Widespread cognitive impairment in psychogenic anterograde amnesia
Sanjay Kumar, PhD, Behavioral Brain Sciences Center, School of Psychology, University of Birmingham, Birmingham, B15 2TT, UK. Email: firstname.lastname@example.org
Abstract A 34-year-old man without a past history of any psychiatric or neurological disorder developed severe anterograde amnesia following a psychological trauma. Initial assessment of neuropsychological functions 3 months after the psychological trauma indicated severe memory deficits for acquiring new information in both verbal and visual modalities with widespread cognitive deficits in attention, executive functions, and intellectual ability. Importantly, working and remote memory were intact. The case illustrates that psychogenic anterograde amnesia might be associated with a wider range of cognitive deficits. Possible neurobiological explanations are discussed to explain large cognitive impairments associated with anterograde psychogenic amnesia.
Organic amnesia is typically restricted to deficits of memory function leaving other cognitive function intact.1,2 Similar restricted memory deficits have also been observed in retrograde psychogenic or dissociative amnesia.3 Retrograde psychogenic amnesia is common but anterograde psychogenic amnesia is rare.4 Some researchers have suggested widespread cognitive impairments in retrograde or mixed anterograde and retrograde psychogenic amnesia.5,6 Here we present a case of pure anterograde amnesia of psychogenic origin that produced widespread cognitive deficits in addition to amnesia following a significant psychological stress.
A 38-year-old married man, without any past history of psychiatric or neurological illness, presented with an acute onset of abnormal behavior following a psychological trauma. He had borrowed money from a friend, which he had been unable to return on the agreed date. This created considerable stress for him. As the evening of the agreed day approached, the patient became very tearful, restless and inconsolable. He kept opening the door to check if his friend had come to collect the money. The patient appeared disoriented, was unable to recognize anyone or register any new information and maintained abnormal postures for several minutes. The patient was hospitalized, following no change in his behavior for 1 day. He was diagnosed with reactive psychosis and treated with antipsychotics and benzodiazepines. Subsequently he also received eight sessions of bilateral modified electroconvulsive therapy (ECT). In the hospital he was noted to have memory problems that would interfere in his daily life, for example he could not remember if he had any visitors. Over a period of 2 weeks his behavior improved but the memory problems and abnormal posture persisted. He was brought to National Institute of Mental Health and Neurosciences (NIHMHANS), Bangalore, with these enduring problems.
The patient was investigated thoroughly for any organic cause of his condition. Plain structural magnetic resonance imaging (MRI), electroencephalogram (EEG), biochemical investigations for renal functions, liver functions, electrolytes, blood glucose, serum ceruloplasmin, serum copper levels, and hematological investigations were within normal limits. He did not have any focal neurological abnormality on examination, nor did he have any hallucinations, delusions, elated, or depressed affect. He scored 8–12 on Mini-Mental Status Examination.7 There was no diurnal variation in his cognitive state or fluctuation of consciousness. During his stay in the hospital he learned the name of only one consultant and was observed to have significant way finding difficulties. He had normal memory for events that had happened before the date he was due to pay back the money, such as the year of his graduation, the date of his marriage and so on and he could identify his relatives and give a detailed account of his business. However, when asked for current date and month, he continued to say it was the date on which he had agreed to pay back the loan.
Neuropsychological assessment 3 months after the onset of disorder
Memory functions were assessed using Auditory Verbal Learning Test, Rey's Complex Figure Test, Passage learning test, verbal working memory test (one-back and two-back test) as part of the NIMHANS Neuropsychology Battery,8 which is specifically adapted to the Indian population, and the Wechsler Memory Scale9 and Face Recognition Memory Test.10 Attention was assessed on the Digit Vigilance Test11 and the Digit Symbol Substitution Test. Executive functions were assessed on the Tower of London Test,12 the Wisconsin Card-Sorting Test13 and the Design Fluency Test; and intelligence on Raven's Standard Progressive Matrices (SPM).14
Neuropsychological assessment at 3 months after the onset of disorder indicated severe deficits in learning new items both verbally and visually, which indicated anterograde amnesia (Table 1). The memory deficits were only of anterograde type and did not include working memory and remote memory deficits. The patient also had other cognitive impairment, such as deficits in attention and executive functions. He had average intelligence on the SPM.
Table 1. Neuropsychological tests
|Anterograde memory functions|
| AVLT trial 1||2||<5th||4||<5th|
| AVLT trial 2||3||<5th||8||30th|
| AVLT trial 3||3||<5th||11||50th|
| AVLT trial 4||5||<5th||7||<5th|
| AVLT trial 5||6||<5th||9||10th|
| AVLT list B||2||5th||2||5th|
| AVLT immediate recall||0||<5th||5||<5th|
| AVLT delayed recall||0||<5th||3||<5th|
| AVLT hits||11||<5th||9||<5th|
| AVLT total learning||19||<5th||39||10th|
| Passage learning immediate recall|| 1/22||<5th||8/22||20th|
| Passage learning delayed recall (after 30 min)|| 0/22||<5th||4/22||<10th|
| WMS: logical memory-I||0.5/22|| ||8/22|| |
| WMS: logical memory-II|| 0/22|| ||7/22|| |
| WMS: paired associate learning|| 6/21|| ||9.5/21 || |
| CFT: immediate recall|| 0/36||<5th||13/36 ||<5th|
| CFT: delayed recall|| 0/36||<5th||11.5/36 ||<5th|
| Face recognition memory (d')||0.62||25th||1.05||50th|
| WMS: visual reproduction|| 5/14|| ||13/14 || |
| WMS: MQ||65|| ||91|| |
| One-back words: hits/total||9/9||100th||9/9 ||100th|
| Two-back words: hits/total||8/9||80th||6/9 ||20th|
| WMS: digit forward||6|| ||6|| |
| WMS: digit backward||4|| ||4|| |
| WMS: personal and current information||6/6|| ||6/6 || |
| Digit vigilance test: time||1580 s ||<5th||796 s||7.5th|
| Digit vigilance test: error||12||18th||0||100th|
| Digit symbol substitution test: time||457 s||<5th||223 s||35th|
| WMS: orientation||3/5|| ||5/5 || |
| WMS: mental control||4/9|| ||6/9 || |
| Category fluency (name of animals)||11||10th||8||<5th|
| Phonemic fluency||8.6||25th||12.3||60th|
| Stroop effect||419||<5th||240||6th|
| Tower of London: total problems solved correctly|| 7/14||40th||12/14 ||95th|
| WCST: % perseverative response||30||40th||44||25th|
| WCST: No. categories||1||5th||3||25th|
| WCST: % conceptual level response||21||<5th||29||10th|
| WCST: Failure to maintain set||2||22nd||0||100th|
| Design fluency: free condition||1||<5th||3||15th|
| Design fluency: fixed condition||1||10th||15||95th|
| Standard progressive matrices||38||50th||52||90th|
| CFT: copy||36/36||100th||36/36 ||100th|
Follow-up neuropsychological assessment
At follow-up assessment at 9 months after the onset of disorder the patient had still not resumed his premorbid life routine. Members of the family reported some improvement in daily functioning but he continued to have memory problems. On the formal neuropsychological tests he had improvement in many cognitive domains (Table 1). Although his over all memory quotient (MQ) improved, on some tests he still showed severe impairments suggesting persisting anterograde amnesia. There was partial improvement in the attention and executive functions. In addition his overall intellectual ability was higher in the second assessment compared to the first.
This case study illustrates the consequences of psychological trauma on cognitive functions including memory. The present patient had no evidence of organic involvement because structural MRI, EEG, hematological and biochemical investigations were unremarkable. Although the patient received ECT, his memory problems and other cognitive deficits pre-dated ECT administration and no further deterioration in his cognitive functioning was observed after ECT. The impaired cognitive functioning cannot be attributed to the effect of medications because there was improvement at the second assessment despite continued medications. Cases with such unexplained etiology often lead clinicians to consider malingering. However, clinically and on neuropsychological tests no evidence of malingering could be established.15
The patient experienced psychological stress immediately prior to the onset of the problem, which seems to be the only possible explanation for his current illness. Therefore we suggest that the patient suffers from psychogenic anterograde amnesia. The memory impairments could have resulted from acute neurotransmitter changes induced by stress that may cause acute, but reversible, metabolic shutdown of medial temporal lobe structures.16
Intriguingly, in contrast to anterograde amnesia of organic origin with a well-defined brain lesion,1,2 the present patient had non-memory cognitive functions impairment as well. De Renzi hypothesized that sudden abnormal excitation of emotional structures can result in inhibition of cognitive systems.17 These widespread impairments may be mediated by increases of glucocorticoids that often occur during experience of stress.18–20 Glucocorticoid receptors are widely distributed in the hippocampus and other brain regions, including the prefrontal cortex.21 Effects of glucocorticoids on prefrontal-mediated cognitive functions have been reported.19 Therefore we suggest that the psychological stress experienced by the present patient had adverse effect on his brain functions that produced a wide range of cognitive dysfunction in addition to severe anterograde amnesia.