Claire L. Isaac

Face processing impairments after encephalitis: amygdala damage and recognition of fear

Face processing and facial emotion recognition were investigated in five post-encephalitic people of average or above-average intelligence. Four of these people (JC, YW, RB and SE) had extensive damage in the region of the amygdala. A fifth post-encephalitic person with predominantly hippocampal damage and relative sparing of the amygdala (RS) participated, allowing us to contrast the effects of temporal lobe damage including and excluding the amygdala region. The findings showed impaired recognition of fear following bilateral temporal lobe damage when this included the amygdala. For JC, this was part of a constellation of deficits on face processing tasks, with impaired recognition of several emotions. SE, YW and RB, however, showed relatively circumscribed deficits. Although they all had some problems in recognizing or naming famous faces, and had poor memory for faces on the Warrington Recognition Memory Test, none showed a significant impairment on the Benton Test of Facial Recognition, indicating relatively good perception of the faces physical structure. In a test of recognition of basic emotions (happiness, surprise, fear, sadness, disgust and anger), SE, YW and RB achieved normal levels of performance in comparison to our control group for all emotions except fear. Their results contrast with those of RS, with relative sparing of the amygdala region and unimpaired recognition of emotion, pointing clearly toward the importance of the amygdala in the recognition of fear.

A comparison of egocentric and allocentric spatial memory in a patient with selective hippocampal damage.

The spatial memory of a single patient (YR) was investigated. This patient, who had relatively selective bilateral hippocampal damage, showed the pattern of impaired recall but preserved item recognition on standardised memory tests that has been suggested by Aggleton and Shaw [Aggleton JP, Shaw C. Amnesia and recognition memory: a reanalysis of psychometric data. Neuropsychologia 1996;34:51-62] to be a consequence of Papez circuit lesions. YR was tested on three recall tests and one recognition test for visuospatial information. The initial recall test assessed visuospatial memory over very short unfilled delays and YR was not significantly impaired. This test was then modified to test recall of allocentric and egocentric spatial information separately after filled delays of between 5 and 60 s. YR was found to be more impaired at recalling allocentric than egocentric information after a 60 s interval with a tendency for the impairment to increase up to this delay. Recognition of allocentric spatial information was also assessed after delays of 5 and 60 s. YR was impaired after the 60 s delay. The results suggest that the human hippocampus has a greater involvement in allocentric than egocentric spatial memory, and that this most likely concerns the consolidation of allocentric information into long-term memory rather than the initial encoding of allocentric spatial information. The findings also suggest that YRs item recognition/free recall deficit pattern reflects a problem retrieving or storing certain kinds of associative information.

Memory for single items, word pairs, and temporal order of different kinds in a patient with selective hippocampal lesions

One kind of between-list and two kinds of within-list temporal order memory were examined in a patient with selective bilateral hippocampal lesions. This damage disrupted memory for all three kinds of temporal order memory, but left item and word pair recognition relatively intact. These findings are inconsistent with claims that (1) hippocampal lesions, like those of the medial temporal lobe (MTL) cortex, disrupt item and word pair recognition, and that (2) hippocampal lesions disrupt temporal order memory and item recognition to the same degree. Not only was word pair recognition intact in the patient, but further evidence indicates that her recognition of other associations between items of the same kind is also spared so retrieval of such associations cannot be sufficient to support within-list temporal order recognition. Rather, as other evidence indicates that the patient is impaired at recognition of associations between different kinds of information, within-list (and possibly between-list) temporal order memory may be impaired by hippocampal lesions because it critically depends on retrieving associations between different kinds of information.

Differential involvement of the hippocampus and temporal lobe cortices in rapid and slow learning of new semantic information.

The present study examined the rapid and slow acquisition of new semantic information by two patients with differing brain pathology. A partial double dissociation was found between the patterns of new learning shown by these two patients. Rapid acquisition was impaired in a patient (YR) who had relatively selective hippocampal damage, but it was unimpaired in another patient (JL) who, according to structural MRI, had an intact hippocampus but damage to anterolateral temporal cortex accompanied by epileptic seizures. Slow acquisition was impaired in both patients, but was impaired to a much greater extent in JL. The dissociation suggests that the mechanisms underlying rapid and slow acquisition of new semantic information are at least partially separable. The findings indicate that rapid acquisition of semantic, as well as episodic information, is critically dependent on the hippocampus. However, they suggest that hippocampal processing is less important for the gradual acquisition of semantic information through repeated exposure, although it is probably necessary for normal levels of such learning to be achieved.

Long-term amnesia: a review and detailed illustrative case study.

Long-term amnesia is a slowly developing form of anterograde amnesia accompanied by retrograde amnesia of variable severity (Kapur, 1996; 1997) often associated with damage to the anterior temporal neocortex and epileptic seizures. The precise neural and functional deficits that underlie this condition are unknown. A patient, JL, who has this condition following a closed-head injury, is described in detail. Her injury caused bilateral anterior temporal neocortex damage that was more extensive on the left and right-sided damage to the perirhinal and orbitofrontal cortices. The hippocampus appeared to be intact bilaterally. Epilepsy developed within two years of JLs injury. Apart from her memory impairments, JLs cognitive functions, including high-level visual perception, attention, semantic memory and executive functions were well preserved. Her memory also seemed well preserved for at least 30 minutes following encoding. The one exception was the patients relatively greater impairment at difficult visual recognition tests for which verbalization may not have been an effective strategy. This problem may have been caused by JLs right-sided perirhinal and orbitofrontal cortex damage. Her recall and recognition was clearly impaired after a three-week delay. She also showed a retrograde amnesia, which appeared to be milder than her remote post-morbid memory deficit. JLs remote memory was preserved for information first encountered in either the pre- or post-morbid period provided the information had received sufficient rehearsal over long periods of time. Her long-term amnesia may have been caused by anterior temporal neocortex damage, possibly in association with her epileptic seizures. Whether the condition is heterogeneous, involves a deficit in slow consolidation, disruption of unconsolidated memories, or blockage of maintenance or disruption of insufficiently rehearsed memories whether or not these have been slowly consolidated is discussed.

The acceptability of computerised cognitive behavioural therapy for the treatment of depression in people with chronic physical disease: a qualitative study of people with multiple sclerosis.

Background: People with chronic physical conditions are at elevated risk of depression. Due to a shortage of Cognitive Behavioural Therapy (CBT) practitioners, computerised CBT (CCBT) is recommended for people with mild to moderate depression. We assessed the applicability of CCBT for the treatment of depression in people with multiple sclerosis (MS). Methods: Depth interviews with 17 people with MS and mild to moderate depression who used one of the two CCBT packages for either eight (Beating the Blues; n = 8) or five (MoodGym; n = 9) weekly sessions were analysed using ‘Framework’. Results: Participants found CCBT-use burdensome due to their physical symptoms. In addition to perpetuating social isolation, the lack of human input meant some participants were unable to define problems, set goals or distinguish between events, thoughts and beliefs as required. CCBT did not legitimise their grief over losses concomitant with their MS. They characterised depression symptom inventories as contaminated by somatic symptoms of their MS. One CCBT package (MoodGym) was perceived as using inappropriate case material for people with the symptoms of MS. Conclusions: It is likely that generic CCBT packages for the treatment of depression will need to be adapted for people with chronic physical conditions to maximise their potential for health benefit.

Cognitive behavioural therapy for the treatment of depression in people with multiple sclerosis: a systematic review and meta-analysis

BackgroundDepression is a common symptom in people with multiple sclerosis. We systematically reviewed published controlled trials on the effectiveness of cognitive behavioural therapy (CBT) for the treatment of depression in people with multiple sclerosis.MethodsPublications were identified using MEDLINE, PsycINFO and the Cochrane Central Register of Controlled Trials to June/July 2013. We combined thesaurus and free-text terms which were synonyms of the concepts multiple sclerosis, depression and cognitive behavioural therapy. We included published controlled trials which compared individual, group CBT, conducted face-to-face or remotely, to no CBT. Two reviewers extracted data to calculate standardized mean differences (SMD) for self-reported symptoms of depression and weighted mean differences (WMD) for the Multiple Sclerosis Impact Scale (MSIS-29), with 95% Confidence Intervals (CIs). We investigated statistical heterogeneity using I2.ResultsSeven eligible studies (n = 433) were identified, which evaluated the effect on depression of CBT delivered individually (3 studies), in a group (3 studies) and by computer (1 study). The summary effect (SMD -0.61, 95% CI -0.96 to -0.26, p=0.0006) was reduced (SMD -0.46, 95% CI -0.75 to -0.17, p=0.002) when an outlying study was removed in a sensitivity analysis to examine statistical heterogeneity. Three studies (n=213) observed a direction of effect using the MSIS-29 which was not statistically significant (WMD -4.36, 95% CI -9.33 to 0.62, p=0.09). There was no between-subgroup heterogeneity (I2=0).ConclusionsCBT can be an effective treatment for depression in MS. Further research should explore optimal durations and modalities of treatment for patients with different characteristics.

Visual paired comparison performance is impaired in a patient with selective hippocampal lesions and relatively intact item recognition

In this study, we have examined visual recognition memory in a patient, YR, with discrete hippocampal damage who has shown normal or nearly normal item recognition over a large number of tests. We directly compared her performance as measured using a visual paired comparison task (VPC) with her performance on delayed matching to sample (DMS) tasks. We also investigated the effect of retention interval between familiarisation and test. YR shows good visual recognition with the DMS task up to 10 s after the familiarisation period, but only shows recognition with the VPC task for the shortest retention interval (0 s). Our results are consistent with the view that hippocampal damage disrupts recollection and recall, but not item familiarity memory.

Memory complaints in epilepsy: An accurate reflection of memory impairment or an indicator of poor adjustment? A Review of the literature

People with epilepsy frequently complain of poor memory. Although organic memory impairment is one possible sequela of neuro-epilepsy variables, these complaints are not consistently supported by performance on objective measures. The current review has two objectives: first, to establish whether inconsistent results are an artifact of methodology and second, to collate existing published literature to identify possible explanations for inaccurate memory self-report in epilepsy. Review of the literature highlights many methodological limitations making it difficult to evaluate findings. However, it is apparent that in people with epilepsy, subjective memory demonstrates a greater relationship with anxiety and depression than with objective memory. We examine the hypothesis that memory complaints in epilepsy are a reflection of difficulties adjusting to, or coping with, the condition. Research has yet to identify any critical variables or pathways through which these factors influence perceptions of memory function. This review proposes a role for illness representations in understanding the nature of memory complaints in epilepsy.

Accelerated long-term forgetting in temporal lobe but not idiopathic generalised epilepsy

Temporal lobe epilepsy (TLE) has been associated with the phenomenon of accelerated long-term forgetting (ALF), in which memories are retained normally over short delays but are then lost at an accelerated rate over days or weeks. The causes of ALF, and whether it represents a consolidation deficit distinct from the one associated with forgetting over short delays, remain unclear. In addition, methodological issues have made results of some previous studies difficult to interpret. This study used improved methodology to investigate the role of seizure activity in ALF. Forgetting was assessed in participants with TLE (who have involvement of temporal lobe structures) and idiopathic generalised epilepsy (IGE; in which seizures occur in the absence of identified structural pathology in the temporal lobes). Learning of novel stimuli was matched between patients with TLE, patients with IGE and healthy controls matched for age and IQ. Results indicated that the TLE group showed accelerated forgetting between 30-min and three-weeks, but not between 40-s and 30-min. In contrast, rates of forgetting did not differ between patients with IGE and controls. We conclude that (1) ALF can be demonstrated in TLE in the absence of methodological confounds; (2) ALF is unlikely to be related to the experience of epilepsy that does not involve the temporal lobes; (3) neither seizures during the three-week delay nor polytherapy was associated with ALF.