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LETTER TO EDITOR
Year : 2014  |  Volume : 62  |  Issue : 4  |  Page : 463-465

Diffusion MRI in transient global amnesia


1 Department of Radiodiagnosis, Kasturba Medical College, Manipal University, Mangalore, Karnataka, India
2 Department of Neuroradiology, Kasturba Medical College, Manipal University, Mangalore, Karnataka, India
3 Department of Neurology, Kasturba Medical College, Manipal University, Mangalore, Karnataka, India

Date of Web Publication19-Sep-2014

Correspondence Address:
Santosh P.V Rai
Department of Radiodiagnosis, Kasturba Medical College, Manipal University, Mangalore, Karnataka
India
Santosh P.V Rai
Department of Radiodiagnosis, Kasturba Medical College, Manipal University, Mangalore, Karnataka
India
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Source of Support: None, Conflict of Interest: None


DOI: 10.4103/0028-3886.141283

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How to cite this article:
Reddy H, Bele K, Misri Z K, Rai SP, Reddy H, Bele K, Misri Z K, Rai SP. Diffusion MRI in transient global amnesia. Neurol India 2014;62:463-5

How to cite this URL:
Reddy H, Bele K, Misri Z K, Rai SP, Reddy H, Bele K, Misri Z K, Rai SP. Diffusion MRI in transient global amnesia. Neurol India [serial online] 2014 [cited 2020 Oct 24];62:463-5. Available from: https://www.neurologyindia.com/text.asp?2014/62/4/463/141283


Sir,

Transient global amnesia (TGA) is clinically defined as sudden onset anterograde amnesia with preserved alertness, attention, and personal identity, which occurs during a period of not more than 24 hours with no long-term sequelae. [1] The precise etiology of TGA is unknown. Diffusion-weighted imaging (DWI) magnetic resonance imaging (MRI) may help in the diagnosis of this condition.

A 52-year-old male presented with acute confusion and memory disturbance. No history of any similar episodes or any medical illness in the past was noted; the family history was negative. Neurological examination showed awake, alert, and well-oriented person with short-term memory loss and long-term memory was intact, was able to remember family members. He kept asking repetitive questions. He had no active hallucinations or delusions, and no speech disturbances or other deficits. The patient returned to baseline normal neurologic state over the course of a 24-hour hospitalized observation period and has not had any further recurrences.

Blood biochemistry and complete blood picture were normal. MRI brain showed no abnormality in conventional T1/T2-weighted and FLAIR (Fluid attenuated inversion recovery) sequences [Figure 1]a-d. However, DWI showed focal punctate area of restricted diffusion in left hippocampus [[Figure 1]e and g white arrow]. Corresponding ADC showed hypointense [[Figure 1]f and h white arrow] area in the region of hyperintensity in DWI. The MR angiography was normal. Electroencephalogram and color-coded carotid Doppler were normal.
Figure 1: Axial Magnetic Resonance (MR) images performed on 1.5 T shows normal FLAIR (a and b) and T2 weighted images (c and d) which shows no abnormality. Diffusion weighted images (e and g) and ADC mapping (f and h) shows focal punctate area of restricted diffusion in the left hippocampus appearing bright on the DWI series (white arrow F) and appearing hypointense on the ADC mapping (white arrow H)

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Although not the first to report TGA, Fisher and Adams [2] were credited with naming the syndrome and monographing it in detail. The etiology and pathogenesis of TGA are uncertain, although several different causes suggested include: Ischemia, migraine, epileptic seizure, venous congestion, and psychological disturbances .[3] In addition, TGA is a well-recognized complication of cerebral angiography with ionic or nonionic contrast agents. [4]

Recent studies have indicated the presence of focal hyperintensities involving the hippocampus in TGA. The typical findings on MRI include hyperintensity signal at the hippocampal area on DWI with corresponding hypointensity on ADC, which support of ischemic etiology. [5],[6] Transient ischemic changes and epileptic events are two major mechanisms proposed etiologies of TGA. [5] Hypothesis of transient cerebral ischemia, especially the hippocampus, is supported by the modern imaging studies. [6] Selective ischemic involvement of hippocampus is not clear. This may be related to the vulnerability of CA-1 (cornu ammonis) of hippocampus (Sommer sector) to ischemic insult. [6] Some triggers in patients with TGA include exertion, emotional stress, or sexual intercourse. These observations lead to the hypothesis of venous congestion mediated by intracranial venous reflux. The intracranial venous reflux may be caused by the valve incompetence of the internal jugular vein or the left brachiocephalic vein occlusion after a precipitating factor such as Valsalva maneuver. [7],[8]

The lesions detected by DWI are small and punctate (1-3 mm) and located within the lateral portion of the hippocampus. [9],[10] The reported frequency of DWI range between 0% and 84%. [9],[11] This discrepancy in the reported rates appears to be related to the timing of imaging from symptoms onset. [9] The combined use of a high b-value (b = 2000) and thin section thickness (3 mm) is preferred for detection of lesions in TGA. If no lesion is detected on initial DWI, especially if performed within several hours of symptom onset, follow-up DWI after several days is recommended .[12]

To summarize, TGA is an important cause of acute transient anterograde amnesia. The characteristic findings on DWI support the clinical diagnosis of TGA. It is important to diagnose this condition as it has benign outcome and treatment is generally not required, and the condition usually does not recur.

 
  References Top

1.Hodges JR, Warlow CP. Syndromes of transient amnesia: Towards a classification-A study of 153 cases. J Neurol Neurosurg Psychiatry 1990;53:834-43.  Back to cited text no. 1
    
2.Fisher CM, Adams RD. Transient global amnesia. Acta Neurol Scand 1964;40:1-83.  Back to cited text no. 2
    
3.Sander K, Sander D. New insights into transient global amnesia: Recent imaging and clinical findings. Lancet Neurol 2005;4:437-44.  Back to cited text no. 3
    
4.Schamschula RG, Soo MY. Transient global amnesia following cerebral angiography with non-ionic contrast medium. Australas Radiol 1994;38:196-8.  Back to cited text no. 4
    
5.Ay H, Furie KL, Yamada K, Koroshetz WJ. Diffusion-weighted MRI characterizes the ischemic lesion in transient global amnesia. Neurology 1998;51:901-3.  Back to cited text no. 5
    
6.Bartsch T, Alfke K, Deuschl G, Jansen O. Evolution of hippocampal CA-1 diffusion lesions in transient global amnesia. Ann Neurol 2007;62:475-80.  Back to cited text no. 6
    
7.Sander D, Winbeck K, Etgen T, Knapp R, Klingehlofer J, Conrad B. Disturbance of venous flow patterns in patients with transient global amnesia. Lancet 2000;356:1982-4.  Back to cited text no. 7
    
8.Chung CP, Hsu HY, Chao AC, Chang FC, Sheng WY, Hu HH. Detection of intracranial venous reflux in patients of transient global amnesia. Neurology 2006;66:1873-7.  Back to cited text no. 8
    
9.Sedlaczek O, Hirsch JG, Grips E, Peters CN, Gass A, Worhle J, et al. Detection of delayed focal MR changes in the lateral hippocampus in transient global amnesia. Neurology 2004;62:2165-70.  Back to cited text no. 9
    
10.Bartsch T, Alfke K, Stingele R, Rohr A, Feritaq-Wolf S, Jansen O, et al. Selective affection of hippocampal CA-1 neurons in patients with transient global amnesia without long-term sequelae. Brain 2006;129:2874-84.  Back to cited text no. 10
    
11.Winbeck K, Etgen T, von Einsiedel HG, Rottinger M, Sander D. DWI in transient global amnesia and TIA: Proposal for an ischaemic origin of TGA. J Neurol Neurosurg Psychiatry 2005;76:438-41.  Back to cited text no. 11
    
12.Weon YC, Kim JH, Lee JS, Kim SY. Optimal diffusion-weighted imaging protocol for lesion detection in transient global amnesia. AJNR Am J Neuroradiol 2008;29:1324-8.  Back to cited text no. 12
    


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