Neurology Primer

Late-life Accompaniments in Middle Age and the Elderly

R. Allan Purdy MD, FRCPC, Professor of Medicine (Neurology), Dalhousie Transient Migraine University, Halifax, NS. Accompaniments (TMAs)

Today, these late-life migraine accompani- Of all the neurological disorders, migraine is one of the most common and fascinating. In impor- ments are considered to be transient tance, the modern neurobiology of migraine places it among other major neurological condi- migraine accompaniments, or TMAs, and tions of a paroxysmal nature. Migraine occurs at all ages and is not uncommon in middle- and are recognised to be generally benign in late-life. It can present with and no or little , and with or without a prior histo- nature but are of important diagnostic inter- ry of migraine in earlier life. Physicians seeing older patients with transient neurological symp- est. Migraine with aura (formerly called toms and headache need to understand the role of migraine in the diagnosis and ensure no “classic migraine”) is distinguished from other sinister etiology exists or coexists. migraine without aura (formerly “common migraine”) by the neurological symptoms Key words: migraine, aura, migraine accompaniment, acephalgic migraine, headache. of aura rather than the headache symp- toms.1 Furthermore, headache can occur in Introduction bances (2); visual symptoms, paresthe- patients with transient ischemic attack Clinicians frequently see patients with sias and speech disturbances (3); visu- (TIA) or ,1,5 although this is not aura symptoms of migraine who have al symptoms, paresthesias, speech always recognised or appreciated. had no headache or very little headache disturbances and weakness (20); visual following the aura. These symptoms are and brainstem symptoms (3) and; no Case Presentation recognised as acephalgic migraine or, lit- visual symptoms (32).3 These cases For five years, a man aged 58 had one or two erally, migraine without headache. This ranged in age from 40–73 years and spells each year of combined visual and speech disorder is classified as “migraine aura 40% had some headache associated disturbance. For six months, spells occurred two without headache” by the International with the neurological symptoms, with or three times a week. In a spell, the ability to Headache Society,1 and is a migraine 65% having a history of recurrent focus was lost and the lateral parts of his visu- variant or equivalent. In the middle-aged headache. He was particularly interest- al field were filled with shimmering pinpoints and elderly patient, this disorder is what ed in patients who had normal cerebral of light.There was a “build-up”for two to three Fisher2 called late-life migraine accom- angiograms. minutes, the symptoms remained at a peak paniments. In both of Fisher’s papers, a signifi- for 30 minutes, and then faded and disap- cant number of patients had headache; peared in one hour.At the height of the episode, Historical Papers thus, not all were totally acephalgic or the patient was unable to read. At the same In 1980, Fisher reported a series of 120 with only aura. The essence of his origi- time, enunciation and fluency of speech were patients with neurological accompani- nal communication was to explain why impaired.There were no paresthesias.The ments of migraine, classified according to patients in the stroke age-bracket (older patient was aware of a slight pressure in the symptoms, as follows: visual symptoms than 40 years) occasionally have unex- head at the onset but did not call it a headache. only (25); visual symptoms and pares- plained transient cerebral ischemic Interestingly, this is Case 12 from thesias (18); visual symptoms and speech attacks in association with normal cere- Fisher’s original series2 and is represen- disturbances (7); visual and brainstem bral angiograms. He emphasized that tative of the cases seen with this disorder. symptoms (14); visual symptoms, pares- these occasional patients probably had This patient had the build-up, progres- thesias and speech disturbances (7); visu- migraine aura mainly, although those sion and march from the neural origin of al symptoms, paresthesias, speech with headache were more clearly suffer- his visual symptoms in his occipital cor- disturbances and paresis (25); recurrence ing migraine. tex to the speech symptoms arising from of old stroke deficit (9) and; miscella- Fisher was not the only one to note his parietal and temporal speech centres. neous symptoms (8).2 Headache the phenomena of significant aura symp- Headache is not seen in all cases, or it occurred in 50% of cases reported. toms without headache. In 1967, Whitty may be mild. In mid-life, as in this case, In 1986, Fisher subsequently report- indicated that migraine auras in middle- there can be a “flurry” of TMAs. ed a study of 85 cases that were similar- age could occur without a headache fol- ly categorised: visual symptoms (21); lowing the aura, and that this was more Mechanisms of TMAs visual symptoms and paresthesias (6); common in people who had prior Although the pathophysiology of visual symptoms and speech distur- migraine in the past.4 TMAs is a matter for speculation, it is

38 GERIATRICS & AGING • June 2003 • Vol 6, Num 6 Transient Migraine Accompaniments probable that the mechanisms of their Diagnosis of TMAs , for example, usually have persist- production are similar to those of Fisher wrote criteria for late-life migraine ent or residual visual symptomology, migraine, as they are really migraine accompaniments that continue to be unlike those who have TMAs. variants or equivalents. It seems that valid today.2 His original criteria are list- Migrainous visual accompaniments TMAs are equivalent to migraine ed in the accompanying Table. These cri- are not rare in late life. Wijman, et al.12 auras, which suggests a neurogenic teria are over 20 years old and would be designed questionnaires to elicit symp- process of cortical spreading depres- modified today due to neuroimaging and toms of TIAs that also may detect late-life sion originating in the posterior pole of other tests, but are still applicable. These transient visual symptoms similar to the the brain, which has been postulated as TMAs display a “build-up” and “pro- visual aura of migraine, often without a possible cause of reduced cerebral gression” of symptoms, which are not headache. In their study, 2,110 subjects blood flow during a migraine attack.6,7 typical of stroke symptoms. Further, the were questioned twice yearly for 17 years It may be that any ischemic mechanism “march” of symptoms from one area of about visual symptoms. Of these, 26 could trigger migraine-like phenome- the body to another—visual to face to (1.23%) had migrainous visual episodes; na in a patient with a migraine ten- arm to hand, for example—is typical of the majority (77%) began after 50 years of dency, but this would still suggest that TMAs but not of stroke. The duration of age and they were stereotypic in 65% of migraine plays a role at some level. A a TMA march (15–25 minutes) is much cases. The episodes lasted 15–60 minutes recent case report of a 65-year-old longer than a march, which is in 50% of subjects, 58% never had woman suggests that an internal usually a minute or two. TIAs are usual- accompanying the episodes, carotid artery stenosis mimicked a ly less than 10 minutes in most patients.10 and 42% had no headache history. Twelve TMA in a patient with a history of percent of subjects sustained a stroke after acephalgic migraine.8 Other Diagnostic Considerations the onset of migrainous visual symptoms. Furthermore, the ability of blood Migraine sensory aura also can involve the However, of those with TIAs, 33% devel- vessels to dilate may be reduced in the tongue and oral mucosa, in contrast to a oped a stroke, two-thirds within six elderly,9 resulting in the absence of TIA in which such involvement is rare.3,11 months of TIA onset. Wijman, et al. con- headache and the emergence of TMAs This is an important clinical clue. As well, cluded that late-life onset transient visual in some cases. Other mechanisms, such TMAs can recur for years without seque- phenomena similar to the visual aura of as down-regulation of serotonin vascu- lae whereas this would be unlikely in migraine are not rare and often occur in lar receptors in menopause, may play a atherothrombotic, embolic or cardioem- the absence of headache. These symp- role, as many menopausal women have bolic stroke, as would full reversibility of toms appear not to be associated with an migraine aura without headache. any symptoms. Patients with occipital lobe increased risk of stroke, and invasive diagnostic procedures or therapeutic Diagnostic Criteria for Late-life Migraine Accompaniments2 measures are generally not indicated. There have been reported cases of per- Scintillations or other visual display in the spell. manent sequelae following late-life – Next in order: paresthesias, aphasia, dysarthria and paralysis. migraine accompaniments,13,14 but this Build-up of scintillations. would be expected since migraine may on 1 – This does not occur in cerebrovascular disease. occasion lead to migrainous infarction, and stroke is common in the elderly. There “March” of paresthesias. are also secondary brain lesions that can – This does not occur in cerebrovascular disease. present with migraine-like symptoms, such as vascular malformations or tumour, Progression from one accompaniment to another, often with delay. which must be considered in all cases. The occurrence of two or more spells. This helps to exclude embolism. Thus, the most important differential diagnosis of TMAs is TIA or stroke. Usu- Headache in the spell. ally, the criteria noted can make diagnosis Episodes last 15–25 minutes. relatively straightforward, especially if the patient had similar symptoms earlier in life Characteristic mid-life flurry of migrainous accompaniments. or many recent repeated stereotypical episodes. The distinctions can be made but A generally benign course. must be done carefully, since risk factors for Normal angiography. stroke in these patients can be similar.15,16 Nevertheless, it is wise to recognise that if Exclusion of cerebral thrombosis, embolism and dissection, , thrombocytopenia, there are any atypical features, then stroke polycythemia and thrombotic thrombocytopenia. or another etiology must be considered.

www.geriatricsandaging.ca 39 Transient Migraine Accompaniments

Investigation of TMAs the biology of migraine may even provide In many patients TMAs are benign events new clues as to the mysterious mecha- and recognised to be so, and do not require nism of migraine.”2 Fisher recognised the investigation. If necessary, magnetic reso- importance of these cases to “students of nance angiography (MRA), echocardiog- migraine”, and his descriptions have raphy, doppler ultrasound or digital broadened our understanding of this angiography can be carried out to exclude common neurobiological disorder. a source of cerebral embolism, such as ath- erosclerotic plaques, dissection of cranial No competing financial interests declared. arteries and cardioembolic sources, where- References as EEG can help exclude . CT and MRA are also useful in detecting the pres- 1. Headache Classification Committee of the ence of stroke and TIA mimics, such as a International Headache Society. Classification and diagnostic criteria for headache disorders, tumour or aneurysm. When indicated, cranial neuralgias, and facial pain. Cephalalgia blood tests should be done to exclude 1988;8(Suppl 7);1-96. platelet disorders, polycythemia and 2. Fisher CM. Late-life migraine accompaniments hyperviscosity syndromes, as well as the as a cause of unexplained transient ischemic attacks. Can J Neurol Sci 1980;7:9-17. presence of lupus anticoagulant, phos- 3. Fisher CM. Late-life migraine pholipid antibodies, other rare coagu- accompaniments—further experience. Stroke lopathies and arteritis if there is an index of 1986;17:1033-42. suspicion that these disorders may be pres- 4. Whitty CMW. Migraine without headache. Lancet 1967;ii:283-5. ent. Diagnosing temporal arteritis, which 5. Portenoy RK, Abissi CJ, Lipton RB, et al. can present with visual symptoms as well Headache in cerebrovascular disease. Stroke as with major systemic symptoms, has to 1984;15:1009-12. be considered in the differential diagnosis 6. Lauritzen M. Pathophysiology of the migraine aura. The spreading depression theory. Brain of all elderly patients with headache. If sus- 1994;117(Pt 1):199-210. pected, an ESR should be done and, if nec- 7. Goadsby PJ, Lipton RB, Ferrari MD. essary, a temporal artery biopsy. Migraine—current understanding and treat- ment. N Engl J Med 2002;346:257-70. Treatment of TMAs 8. The late-life migraine “accompaniment” that wasn’t. AP Headache 2003;43:293. There is no evidence-based information 9. Meyer JS, Terayama Y, Konno S, et al. Age- on how to treat TMAs, and they may not related cerebrovascular disease alters the need any specific intervention. Standard symptomatic course of migraine. Cephalalgia 1998;18:202-8. migraine therapy is suggested if there is 10. Mohr JP, Gautier JC, Pessin MS. Internal headache, although vasoconstricting carotid artery disease. In: Barnett HJM, Mohr agents such as ergotamines and triptans JP, Stein B, et al., editors. Stroke. New York: should probably be avoided in these age Churchill Livingstone, 1998:355-400. 11. Raskin N, Appenzeller O. Headache. Major groups, especially if there are any signif- problems in internal medicine. Philadelphia: icant cardiovascular or cerebrovascular W.B. Saunders, 1980. risk factors. Preventive therapeutic sug- 12. Wijman CA, Wolf PA, Kase CS, at al. Migrain- gestions are anecdotal and have not been ous visual accompaniments are not rare in late life: the Framingham Study. Stroke validated in large trials. 1998;29:1539-43. 13. Shuaib A, Lee MA. Cerebral infarction in Conclusions patients with migraine accompaniments. The mechanisms of TMAs have interest- Headache 1988;28:599-601. 14. Fisher CM. An unusual case of migraine ed clinicians for many years, as older accompaniments with permanent sequela—a patients presenting with TMAs are not case report. Headache 1986;26:266-70. uncommon. There is no diagnostic test for 15. Dennis M, Warlow C. Migraine aura with- migraine, and clinicians need to be very out headache: transient ischaemic attack or not? J Neurol Neurosurg Psychiatry diligent in the differential diagnosis of 1992;55:437-40. patients with suspected TMAs, as this 16. Claiborne Johnston S, Sidney S, Bernstein AL, diagnosis is always one of exclusion. In et al. A comparison of risk factors for recurrent concluding his original paper, Fisher stat- TIA and stroke in patients diagnosed with TIA. Neurology 2003;60:280-5. ed: “The added knowledge concerning

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