Since the age of 11 one-two times per year, the patient has been experiencing attacks of intensive bilateral throbbing headache without associated symptoms lasting 8–12 h usually aborted with sleep. At the age of 22 for the first time, he experienced visual symptoms described above with the duration of 20–30 min. Until the age of 35, visual symptoms were followed by headache phase every time. At the age of 35, the headache attacks stopped while visual symptoms have persisted until now. In his 40s the patient noticed that the duration of visual episodes increased to 40–60 min and began to be accompanied by difficulties in speech (dysarthria); after the disappearance of visual symptoms, speech is completely recovered. Among factors provoking these episodes, the patient mentions bright light and intensive visual activity while using PC. A 19-year-old son of the patient since childhood has been suffering from similar headache attacks preceded by visual phenomena.

Without any significant findings, the patient is overweight; there is bilateral tenderness of the pericranial and cervical muscles during manual palpation; the patient looked very depressed and expressed anxiety associated with his condition (Fig. 16.1).

Depressed mood, anxiety, episodic back and neck pain, sleep disturbances and arterial hypertension.

Complete blood count and biochemical analysis: the parameters are in normal range; cholesterol on the upper range. BP, 135/90; Brain MRI and MR angiography did not reveal any organic lesions. Ophthalmologic investigation: hypertensive retinal angiopathy.

Late-life migrainous equivalent (LLME, Fisher’s syndrome), migraine with aura (in the past), anxiety and depression syndrome and pericranial muscles dysfunction.

For his arterial hypertension for the last 15 years, the patient received beta-blockers. Taking into account his severe depression and anxiety, the combination of antidepressant and neuroleptic (escitalopram + ticersin) was recommended for 6–8 months.

When seen repeatedly over 2 years (at the age of 54), the patient demonstrated the same visual and occasionally speech defect symptoms; his mood has significantly improved; no complications or new symptoms were registered. The possibility of adding calcium channel blockers (nimodipine) should be considered in the future.

Two presented cases illustrate different ways of migraine evolution in elder age. The 1st demonstrates the severe migraine course (migraine persistence) in a woman aged 57 and the 2nd, the incomplete migraine cessation (preservation of migraine aura without pain episodes) in a 53-year-old man which could be classified as late-life migrainous accompaniment (LLMA).

In the 1st case despite menopause lasting for 5 years, an elderly woman keeps on developing typical migraine attacks with the same accompanying symptoms, pain characteristics and triggers that were present in the young age. It is worth mentioning the following details of this case:

Thus main predictors/risk factors of migraine persistence in this patient include:

The 2nd case illustrates age-related transformation of migraine with visual aura into more complicated aura (visual and speech disturbances) without headache (“headless migraine”). Such complex of symptoms was described by C. M. Fisher in 1986 and is also called “late-life migrainous accompaniment”. The past history of typical migraine without aura, normal instrumental examinations and benign course of the condition allowed us to exclude the possibility of other causes of aura symptoms. At the same time considering risk factors in our patient (arterial hypertension, mild obesity, elevated cholesterol and smoking), possible preventive therapy with calcium channel blockers could be further recommended.