 In addition, it may be difficult to discern between ACM and seizures with dyscognitive symptoms and peri-ictal headache. Transient epileptic amnesia (TEA) is a peculiar, probably under recognized, epileptic condition in which the main ictal manifestation is isolated memory loss of quite variable duration (from seconds to hours).11 It represents an underrecognized type of temporal lobe epilepsy. The onset of the attacks is common in latemiddle or old age. Diagnostic criteria for TEA include: (1) a history of recurrent episodes of transient amnesia; (2) normal cognitive functions apart from memory during typical episodes; and (3) evidence for diagnosis of epilepsy (at least 1 among EEG abnormalities, ictal features of temporal lobe epilepsy [ie, oro-alimentary or bimanual automatisms], or clear-cut response to antiepileptic drugs).11 Della Volta et al1 excluded the diagnosis of epilepsy
July/August 2014 mainly based on the absence of clear interictal epileptiform abnormalities at EEG. However, interictal EEG can be normal in patients with late-onset temporal lobe epilepsy12 and, in particular, in TEA. Moreover, several other characteristics challenge the diagnosis of migraine in this patient, such as late age at onset of “amnestic episodes,” lack of other symptoms suggestive of migraine aura, and absence of response to flunarizine. Finally, the prompt disappearance of episodes following valproate introduction did not allow discrimination between migraine and epilepsy. In ACM, aura is usually accompanied by other suggestive neurological deficits such as visual phenomena, hemisensory loss or paresthesia, aphasia, hemiparesis. Such symptoms did not occur in the patient reported by Dalla Volta et al.1 To exemplify a typical ACM picture, we briefly report a 40-year-old man who recently came to our observation for an episode characterized by visual disturbance (blurred vision with zigzagging lines) lasting for about 10 minutes, followed by right-sided perioral and hand tingling sensation lasting for about 15 minutes, then amnesia (impossibility of remember his friends and his relatives when he listened to their names) accompanied by agitation, for about 15-20 minutes.A typical left-sided migraine headache accompanied the symptoms and lasted for the following 12 hours, resolving after sleep. Post-ictal neurological examination was normal. Several diagnostic examinations (EEG, brain magnetic resonance imaging, transcranial Doppler with bubble study, transthoracic echocardiography with contrast, vast hematological panel including thrombophilia screening and autoimmunity) were unremarkable. We believe that the clinical features of the episode presented by our patient represent a paradigmatic example of TGA. The sequence of focal neurological symptoms clearly recalls the progression of the cortical spreading depression from the occipital and parietal cortices to the mesial temporal structures. We believe that ACM should be included in the International Classification of Headache Disorders as a variant of migraine with aura in order to lead physicians toward a proper diagnosis of this challenging condition.
Headache Edoardo Ferlazzo,* MD, PhD; Domenico Italiano,* MD, PhD; Vincenzo Belcastro, MD, PhD; Sara Gasparini, MD; Edoardo Spina, MD, PhD; Umberto Aguglia, MD From the Department of Medical and Surgical Sciences, Magna Graecia University, Catanzaro, Italy (E. Ferlazzo, S. Gasparini, and U. Aguglia); Regional Epilepsy Centre, Bianchi-Melacrino-Morelli Hospital, Reggio Calabria, Italy (E. Ferlazzo, S. Gasparini, and U. Aguglia); Department of Clinical and Experimental Medicine, University of Messina, Messina, Italy (D. Italiano and E. Spina); Neurology Unit, S. Anna Hospital, Como, Italy (V. Belcastro)
REFERENCES 1. Dalla Volta G, Zavarise P, Ngonga G, et al. Transient global amnesia as a presenting aura. Headache. 2014;54:551-552. 2. Santoro G, Casadei B, Venco A. The transient global amnesia-migraine connection. Case report. Funct Neurol. 1988;3:353-360. 3. Schmidtke K, Ehmsen L. Transient global amnesia and migraine. A case control study. Eur Neurol. 1998;40:9-14. 4. Quinette P, Guillery-Girard B, Dayan J, et al. What does transient global amnesia really mean? Review of the literature and thorough study of 142 cases. Brain. 2006;129(Pt 7):1640-1658.
1235 5. Schipper S, Riederer F, Sándor PS, Gantenbein AR. Acute confusional migraine: Our knowledge to date. Expert Rev Neurother. 2012;12:307-314. 6. Sathe S, DePeralta E, Pastores G, Kolodny EH. Acute confusional migraine may be a presenting feature of CADASIL. Headache. 2009;49:590-596. 7. Headache Classification Committee of the International Headache Society (IHS). The International Classification of Headache Disorders, 3rd edition (beta version). Cephalalgia. 2013;33:629-808. 8. Bernasconi A, Andermann F, Bernasconi N, Reutens DC, Dubeau F. Lateralizing value of periictal headache: A study of 100 patients with partial epilepsy. Neurology. 2001;56:130-132. 9. Parisi P, Striano P, Negro A, Martelletti P, Belcastro V. Ictal epileptic headache: An old story with courses and appeals. J Headache Pain. 2012;13:607613. 10. Italiano D, Grugno R, Calabrò RS, Bramanti P, Di Maria F, Ferlazzo E. Recurrent occipital seizures misdiagnosed as status migrainosus. Epileptic Disord. 2011;13:197-201. 11. Butler CR, Graham KS, Hodges JR, et al. The syndrome of transient epileptic amnesia. Ann Neurol. 2007;61:587-598. 12. Labate A, Gambardella A, Andermann E, et al. Benign mesial temporal lobe epilepsy. Nat Rev Neurol. 2011;7:237-240.
Response to “Transient Global Amnesia as a Presenting Aura or Epilepsy?” We appreciate the opportunity to reply to the letter of Ferlazzo and colleagues about our recent publication: “Transient Global Amnesia as a Presenting Aura.”1 We consider of significant interest the aforementioned report by Ferlazzo and collaborators, to support the concept of acute confusional migraine (ACM) as a distinct clinical entity, requiring careful anamnesis and clinical evaluation, as well as diagnostic studies (radiological and neurophysiological), to rule out other alternative conditions. However,
several significant differences were present in our patient, supporting our idea that Transient Global Amnesia (TGA) could represent an atypical aura of migraine attack. First of all, the amnesic episodes experienced by our patient were not a simple epiphenomenon of a state of confusion and/or disorientation, but the main aspect of the episode, with all the other peculiar aspects of TGA amnesic crisis, in particular: (1) repetitive questioning; (2) an amnesic state for the entirety of the event itself (as a key symptom