Transient global amnesia

LEARNING BY IMAGES

Transient global amnesia

Juliana Frota Guimarães; Cristiane Wosny; Alcino Alves Barbosa Junior

Department of Diagnostic Imaging, Hospital Israelita Albert Einstein – HIAE, São Paulo (SP), Brazil

^{Corresponding author}

A 65-year-old male patient with no past medical history, complains of sudden loss of memory that lasted about four hours. He was submitted to a magnetic resonance image (MRI) of the cranium, which showed no alterations. Follow-up MRI 48 hours later showed a diffusion restriction focus in the left hippocampus, consistent with the clinical hypothesis of transitory global amnesia (Figures 1 and 2).

Transient global amnesia (TGA) is a syndrome characterized by transient sudden loss of memory and incapacity to acquire new information, lasting a few hours. Complete remission occurs within 24 hours⁽¹⁾.

Recent studies on the diffusion technique have demonstrated hyperintense lesions in the hippocampal region or in limbic system structures in patients with TGA, comparable to patients with cerebral ischemia⁽²⁾. A current study published by Sedlaezek suggests that these lesions are usually not visible until 48 hours after the onset of symptoms. Therefore, early MRIs performed in the first 24 hours might not detect a lesion^(3,4).

These hyperintense hippocampal lesions are small in size (1 to 2 mm), with low apparent diffusion coefficients (ADC), and generally remit within two weeks^(2,5). However, these image changes in patients with TGA, despite being seen in ischemia of arterial origin, are not specific and may occur due to prolonged ictal activity, multiple sclerosis, hypoglycemia, venous thrombosis, phenylketonuria, emotional stress, pain, sexual intercourse, and physical activity^(1,3).

If the clinical presentation is typical, no additional evaluation is mandatory. In case of doubt, imaging studies may be necessary in order to exclude other differential diagnoses⁽³⁾. One must consider that amnesia may be a part of the clinical picture of other diseases, hindering the distinction from TGA based merely on the clinical presentation⁽⁶⁾. There are data that suggest hypoperfusion of the hippocampal region as cause of the disease, and the cerebral image study indicated should be MRI with the diffusion technique, emphasizing that during the first 24 hours, the lesion might not be detected^(3,5).

ACKNOWLEDGMENT

To Dr. Ayrton Massaro, neurologist that assisteded this pacient.

Received on: Mar 27, 2012

Accepted on: Apr 23, 2012

• 1. Quinette P, Guillery-Girard B, Dayan J, de la Sayette V, Marquis S, Viader F, et al. What does transient global amnesia really mean? Review of the literature and thorough study of 142 cases. Brain. 2006;129(Pt 7):1640-58.
• 2. Godeiro-Junior C, de Miranda-Alves MA, Massaro AR. Diffusion magnetic resonance imaging in transient global amnesia. Arq Neuropsiquiatr. 2009; 67(1):130-1.
• 3. Berli R, Hutter A, Waespe W, Bachli EB. Transient global amnesia - not so rare after all. Swiss Med Wkly. 2009;139(19-20):288-92.
• 4. Sedlaezek O, Hirsch JG, Grips E, Peters CN, Gass A, Wöhrle J, et al. Detection of delayed focal MR changes in the lateral hippocampus in transient global amnesia. Neurology. 2004;62(12):2165-70.
• 5. Tong DC, Grossman M. What causes transient global amnesia? New insights from DWI. Neurology. 2004;62(12):2154-5. Comments on: Neurology. 2004; 62(12):2165-70.
• 6. Zukerman E, Andrade LA, Bertolucci PH. [Transient global amnesia: study of 26 cases]. Arq Neuropsiquiatr. 1985;43(1):39-47. Portuguese.

Publication Dates

• Publication in this collection
  20 Sept 2012
• Date of issue
  June 2012