• dihydroergotamine;
  • sumatriptan;
  • transient global amnesia;
  • thalamic infarct


  1. Top of page
  2. Abstract

This case report describes an episode of transient global amnesia that occurred during a migraine attack, which had been treated with vasoconstrictors. Magnetic resonance imaging showed a small lesion with an ischemic appearance in the right thalamus.


transient global amnesia


single photon emission computed tomography

Transient global amnesia (TGA) is a frequent transient neurological event, with an incidence of 23.5 cases per year per population of 100 000 over the age of 50 years. 1 Its pathophysiology remains unknown, as various hypotheses, including epilepsy and embolic or vasospastic transient ischemic attack (often associated with migraine, in the latter case), have not yet been formally demonstrated by clinical and epidemiological studies. We recently observed an episode of TGA in a patient with migraine, apparently following the injection of vasoconstrictors.


  1. Top of page
  2. Abstract

A 54-year-old woman had had migraine without aura since the age of 20 years, with a frequency of three to four episodes per month. She had been treated with nasal dihydroergotamine (Diergospray) or sumatriptan, 100-mg tablets (Imigrane), for several years, with no particular adverse effects.

Starting at about 9 pm on a Friday, the patient had an attack of migraine without aura that was similar to her usual episodes. She took dihydroergotamine that night. As the migraine persisted, she took a second dose of the nasal spray at 4 pm the next day with three or four Propofan (paracetamol, caffeine, dextropropoxyphene) tablets. She went to bed at about 11 pm and woke up at 6 am on Sunday with migraine. At about 6:15 or 6:30 am, the patient, who had a persistent and severe hemicrania, asked her husband to administer a 6-mg subcutaneous injection of sumatriptan in her thigh. This was the first time she had taken such medication, and her husband administered it without difficulty. Approximately 30 to 45 minutes later, the patient could repeat questions and comments but immediately forgot the answers to questions regarding her children. However, her husband did not report any other abnormality apart from the acute memory disorder. There was no speech disorder or confusion, as the patient clearly recognized her husband and her apartment, nor was there any visual or motor disorder.

Two or 3 hours later, the patient went back to sleep. She woke up on Sunday at 11 am for the arrival of her family doctor who had been called by her husband. At this time, all the symptoms (migraine, TGA) had disappeared without any disability remaining other than partial amnesia regarding this episode. The findings of the neurological examination were normal, as were her blood pressure (130/80 mm Hg) and heart rate.

The patient had no history of neurological or cardiovascular disorders. Clinical examination, with memory testing, laboratory assessment (search for a thrombophilic state, platelets, monoclonal Ig, proteins C or S, factor V Leiden, antithrombin III, antiphospholipid antibodies, etc), cervical and transcranial ultrasound assessments, and transesophageal ultrasonography, performed after the TGA, was normal. Magnetic resonance imaging (MRI) was, unfortunately, only obtained 5 weeks after the episode and consequently gadolinium was not injected. The MRI showed a small ischemic lesion of indeterminate age in the antero-inferior part of the right thalamus. The same investigations were also negative 12 months later, except for the persistence of the right thalamic lacune.

This patient has not developed any further episodes of TGA or any other disease, over the 2 years since the episode reported here. Migraine still occurs at a frequency of two to three attacks per month. During these attacks, the patient has taken nasal dihydroergotamine or oral sumatriptan (but not together) on five or six occasions with no particular problems.


  1. Top of page
  2. Abstract

Transient global amnesia has been defined 2 by the following criteria:

  • • 
    There must be clear-cut anterograde amnesia during the attack.
  • • 
    Clouding of consciousness and loss of personal identity must be absent, and the cognitive impairment must be limited to amnesia.
  • • 
    There should be no accompanying focal neurological symptoms or functionally relevant focal signs.
  • • 
    Epileptic seizures must be absent.
  • • 
    Attacks must be resolved within 24 hours.
  • • 
    Patients with recent head injury or known active epilepsy are excluded.
  • • 
    There must be a witness to the attacks.

These criteria rule out other amnestic disorders such as amnestic seizures and amnestic strokes. According to nosology, TGA associated with other neurological deficits is defined as an amnestic stroke. 3

A vascular cause of TGA has been suggested frequently, but this hypothesis remains controversial. Although it is difficult to accept the hypothesis of an embolic cause for this type of neurological event, many authors have suggested the role of vasospasm or, similar to that proposed for migraine, Leão's spreading depression in the physiopathology of TGA, 4 as recently suggested by diffusion-weighted MRI. With this technique, Strupp et al 5 showed an elevated signal intensity in 7 of 10 patients with pure TGA (unilaterally in the left mesial temporal region for four patients, and in both mesial temporal lobes for the other three). These changes were reversible. In contrast, conventional T1- and T2-weighted images were normal.

Several elements support the hypothesis of a migrainous origin of TGA. A personal and family history of migraine is significantly more frequent in patients with TGA than in individuals without TGA, or in patients with transient ischemic attacks. 6-9 Some cases of TGA occurring during a migraine attack are described in the literature. 10-13 Generally, TGA is associated with migraine with aura; six of seven patients had migraine with aura in the Caplan et al series. 6 In most cases, TGA was preceded by the migrainous attack as in our patient.

Few authors have studied brain computed tomography (CT) scans in patients with TGA. There is rarely evidence of infarction. However, some scans have shown definite lesions: in 3.3 % of patients with TGA in one study 3 and 9.3 % in another. 14 Low resolution may explain why patients with TGA may have normal CT scans, but a circumscribed lesion in the left hippocampus shown on MRI was described by Tanabe et al. 15 Unfortunately, systematic studies of patients experiencing TGA during a migraine attack have not been published.

Transient global amnesia can also occur in a context of cardiovascular disease (atherosclerosis, cardiac arrhythmia, etc), but in this situation it is generally associated with other symptoms (either during the episodes or previously) such as drop attacks, cortical blindness, hemianopia, and cerebellar or vestibular syndromes. More rarely, TGA has been reported immediately after trauma and exceptionally associated with certain tumors or toxins. However, in our experience, these potential causes are not common.

Clinical and biological investigations were unable to explain the thalamic infarct in our patient, therefore, in our opinion, ischemia may have been responsible. Apart from the migraine phenomenon itself, treatment with vasoconstrictors, namely, nasal dihydroergotamine 17 and 9 hours before sumatriptan by injection, followed 45 minutes later by the onset of TGA, suggests a triggering role for one of these drugs or more probably the association of the two vasoconstrictor drugs with the neurological event. Conversely, Bates et al 16 administered subcutaneous sumatriptan during the aura (the phase thought to be related to vasoconstriction and ischemia) and found no change in aura duration or aura symptoms.

Transient global amnesia classically occurs after cerebral or coronary angiography, even when the findings are normal, suggesting a role for vasospasm. Juni et al 17 even visualized spasm of the basilar artery and concomitant onset of TGA during vertebral angiography. In the patient described here, repeat angiography, 3 months later, was normal, and an ischemic lesion in the thalamus was demonstrated on MRI. Investigation of isolated TGA usually does not reveal any abnormality of the cervical vessels, and transcranial ultrasound assessment and CT scan are generally normal. However, as previously noted, infarction has sometimes been demonstrated on CT scans. In other studies, the CT scan was normal, but MRI or single photon emission computed tomography (SPECT) revealed abnormalities. Lin et al 18 observed multiple perfusion defects on SPECT in both occipital lobes, the left temporal lobe, and the left thalamus 6 hours after the onset of TGA. The SPECT was normal 28 days later. These findings, therefore, suggest the existence of ischemia in the territory of the posterior cerebral arteries during TGA. A reduction of thalamic perfusion was also recently reported by Goldenberg et al, 19 again by means of the SPECT technique. These authors observed a marked reduction of the regional blood flow in the left thalamus and a less marked reduction in the right thalamus. Forty days later, the thalamic blood flow on SPECT had returned to normal. In our case, it is, therefore, likely that migraine and vasoconstrictors induced ischemia of this territory, sufficient to be visualized as a persistent defect on MRI.

Finally, this observation suggests care in the use of vasoconstrictors in severe and lasting migraine and the need to respect the recommended delay of 24 hours after the use of ergot derivatives before prescribing sumatriptan.


  1. Top of page
  2. Abstract
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