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  • Updated 07.11.2022
  • Released 11.04.1993
  • Expires For CME 07.11.2025

Late-life migrainous accompaniments

Introduction

Overview

Late-life migrainous accompaniments remain important in neurologic practice as the diagnosis is largely dependent on history, taken carefully, to eliminate mimics and other neurologic disorders and diseases. Reviews relating to late-life migrainous accompaniments and migraine aura without headache are still reported in the literature and an ongoing discussion of mechanisms remains of interest to clinicians and patients as well. Neuroimaging maybe necessary to rule out secondary causes before making the diagnosis of late-life migrainous accompaniments. One suggestion is to consider that cerebral MRI with or without contrast, including DWI, T2*GRE, or susceptible weighted imaging sequences, may be the best tools for early detection of underlying pathology. Thus, it is important to be able to identify late-life migrainous accompaniments and sort them from a myriad of other mimics, particularly cerebrovascular diseases.

Key points

• Visual symptoms are common.

• They build up over time and march across the visual cortex.

• They are stereotyped and last 15 to 25 minutes.

• Some people still do have headache.

• There is a midlife flurry of attacks.

• There is usually a benign course.

• Imaging is normal in most cases.

Historical note and terminology

Late-life migrainous accompaniments, a topic of historical interest, is a clinical concept that is still important to modern-day neurologic diagnosticians and students of migraine. Miller Fisher published his 2 seminal articles on late-life migrainous accompaniments in 1980 and 1986. In his combined case series of 205 patients, Fisher was attempting to differentiate late-life migrainous accompaniments from the symptoms and signs of transient ischemic attacks (17; 19).

In his first series, Fisher reported 120 patients with neurologic accompaniments of migraine classified according to the following symptoms: visual accompaniments (excluding patients who had only ordinary scintillating scotoma) (25); visual symptoms and paresthesias (18); visual symptoms and speech disturbances (7); visual and brainstem symptoms (14); visual symptoms, paresthesias, and speech disturbances (7); visual symptoms, paresthesias, speech disturbances, and paresis (25); recurrence of old stroke deficit (9); and miscellaneous symptoms (8). Diagnosis was facilitated when 2 or more similar episodes occurred or migraine-like scintillations were present (17). Headache occurred in 50% of the patients.

In the second series, Fisher reported 85 cases that were similarly categorized: visual symptoms (21); visual symptoms and paresthesias (6); visual symptoms and speech disturbances (2); visual symptoms, paresthesias, and speech disturbances (3); visual symptoms, paresthesias, speech disturbances, and weakness (20); visual and brainstem symptoms (3); and no visual symptoms (32) (19). These patients ranged in age from 40 to 73 years. Forty percent had some headache associated with the neurologic symptoms, with 65% having a history of recurrent headache. Fisher was particularly interested in patients who had migrainous accompaniments and normal cerebral angiograms. Headache was present in 40% of cases in this series.

In both of Fisher’s studies, many patients had headache; thus, all were not totally acephalgic (only aura). The essence of his original communication was to explain why patients in the stroke-age bracket (older than 40 years) occasionally have unexplained transient ischemic attacks in association with normal cerebral angiograms. He believed that these patients probably had migraine aura; those with headache were more typical migraine. Fisher was not the only one to note the phenomenon of aura symptoms without headache. Whitty reported that in middle-age, migraine auras could occur alone, without a headache; this was more common in people who had had typical migraine in the past (48).

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