
Self-limiting antegrade amnesia
› In absence of other causes


Witnessed
Antegrade amnesia
› Unable to form new memories
› Perserveration
 “Broken record”
› Sometimes also retrograde

No other cognitive impairment or altered consciousness
› Otherwise, alert and well

Duration of episode resolves within 24hrs
› 1-10 hrs, average 6hrs

No other neurological deficit/epileptic features/head trauma
› Diagnoses of exclusion

Precipitating event
No concensus
 Theories include:

› Vascular dysfunction
 Arterial or Venous
› Paroxysmal neuronal discharge/Epileptic phenomena
 Self propagating wave of neuronal depolarisation

Nothing
› Self resolving

Exclude other causes
› Diagnosis
 treatment
› Prognosis
DDx
DDx
Clinical Findings
MRI findings
Transient epileptic
epileptic
Transient
amnesia
amnesia
<1hr, multiple
attacks at time of
presentation
Increased T2/FLAIR in
hippocampus, thalamus and
cortex
Amnesia in absence
of other focal
neurodeficits rare
DWI in vascular territories
More global
amnesia and
inattention
Symmetrical increased T2/FLAIR
in mammillary bodies, medial
thalami, tectal plate and
periaqueductal area
Antegrade amnesia
<24hrs
DWI punctate (1-3mm) foci in
hippocampus, uni/bilateral
TIA/CVA
TIA/CVA
Wernickes
Wernickes
encephalopathy
encephalopathy
TGA
TGA
tectal region (white arrows), periaqueductal area
(black arrowheads), and mamillary bodies (white
arrowheads

Fn
› Involved in learning & memory

Part of mesial temporal lobe
› Below temporal horn of lateral ventricles
› Seahorse
› Made up of dentate gyrus, C1-4.

Blood supply:
› PCA
 hippocampal arteries
› AChA
 Branch of ICA

5 TGA cases presented to the Calvary Hospital
› Between March 2013 to February 2015

All had MRI findings typical of TGA
61 yo male
 No significant PMHx


Acute confusion and amnesia
› Repetitive questioning

Alert

Ix:
› CTB: NAD
› LP: NAD
Day 1 MRI
 2 punctate DWI lesions in left hippocampus

66yo male
 PMHx: T2 DM, hypertension and hypercholesterolaemia
 Acute onset of amnesia and confusion

Alert
 Repetitive questioning


CTB: NAD
Day 1 MRI
 Punctate DWI lesion in left hippocampus

62yo female
 PMHx: Meniere’s disease, migraine and hypertension
 Sudden onset of anterograde and retrograde amnesia
 Nausea and vomiting, worse than usual Meniere’s


Alert

CTB: NAD
Day 2 MRI
 5mm DWI hyperintense focus in the left hippocampus

63yo female
 Sudden onset confusion and amnesia at work
 PMHx: NAD


Alert
› No memory of days events

CTB: NAD
Day 2 MRI
 4.5mm DWI hyperintense focus in the left hippocampus

64yo female
 PMHx: OA
 Amnesic events at the gym and whilst doing errands

Day 2 MRI
 5mm DWI lesion in left hippocampus


Left hippocampal DWI lesion
81yo female
 PMHx: AF, AV replacement
 Acute confusion and dysphasia

› Resolved next day

Acute left hippocampal infarction

Left hippocampal DWI focus
78yo male
 PMHx: EtOH, COPD


Recurrent episodes of decreased levels of
consciousness
› Staring and not responding
› Over last few months
› Lasts 10mins
 Followed by 2-3 hrs of fatigue

Complex partial seizures

Cases demonstrating DWI focus in hippocampus
› BUT not TGA clinically
Hippocampal DWI Lesions ≠ TGA
Total 99 patients
› 52 had DWI changes
 45 in hippocampal region
 25 left, 9 bilateral, 11 right
› Sedlaczek et al.
 26 out of 31 had punctate hippocampal
DWI lesions

All 5 TGA cases showed hippocampal DWI lesion
Sander & Sander, Lancet Neuro. 2005

Small case series
 Reflective of literature

Diagnosis to consider
 Review area


Clinical diagnosis
“Clinical correlation is recommended”
Dr Yash Gawarikar
 Dr Alexander Lam
 Dr Brett Jones
 Dr Yun Tae Hwang


Consistent with other studies

MRI findings supports clinical diagnosis
› Treatment and prognosis

100% MRI detection rate
› Why?
 Optimised protocol
 t = 24-72 hrs
 b = 2000
 3mm thick slices
Previously brain imaging normal
Now…
Improvements in MRI:
 Small punctate (1-3mm) DWI hyperintense foci in lateral
hippocampus (CA1 sector of hippocampus)
 Often Unilateral and left sided
› Selective vulnerability of this region to metabolic stressors
 glutamate excitotoxicity and Ca2+ influx

MR-spectroscopy of hippocampal DWI lesion
› Lactate peak  further evidence for CA1 neuronal dysfuction
No abnormality in vessels on MRA
 Dy/dx with Wernicke encephalopathy
 DWI in medial thalami, mammillary bodies,
periaqueductal region, tectal plate


Frequency of detection 0-84%
›
›
›
›

Large range!
Likely related to timing of MRI from onset of symptoms
Sedlaczek (2004) - 6% detection rate when Mri done within 8 hrs of onset
Increased to 84% at 48hrs post onset
B values >1000
› Weon (2008) – detection rate @ B= 1000 (3mm thickness) was 38%, @ B=2000 (3mm
thickness) was 54%. No difference between B=2000 and B=3000.
As B value increases  diffusion weighting increases  increases detection
 Slice thickness <5mm

› Weon- detection rate within 24 hrs @5mm thickness – 13%, then increased to 38% at 3mm

Increase detection of small punctate lesions by decreasing partial volume
averaging effects








Ahn – overall time to MRI was 6hrs . However, those with MRI
changes is 9 hrs
16 out of 203 TGA over 7yrs with DWI hippocampal changes
Bartsch – found that lesions localised to CA1 of
hippocampus in 29 TGA patients in 24-72 hrs
Peak incidence at 12-72hrs
DWI normalisation on Day 10
Similar to time course of ischaemic
 careful timing to find abnormalities
Lesions resolve on F/U imaging in 1-6 months
3T magnet
 Acquisition between 24 to 72 hours
 3mm DWI slice thickness


Detection increased 88% when scan performed 2-3
days post event, DWI with resolution B=2000, slice
thickness 2-3mm.