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444 Emergency casebook

neurology consultant agreed with our


The diagnosis and management of diagnosis. He saw the patient in a
follow-up clinic where he reassured
transient global amnesia in the her about the diagnosis and then
discharged her with a letter to her
emergency department general practitioner to monitor her risk
factors for CVA.
Magnus Harrison, Mark Williams
DISCUSSION
The incidence of TGA is approximately
Transient Global Amnesia (TGA) is a benign and temporary loss of anterograde 2.910/100 000 worldwide.1 Arterial
memory with the preservation of remote memories and immediate recall. TGA was first ischaemia (TIA), epileptic seizures and
described in 1956 and since then epilepsy, transient ischaemic attacks (TIA), migraine migraine were previously thought to be
and now intracranial venous stasis have been implicated in its aetiology. Precipitants of the most likely factors causing TGA.4 5
TGA include physical exertion and valsalva-like manoeuvres. In order to diagnose TGA Now the most likely cause of this
the criteria created by Hodge and Warlow in 1990 can be used. This requires the condition is thought to be intracranial
episode of memory loss to be witnessed and involve anterograde amnesia. The patient venous congestion leading to ischaemia
must not have any evidence of neurological signs or deficits, features of epilepsy, active in the hippocampus and other mesio-
epilepsy or recent head injury. Finally the episode must have resolved within 24 h. In this temporal structures of the brain asso-
case study the patients symptoms are mistakenly attributed to a TIA. There is no ciated with creating and storing
increased risk of TIA or CVA in patients who have had TGA and there are no increased memories.1 4 5 This is caused by
levels of mortality amongst these patients. In this article we aim to help doctors working Valsalva-like manoeuvres increasing
in the emergency department to diagnose and manage TGA. the intrathoracic pressure and causing
venous reflux in the vessels draining
the brain.1 5 6 A study published in

T
ransient global amnesia (TGA) is a husband was still worried when her
benign, temporary loss of antero- symptoms did not resolve, so he took Neurology used three-dimensional
grade memory with sparing of her to the emergency department. time-of-flight magnetic resonance
immediate recall and remote memories. The patient had no history of hyper- angiography and upper extremity digi-
Worldwide, its incidence is approxi- tension, raised cholesterol, previous tal subtraction venography to show
mately 2.910/100 000 and it is thought myocardial infarction or CVAs, transi- that left brachiocephalic vein occlusion
to be due to intracranial venous stasis ent ischaemic attacks, recent head caused retrograde intracranial venous
leading to ischaemia in the areas of the injury, epilepsy or migraine. She did flow in 50% of those having TGA
brain associated with memory. There not drink and had quit smoking a few compared with none in the control
are many precipitants including physi- years ago, having smoked 20 cigarettes group (p,0.001).6
cal exertion and valsalva-like man- per day for approximately 45 years. The Pre-attack factors associated with
oeuvres. TGA can be diagnosed using only medication she took regularly was TGA include physical exertion, swim-
the Hodges and Warlow criteria created diclofenac that was prescribed for ming, sexual intercourse and use of
in 1990. The most important part of osteoarthritis in her left hand. marijuana and Viagra.1 5 7 The greatest
managing an episode of TGA is the On examination she appeared risk factor for TGA is a history of
psychological support of the patient relaxed. Her airways were open with migraines.7 Patients who have had an
and his or her relatives. no crackles or wheezes, her respiratory episode of TGA have no increased risk
TGA was first described by M Bender rate and oxygen saturation were nor- of having a TIA or CVA, as they have
in 1956.1 Although this is not an mal, her heart rate was 64 beats per different risk factors.4
uncommon presentation of acutely minute and had a regular rhythm, and In order to diagnose TGA the patient
altered neuropsychiatric status, it may her blood pressure was raised at must satisfy the following criteria,
be new to the members of an emer- 180 mm Hg systolic and 84 mm Hg created by Hodge and Warlow in 19908:
gency department.2 TGA needs to be diastolic. Her Glasgow Coma Scale was (1) The attack was witnessed and
differentiated from the diagnosis of 15/15 and her abbreviated mini-mental reported.
cerebrovascular accident (CVA) and test score was 9/10 (her immediate (2) There was obvious anterograde
subarachnoid haemorrhage.3 recall of three words was spared, but amnesia during the attack.
In this case study we give an example she was unable to remember any of the (3) There was an absence of clouding
of a presentation of TGA to the emer- three words after three minutes). Her of consciousness.
gency department along with impor- cranial and peripheral nerves were (4) There were no focal neurological
tant facts that will help doctors to normal. She was apyrexic and her signs or deficits during or after the
manage these patients. capillary blood glucose was 5.2 mmol/ attack.
l. Her ECG and urinalysis were normal (5) There were no features of epi-
CASE STUDY and her full blood count, urea and lepsy.
A woman was strenuously cutting her electrolytes and cholesterol were all (6) The attack resolved within 24 h.
hedge when she suddenly froze. within normal ranges. (7) The patient did not have any
Afterwards she had no recollection of The diagnosis of the patients pro- recent head injury or active epilepsy.8
the previous 2 h and was unable to retain blems was transient global ischaemia. As the prognosis of TGA is very good
any new information for longer than a By this time her anterograde amnesia (it has a small recurrence rate and no
few minutes. She had no other symp- was beginning to resolve. After discus- increased mortality rate), the most
toms such as headache or confusion. sion with a neurology registrar she was important part of management after
After visiting her general practitioner she admitted to the neurology ward where diagnosis is looking after the psycholo-
was diagnosed as having had a transient she received a CT scan of her brain that gical needs of the patient and his or her
ischaemic attack (TIA). However her showed old ischaemic change. The relatives.2 Seeing a once competent and

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Emergency casebook 445

healthy partner, sibling or parent Stoke-on-Trent, Staffordshire ST4 7LN, UK; Clinical and laboratory findings in a particular type
m.williams@doctors.org.uk of acute global amnesia. Eur J Emerg Med
become incapable of remembering 2000;7:2913.
what was said only a minute ago is Accepted 17 January 2007 4 Pinol-Ripoll G, de la Puerta Gonzalez-Miro I,
very distressing, and hence it is often Martinez L, et al. A study of risk factors in transient
Competing interests: None declared. global amnesia and its differentiation from a
the relatives who will require reassur- transient ischaemic attack. Rev Neurol
ance. Informed consent was obtained for publication of 2005;41:5136.
the persons details in this report. 5 Rashid J, Starer J. Transient global amnesia
Emerg Med J 2007;24:444445. following a transoceanic flight. Psychiatry Clin
doi: 10.1136/emj.2007.046565 Neurosci 2006;60:516.
6 Chung CP, Hsu H, Chao A, et al. Detection of
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transient global amnesia. Neurology
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Hospital of North Staffordshire, Stoke-on-Trent, of the literature and thorough study of 142 cases. Branas F, et al. Transient global amnesia.
UK Brain 2006;129(Part 7):164058. Casecontrol study of 24 cases. Rev Neurol
2 Basior J, Vogel S, Mitton J. Transient global 1996;24:5547.
amnesia in the emergency department. Am J Emerg 8 Hodges JR, Warlow CP. Syndromes of transient
Correspondence to: Dr M Williams, University Med 1985;3:3527. amnesia: towards a classification; a study of 153
Hospital of North Staffordshire NHS Trust, North 3 Monzani V, Rovellini A, Schinco G, et al. Transient cases. J Neurol Neurosurg Psychiatry
Staffordshire Royal Infirmary, Princes Road, global amnesia or subarachnoid haemorrhage? 1990;53:83443.

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