Journal of Clinical Anesthesia 37 (2017) 159–161

Contents lists available at ScienceDirect

Journal of Clinical Anesthesia

Case report

Transient global amnesia in immediate postoperative period: A
diagnostic dilemma
Anudeep Jafra a,⁎, Tanvir Samra b, Vasudha Gupta b, M Seran Kumar Reddy b
a
b

Department of Anaesthesia and Intensive Care, Post Graduate Institute Of Medical Education and Research, Sector-12, 160012 Chandigarh, India
Post Graduate Institute Of Medical Research and Education, Sector-12, 160012 Chandigarh, India

a r t i c l e

i n f o

Article history:
Received 7 May 2016
Received in revised form 1 November 2016
Accepted 7 December 2016
Available online xxxx
Keywords:
Memory
Amnesia
Transient global amnesia

a b s t r a c t
Introduction: Transient Global Amnesia (TGA) is short-term inability to form new memories despite otherwise
normal neurological function. There is associated anterograde and retrograde amnesia. The memory loss is
often accompanied by repetitive questioning and temporal disorientation while higher cognitive functions are
preserved. The symptoms usually resolve by 24 h.
Case report: We present an interesting case of 31 year old female who was planned for robotically assisted right
sided pyeloplasty. 30 min after emergence from anaesthesia patient was disoriented, with retrograde and anterograde amnesia, but neurological function was intact. Neurologic imaging revealed no abnormality. 36 h later patient was able to recall everything.
Discussion: The pathogenesis of TGA has more recently been attributed to cerebral venous hypertension resulting
from retrograde jugular venous flow. Precipitating events are Valsalva manoeuvre, emotion/stress/pain, Excessive exertion, sexual intercourse and swimming in cold water.
Conclusion: TGA presents dramatically, it needs to be differentiated from cerebral event. It resolves on its own. But
one needs to be aware of existence of such an entity.
© 2016 Elsevier Inc. All rights reserved.

1. Introduction

2. Case report

Transient global amnesia (TGA) is characterized by temporary disruption of short term memory. There is inability to form new memories,
anterograde amnesia which is abrupt in onset and associated retrograde
amnesia which ranges from few hours to years [1]. The imperative feature is patient is alert, attentive and there is no clouding of consciousness or loss of personal identity. Usually the symptoms resolve by
30 min to 24 h. Once the attack is over there occurs rapid and complete
return of anterograde memory, but retrograde memory is slow to return
to normal and patient is not able to recall the present episode of memory loss. We present a case of TGA in a young female following robotically assisted laparoscopic pyeloplasty under general anaesthesia and
highlighting the differential diagnosis, precipitating events and treatment of this rare neurological entity.

31 year old female patient belonging to American Society of
Anaesthesiologists physical status classification 1, weighing 42 kg was
administered general anaesthesia for robotically assisted laparoscopic
pyeloplasty. Her biochemical and hematological investigations were in
normal limits and past medical history was insignificant. Patient was
premedicated with H2 blocker (ranitidine 150 mg) and benzodiazepine
(alprazolam 0.25 mg). Intraoperative monitoring included electrocardiogram, pulse oximetry, end tidal carbon dioxide measurement, noninvasive blood pressure measurement and temperature monitoring.
Patient was induced with 100% oxygen using propofol 2 mg/kg, Muscle
relaxation was achieved using vecuronium 0.1 mg/kg, for analgesia4.5 mg morphine was given, airway was secured with 7.5 mm endotracheal tube. Anaesthesia was maintained using desflurane in 50% oxygen
in air mixture. Patient was operated in left lateral decubitus position and
surgery lasted for two hours. Intraoperatively hemodynamics remained
stable with no episode of hypotension. Extubation was smooth and uneventful; patient was conscious and responding to commands.
30 min after surgery, in postanaesthesia care unit patient was not
able to recall names of family members and was repeatedly asking
‘where am I’. Patient was conscious and oriented but there was total amnesia of her hospitalization for the surgery. Neurological examination
including higher mental functions and cranial nerve examination were

⁎ Corresponding author: Post Graduate Institute of Medical Education and Research,
Sector-12, Chandigarh 160012, India.
E-mail addresses: anu_gmch@yahoo.co.in (A. Jafra), drtanvirsamra@yahoo.in
(T. Samra), dr.vasudhagupta@gmail.com (V. Gupta), seranreddy.m@gmail.com (M. Seran
Kumar Reddy).

http://dx.doi.org/10.1016/j.jclinane.2016.12.005
0952-8180/© 2016 Elsevier Inc. All rights reserved.

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A. Jafra et al. / Journal of Clinical Anesthesia 37 (2017) 159–161

Table 1
Postoperative investigations.

Postoperative

Hb-10.6 g%
Blood sugar-110 mg%

Na+ – 142 meq/l
K+ – 3.8 meq/l

ABG-pH -7.36/paO2-80/paCO2-38/HCO3-22.8/BE-1.5/Cl−-98.9

normal. Electrolyte/metabolic abnormality were ruled out on normal
values of arterial blood gas analysis and biochemical investigations
(Table 1). Non-contrast computed tomography scan of head (Fig. 1)
was done 6 h later but it was normal. A detailed neurological and psychiatric evaluation was done and patient failed in all tests for short
term memory. Patient was shown five objects which 30 s later when
again shown to her she was not able to recognize and refused that she
was shown these before. Mini Mental State Examination (MMSE)
score was 26; deficit was seen only in amnestic components. Patient
was closely observed and monitored and no active intervention was
done on second postoperative day. She was not able to recall any past
events, not able to recognize her own children but there was no loss
of personal identity. After 36 h patients memory recovered and she
was able to recall all her past and present history but was not able to recall this event of memory loss and the surgery she had undergone.
MMSE score after the episode was 30/30.

3. Discussion
TGA was first described by Fischer and Adams in 1958; it is characterized by transient loss of memory in an otherwise healthy patient
[2]. The annual incidence ranges from 3 to 32/100,000/year, with slight
female preponderance. There is a brief period of anterograde amnesia
and retrograde amnesia which extends to days or weeks to years
which subsequently shrinks over time and finally patient is left with
permanent amnesia for a short duration when new memories were
not formed. This is accompanied by repetitive questioning by the patient as to “where am I”, “Why I am here” and associated temporal dissociation could be there. But there are no focal neurological symptoms
and all higher cortical functions like language, calculations, reasoning,
abstract thinking are intact and patient is calm but disoriented to time
and place. Though a rare entity, the literature search shows its existence
after both general and spinal anaesthesia [3,4].
In our case the following differential diagnosis were made; acute
confusional states (ACS), complex partial seizures, transient epileptic

amnesia (TEA), transient ischaemic attack (TIA), toxic metabolic states,
psychogenic amnesia, migraine and paradoxical embolism from patent
foramen ovale. In ACS patients are inattentive and there is loss of stream
of thoughts so it was ruled out. There was no episode of seizure in our
patient so possibility of complex partial seizures was not there. TEA is
a manifestation of temporal lobe epilepsy, and patients will have multiple episodes characterized by amnesia and symptoms usually last for
less than one hour which did not occur in our case. In psychogenic amnesia there is profound retrograde amnesia with loss of personal identity but intact anterograde memory, which did not correspond to the
symptoms in our patient. TIA was ruled out as there was no motor
and sensory loss in our patient and also CT scan of the patient was normal. In contrast the CT images in acute embolic stroke might show early
ischaemic changes. We labeled our patient with TGA after excluding all
the above causes and using diagnostic criteria (Table 2) laid down in
1990 by Hodges JR and Warlow CP [5].
Etiology of TGA is obscure; large number of hypothesis has been
given. Most commonly affected areas of brain linked to TGA are
mediobasal temporal, hippocampus and parahippocampus. Neuroimaging modalities like single photon emission computed tomography
scan show decreased blood flow in these areas in TGA patients. Also diffusion weighted imaging studies show changes in the mentioned areas
after 48 h of the event [6,7]. And before onset of TGA most patients have
Valsalva like precipitating activities like swimming, sexual intercourse,
acute pain, coughing, straining and immersion in cold water. Lewis suggested Valsalva manoeuvre allows brief retrograde transmission of high
venous pressure to the cerebral venous system, due to jugular valve incompetence resulting in venous ischaemia [8]. Sander D et al. studied
the venous flows in internal jugular vessels in 21 patients with TGA
and 21 controls using two Valsalva manoeuvres and concluded that
TGA was attributable to venous congestion and consequent venous ischaemia to bilateral diencephalic or hippocampal structures [9]. During
perioperative period patients may undergo substantial pain, emotional
and physical stress which leads to increase intrathoracic pressure, leading to decreased cerebral venous return from the superior vena cava and
increased cerebral venous pressure, thereby causing venous ischemia
due to cerebral venous congestion and hence can trigger an episode of
TGA [10]. Pantoni et al. suggested the contribution of psychological factors and reported that 50% patients with TGA had a phobic personality
trait [11]. Recently, a unifying hypothesis has been put forward by
Winbeck et al. which suggests that TGA can result from transient ischaemia of memory-relevant structures either from arterial emboli or from
venous ischaemia with Valsalva-like activities before the onset of symptom [7].
Factors like coughing during extubation, generation of large levels of
negative pressure by patient during extubation, positive end expiratory
pressure and Valsalva manoeuvre might have lead to increased intrathoracic pressure and venous backflow in our patient. Perioperative factors like anxiety, pain, emotions and stress could also have acted as
precipitating factors. The drugs used in the patient were all short acting
(including desflurane- low blood gas solubility): it is unlikely that such
prolonged amnesia was due to residual pharmacological effects of
drugs. Usually the attack lasts for less than 24 h duration but the diagnostic criteria which have been laid out have not been validated as to

Table 2
Diagnostic criteria.

Fig. 1. Non-contrast computed tomography scan of head - normal.

1.
2.
3.
4.
5.
6.
7.
8.
9.

Attack must be witnessed
Acute onset of anterograde amnesia during the attack
No clouding of consciousness
No cognitive impairment other than amnesia (no aphasia or apraxia)
No loss of personal identity
No focal neurology or epileptic features must be present
Patients with recent head trauma or seizures were excluded
Attack must resolve within 24 h
Other causes of amnesia must be excluded

A. Jafra et al. / Journal of Clinical Anesthesia 37 (2017) 159–161

whether they can be successfully applied in clinical practice to this subset of patients with postoperative amnesia. If diagnosis can be made on
basis of history and examination no further testing or investigations are
required. Though in 1995, Sandson and Price suggested a myriad group
of investigations including electro encephalogram, echocardiography,
Doppler, magnetic resonance imaging, magnetic resonance angiography, holter monitoring and toxicology screening [12]. Diffusion weighted magnetic resonance imaging (DW-MRI) was the next imaging
modality of choice in our patient but due to absence of any localising
signs it was postponed. Sedlaczek et al. showed with serial imaging
DWI changes were rarely noted in the acute phase but were evident at
48 h [13]. However some investigators report no detectable DWI changes [7].The recurrence is rare with an incidence of 3–20% in 5 years. It
does not lead to any long term neurological sequelae and no treatment
is required.

4. Conclusion
TGA presents in a very dramatic manner, is a self-limiting condition
and does not lead to any long term neurological deficit. But it needs to
be differentiated from acute cerebral ischaemic event and thorough
neurological examination is a must. One needs to be aware of existence
of such an entity to relieve the anxiety of patient's relatives and reassure
that the event will resolve spontaneously.

Conflict of interest
No conflicts of interest.

161

Funding
This case report did not receive any specific grant from funding
agencies in the public, commercial, or not-for-profit sectors.
Acknowledgement
Published with written consent of the patient.
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