Int J Legal Med (2015) 129:223–226 DOI 10.1007/s00414-014-1038-5
Transient global amnesia in legal proceedings Martin Griebe & Hansjörg Bäzner & Micha Kablau & Michael G. Hennerici & Kristina Szabo
Received: 8 October 2013 / Accepted: 16 June 2014 / Published online: 25 June 2014 # Springer-Verlag Berlin Heidelberg 2014
Abstract Transient global amnesia (TGA) is a neurological disorder characterized by an acute onset of severe anterograde amnesia. While retrograde amnesia may be present—although to a lesser extent—patients have no further cognitive disturbances or neurological signs. These symptoms resolve fully within several hours leaving a permanent memory gap for the duration of the episode and do not lead to long-term neurological deficits. In addition to well-defined clinical diagnostic criteria, in up to 80 % of patients, small, point-shaped lesions in the hippocampus are detected 24–48 h after symptom onset on diffusion-weighted magnetic resonance images. Despite several etiological hypotheses, to date, there is no scientific proof for the etiology of TGA or the small hippocampal lesions. Interestingly, in a large number of cases, an emotionally or physically straining event precipitates the onset of TGA, suggesting a stress-related mechanism. We report two cases of TGA occurring in legally relevant settings: affecting the victim of brutal burglary and the key witness in a murder trial. In the context of forensic medicine, the knowledge of this disorder and recognition of its typical features are essential. Keywords Transient global amnesia . Amnesia . Emotional stress . Hippocampus . MRI Transient global amnesia (TGA) is characterized by a sudden and severe anterograde memory disturbance accompanied by various degrees of retrograde amnesia affecting mostly elderly M. Griebe (*) : M. Kablau : M. G. Hennerici : K. Szabo Department of Neurology, UniversitätsMedizin Mannheim, University of Heidelberg, Theodor-Kutzer-Ufer 1-3, 68135 Mannheim, Germany e-mail: [email protected]
H. Bäzner Department of Neurology, Klinikum Stuttgart, Stuttgart, Germany
individuals [1, 2]. During the episode, patients cannot remember new episodic information (e.g., how they were brought to hospital or the doctors they have met) and repeatedly ask the same questions about their present whereabouts and situation (“How did I get here?” or “What am I doing here?”). They are cooperative, alert, and fully oriented to person, but not accurately to time and place [3, 4]. As required by diagnostic criteria of TGA, there are no additional neurological deficits; however, a number of associated symptoms have been reported in the literature, such as headache, nausea, emesis, dizziness, chills/flushes, fear of dying, and emotionalism [1, 3]. The exact duration of a TGA episode is often difficult to determine, as recovery is mostly gradual. TGA must resolve within 24 h; however, the typical duration reported is in general shorter, estimated around 4 and 6 h [1, 4]. TGA patients are left with a permanent memory gap for the duration of the attack. The diagnostic criteria still in use today were first established in 1985 by Caplan and elaborated in 1990 by Hodges and Warlow; these criteria demand that there is no clouding of consciousness, other impairments of cognition, or a history of epilepsy or head trauma [3, 5]. While in rare cases TGA might occur repeatedly, in most patients, it is a singular event . TGA is considered a benign disorder as memory deficits resolve completely and do not lead to long-term symptoms . Fisher and Adams, who first used the term TGA in 1958, already described the presence of certain events occurring immediately before the attack— such as swimming in cold water, taking hot showers, pain, and sexual intercourse . In a more recent analysis, in up to 90 % (32–89.1 %) of reported TGA cases, a precipitating event—mainly described as physical, emotional, or behavioral stress—was reported . In addition to those mentioned above, typical events include stressful medical examinations, arguments, funerals, exhausting physical work, and celebrations.
Case 1 A 63-year-old woman without a history of neurological or psychiatric diseases was brought to the emergency room by paramedics. The police had found her at a crime scene and believed she was in a state of shock. She told us that she worked as a cashier in a small bakery. The last thing she could recall from that morning was opening the backdoor for the delivery man. Neurological examination showed a fully alert but restless patient. She presented with the typical clinical picture of a TGA: she was not fully oriented to time and space but was able to give correct information concerning her person. She repeatedly asked “Why am I here?” In the course of neurologic examination, she could not remember new information presented to her (e.g., the name of the hospital). As we learned from the police, a man had entered the bakery and had attacked her 2 h earlier. He had held a knife to her throat and forced her to hand over the money in the cash register. The patient’s memory functions returned to normal on the evening of the same day; however, she never recalled what had happened that morning. MRI performed on the next day showed small hyperintense lesions in both hippocampi on diffusionweighted images (DWI; Fig. 1a).
Case 2 A 52-year-old, healthy man was to appear as a witness in a murder trial. Six months previously, he had observed from a second floor window of his apartment how a man was shot multiple times in broad daylight. On the day in court, as he was about to step up to the witness stand and begin his testimony, he suddenly became agitated and started asking Fig. 1 Axial (left) and coronal (middle) diffusion-weighted MRI show typical hyperintense dotlike lesion in the hippocampus bilaterally in a patient with assault-induced TGA (a) and in the left hippocampus in a patient developing TGA while appearing as an eye-witness in a murder trial (b). Yellow arrows mark the hippocampal lesions with magnified image sections on the far right
Int J Legal Med (2015) 129:223–226
repeated questions about the circumstances and the time of day. The hearing was stopped, and he was rushed to the emergency room. There, he was only oriented to person and could not remember any novel information. He could not recall what had happened and why he was brought to the hospital. His family told us that he had been very anxious in the morning before the trial knowing that he would have to speak in front of the murder suspect. The memory disturbance gradually improved over the course of 5 h but left a permanent amnesia for the events at court. DWI 24 h later displayed a small hyperintense lesion in the left hippocampus (Fig. 1b).
Discussion Memory function and its disturbances are common issues in legal cases. Crime-related amnesia is most often reported as a phenomenon in offenders claiming memory loss for the criminal act. However, such issues are also discussed in victims as well as eye-witnesses—although with different implications. In the context of forensic medicine, the causes of amnesia in subjects involved in judicial proceedings include organic causes (including post-traumatic stress disorder), substanceinduced amnesia, dissociative disorders, and malingering . The clinical presentation of TGA is especially distinct from that of malingering; while TGA presents as a more or less isolated and stereotypic disturbance of anterograde episodic long-term memory, patients with malingering over-endorse a wide variety of symptoms inconsistent with any neuropsychiatric disorder [9–12]. Table 1 lists some of the typical characteristics of TGA versus malingering. In both cases reported here, the patients exhibited the typical and distinct features of TGA according to established clinical diagnostic criteria .
Int J Legal Med (2015) 129:223–226 Table 1 Typical characteristics of TGA versus malingering
Typical characteristics of TGA
Typical characteristics of malingering
Isolated disturbance of learning and recalling novel episodic information Lack of additional neurological symptoms Patients repeatedly ask the same question concerning situation Cooperative, alert, and fully oriented Associated symptoms include headache, nausea, emesis, dizziness Transient, typically lasts 4–6 h
Mix of symptoms not consistent with any mental illness Exaggeration of wide variety of symptoms Endorsement of positive rather than negative symptoms Approximate answers Positive response to suggested symptoms
While a stress-related etiology of TGA has been postulated—although to date there is no evidence for the exact underlying mechanism—there is no doubt among experts that emotionally distressing events can trigger TGA [2, 13]. Three interesting cases involving crime have been published previously: in 1998, Pillmann and Broich described a 72-year-old woman who suffered an attack of TGA after discovering a burglary in her home . In 2010, Stöllberger et al. reported a woman with assault-induced Takotsubo cardiomyopathy (TTC) and anterograde amnesia, with features suggestive of TGA . The 77-year-old woman had been assaulted by a person sneaking up to her when she was unlocking the door of her apartment. Unfortunately, the authors did not report whether she had fulfilled clinical criteria for TGA and whether neuropsychological testing or MRI had been performed. It is noteworthy that precipitating stressful events have also been observed in TTC patients . In his case series published in 1982, Fisher reports precipitating activities in TGA patients: one of his patients was robbed in his drugstore by thieves. He became amnestic immediately after he told the police of the robbery . Based on the nature of clinical impairment during TGA with the inability to form new long-term memories, a transient dysfunction of the medial temporal lobes, especially of the hippocampus, has been repeatedly postulated to underlie TGA . Neuroimaging studies in single patients or small case series using PET or SPECT have shown alterations of perfusion or metabolism during the acute or post-acute phase of TGA in the thalamus, the amygdala, the medial temporal lobes, or the prefrontal cortex [19–22]. In 1999, Gass et al. examined patients with acute TGA using MRI and found no signs of hyperintensity on diffusion-weighted MRI (DWI) that would imply the regional decrease of water mobility or acute T2 signal changes . The lack of such findings suggested that mechanisms other than ischemic infarction cause TGA. Extending this research in a follow-up study, the group used a modified study design to investigate TGA patients that included serial DWI measurements performed from the day of symptom onset through days 1 and 2 . As a result, they were able to demonstrate that more than 80 % of patients
Symptoms lessen with fatigue
developed small, point-shaped, uni- or bilateral DWI lesion in the lateral aspect of the hippocampal formation that became detectable 24–48 h after symptom onset. In both of our patients, MRI performed on the day following TGA showed these typical hippocampal lesions. While these findings actually link the disorder to the hippocampus anatomically, the exact etiology of these small lesions remains uncertain . In conclusion, TGA must be considered a differential diagnosis of amnesia in legal proceeding, especially if preceded by stressful events. Subjects with acute onset of amnesia in such situations need to be evaluated by neurologists who are able to recognize the features of TGA. MRI should be considered to affirm the diagnosis.
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