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PubMed1996

The effect on memory of chronic prednisone treatment in patients with systemic disease.

There have been no systematic investigations of the effects of glucocorticoid treatment on memory in a clinical population despite experimental and clinical evidence that such treatment could cause memory disturbance. We conducted both cross-sectional and longitudinal studies. In Study 1, we administered tests of both hippocampal-dependent explicit memory and hippocampal-independent implicit memory to twenty-five prednisone-treated patients with systemic disease without CNS involvement and 25 matched clinical controls. All treated patients were taking doses of 5 to 40 mg of prednisone daily for at least 1 year. The glucocorticoid-treated group performed worse than the controls on tests of explicit memory, but the groups did not differ on the implicit memory task. Multiple regression analyses suggested that elderly patients are more susceptible to memory impairment with less protracted treatment. The results of Study 2, a prospective, longitudinal study of the effects of prednisone on memory across 3 months of therapy, suggest that even acute treatment can adversely affect memory. The observed alteration in memory was not secondary to inattention, affective disturbance, generalized global cognitive decline, or severity of disease. Results reported here, combined with previous clinical and experimental reports, indicate that the risk of memory impairment should be carefully considered before initiating treatment with glucocorticoids. Conversely, use of glucocorticoids should be considered in the differential diagnosis of memory loss. Finally, the potential benefit of anti-inflammatory treatment in Alzheimer's disease might be counterbalanced by possible iatrogenic memory impairment, at least when synthetic glucocorticoids are considered.

Adult↗

PubMed2000

Short- and long-term memory: differential involvement of neurotransmitter systems and signal transduction cascades.

Since William James (1890) first distinguished primary from secondary memory, equivalent to short- and long-term memory, respectively, it has been assumed that short-term memory processes are in charge of cognition while long-term memory is being consolidated. From those days a major question has been whether short-term memory is merely a initial phase of long-term memory, or a separate phenomena. Recent experiments have shown that many treatments with specific molecular actions given into the hippocampus and related brain areas after one-trial avoidance learning can effectively cancel short-term memory without affecting long-term memory formation. This shows that short-term memory and long-term memory involve separate mechanisms and are independently processed. Other treatments, however, influence both memory types similarly, suggesting links between both at the receptor and at the post-receptor level, which should not be surprising as they both deal with nearly the same sensorimotor representations. This review examines recent advances in short- and long-term memory mechanisms based on the effect of intra-hippocampal infusion of drugs acting upon neurotransmitter and signal transduction systems on both memory types.

Animals↗

PubMed2005

[A case of primary progressive multiple sclerosis with onset of memory impairment].

We report a 52-year-old woman with primary progressive multiple sclerosis (PPMS) presenting with chronic progressive memory impairment. From a couple of years prior to admission, she had developed impairment of her short-term memory. For example, she forgot her nephew's name, and spoke the same phrases again and again. She also sometimes forgot to turn off her gas stove and forgot things she bought in shops. Moreover, her mental activity gradually decreased and she became apathetic. However, she did not note her memory impairment, and had no hallucinations. She was admitted to our hospital on 20 May, 2003 because donepezil had been ineffective for treating her memory impairment. Neurologically, she showed bilateral horizontal gaze nystagmus, mild limb ataxia on the left and mildly ataxic gait. Neuropsychological examinations showed mildly impaired cognitive function, e.g., MMSE 25/30, WAIS-R full IQ 69 and especially in verbal short memory, which may represent temporal lobe dysfunction. Moreover, Benton's visual memory test revealed marked visual short-term memory impairment, while impaired performance on a Kana picking up test suggested mild to moderate attention impairment, which could have represented frontal lobe dysfunction. Brain MRI showed multiple T2-high plaque lesions close to the bilateral lateral ventricles, and bilateral optic nerve lesions enhanced by gadolinium. Also, spinal cord MRI showed a gadolinium enhanced lesion at Th5 on the left. Cerebral spinal fluid (CSF) examination showed normal cell count and protein level, and undetectable oligoclonal bands (OCB), but an elevated IgG index (1.1, normal < 0.85). Visual evoked potentials (VEPs) showed prolonged P100 latency bilaterally, indicating subclinical optic nerve lesions. She was thus diagnosed as having PPMS according to McDonald's diagnostic criteria for MS. 99mTc Single photon emission computed tomography (SPECT) showed a decreased cerebral blood flow (CBF) in the bilateral frontal and temporal lobes, which was consistent with her clinical features. PPMS patients generally present with chronic progressive spastic paraparesis and/or cerebellar ataxia. Cognitive impairments observed in PPMS are generally thought to be due to white matter lesions, i.e., subcortical dementia. However, some recent reports have shown MS patients with short-term memory impairment (antegrade amnesia) similar to cortical dementias such as Alzheimer's disease (AD). In such MS cases, visual short-term memory impairment seems characteristic of their cognitive impairment compared to AD cases. As well, the present case showed visual memory impairment as evaluated by Benton's memory test. Parietal and frontal lobes are reported to be important for verbal and visual working memory, respectively. Thus, in the present case, decreased CBF in the frontal and temporal lobes, which could have been due to a disconnection between cortices and subcortices caused by the white matter lesions, is consistent with the type of her cognitive dysfunction, i.e., notable visual memory impairment. PPMS may thus be an important disease as a differential diagnosis for chronic progressive dementia. Further neuropsychological and functional imaging studies will be necessary to achieve a better understanding of the mechanisms of cognitive impairment in PPMS.

Brain↗

PubMed2000

Dissociation of memory retrieval and search processes: an event-related fMRI study.

A cognitive task can often be subdivided into several subprocesses, which follow a specific temporal order. Here, we report an event-related functional magnetic resonance imaging (fMRI) experiment on memory search, in which the temporal onset of search in primary memory was varied relative to retrieval from secondary memory. Furthermore, previous behavioral studies demonstrated that search times in primary memory depend on the number of items in a memory set, whereas retrieval from secondary memory is a set-size independent process. We analyzed the dependency of the blood oxygenation level dependent (BOLD)-response on the temporal onset of memory search on the one hand and on memory set size on the other hand to differentiate the contribution of retrieval from secondary memory, maintenance in primary memory, item search in primary memory, and response-related processes. The timing of activation followed cue presentation bilaterally in the middle frontal gyri (Brodmann area (BA) 9,46) and the inferior parts of the precentral gyri (BA6). In all other regions of interest (ROI), supplementary motor area (SMA), posterior parietal cortex, antero-superior insula, and primary motor cortex, the onset of activation was delayed with delayed probe presentation, ruling out participation in retrieval from secondary memory. The amplitude of the BOLD-response increased with increasing memory set size in all ROI except primary motor cortex and left posterior parietal cortex. All areas with cue-associated BOLD onset, suggesting involvement in retrieval, showed prolonged BOLD activation, suggesting that they also support maintenance of the retrieved information.

Adult↗

PubMed2006

The effect of alcohol and repetition at encoding on implicit and explicit false memories.

RATIONALE: Alcohol impairs explicit memory, whilst leaving implicit memory relatively intact. Less is known about its effects on false memories. AIM: The present study examines the effects of alcohol on explicit and implicit false memories using study list repetition as a tool for modulating learning at encoding. METHODS: Thirty-two participants were given either an alcohol (0.6 g/kg) or placebo beverage before undergoing an encoding phase consisting of 10 lists of nine associated words (veridical items). Each list was associated to a word, which was not presented at encoding (semantically associated non-studied lure; critical item), serving as the measure for false memory. Half of the lists were presented once, and half were repeated three times. The next day, participants underwent an implicit (stem completion and post hoc awareness measurements), and an explicit (free recall) task. RESULTS: Alcohol decreased veridical and false explicit memory for singularly presented lists compared to placebo; no group difference existed for repeated lists. Implicit veridical memory was not affected by alcohol. Awareness memory measures demonstrated in placebo participants an increased ability with repetition in rejecting false memories. The reverse was found in intoxicated participants who with repetition accepted more false memories. CONCLUSION: Alcohol appears to decrease semantic activation leading to a decline in false memories. Increased learning with repetition, which increases the rejection of false memories under placebo, is reversed under alcohol leading to a decrease in rejection of false memories. The latter effect of alcohol may be due to its ability to impair monitoring processes established at encoding.

Adolescent↗

PubMed1998

Glucose and memory: fractionation of enhancement effects?

Recent research findings indicate that glucose administration enhances some aspects of cognitive functioning. To date, those studies which have investigated the effects of glucose on memory in human participants have concentrated on its apparent ability to attenuate memory impairment. Relatively little research has been done in humans investigating the effects of glucose on memory performance in young healthy participants in whom no memory deficits exist. Moreover, the work which has been conducted in this population has produced somewhat equivocal findings. In this study, after overnight fasting the influence of a 25 g oral dosage of glucose on a range of measures of memory performance was investigated in healthy young female participants. Two control treatments (saccharin and water) were also administered. There was a significant glucose facilitation effect upon performance of long-term verbal free and cued recall tasks which did not vary with test delay. Performance on these free and cued verbal recall measures correlated significantly with blood glucose levels across all participants. No glucose-related facilitation was observed on either a test of short-term verbal memory (forwards/backwards digit recall) or a test of long-term non-verbal memory (complex figure reproduction). However, the significant glucose-related effects observed with long-term free and cued recall remained after controlling for participants' differential baseline blood glucose levels and individual levels of immediate memory performance. Therefore, memory improvement after glucose ingestion was not merely a consequence of lower baseline blood glucose or lower immediate memory performance in the glucose treatment group. These findings indicate that there may be some fractionation in the memory facilitation effects of glucose: the memory enhancing effect of glucose administration in healthy young adults may be greatest on tests of long-term verbal recall. The results suggest that glucose may enhance retention in and/or retrieval from long-term verbal memory.

Adolescent↗

PubMed1996

Working memory in temporal lobe epilepsy: an event-related potential study.

Event-related potentials (ERPs) were recorded to a digit-probe identification and matching task (modified 'Sternberg paradigm') in 29 patients with temporal lobe epilepsy (TLE) and 26 healthy subjects. Our main aim was to identify the neurophysiological correlates of abnormal short term memory function in patients with TLE. Neuropsychological tests allowed the definition and comparison of two patient groups according to the presence or absence of memory dysfunction. These two groups did not differ significantly in mean age, education years, IQ, seizure duration, seizure frequency, anti-epileptic drug (AED) regimes, or on findings on neuroimaging. ERPs recorded under different levels of memory load were analysed both by conventional component identification and by an objective computer method of determining mean amplitudes of multiple 50 ms epochs (MMA analysis). We found that some significant abnormalities were common to both groups of patients; these included slow reaction times, a reduced amplitude of the N170 wave (and the corresponding 157-210 ms epoch in the MMA analysis) and a broad late negative shift between 577 and 735 ms. Other findings, including a significantly reduced performance accuracy as the level of memory load increased, were restricted to patients with abnormal memory function. The ERP changes that were specific to these patients occurred within a latency band of 200-420 ms and included a relatively preserved, but delayed P250 component and a delayed and attenuated N290 wave. When compared with either healthy subjects or with patients with normal memory, the responses in patients with abnormal memory showed an abnormal 'positive shift' between 262 and 315 ms after probe presentation and a further positive shift between 315 and 420 ms as memory load increased. These abnormalities of 'memory scanning' ERPs in patients with TLE which paralleled neuropsychological and behavioural evidence of memory dysfunction, and which occurred in the section of the response that is sensitive to memory loading in healthy subjects, provide further objective evidence that abnormalities of short term memory processes contribute to the memory deficits of TLE.

Adult↗

PubMed1996

Semantic and episodic memory in aphasia.

Within the framework of the distinction between episodic and semantic memory, it has been argued that these two memory Systems are organised in a hierarchical way. The hierarchical hypothesis assumes that episodic memory is a specific subsystem of semantic memory and therefore implies that episodic memory cannot exist without semantic memory. If this hypothesis is correct, it should be expected that (episodic) yes/no recognition performance would improve in patients with preserved semantic memory, following semantic encoding. In the present study we investigated the influence of semantic encoding on recognition memory performance in a population of 28 aphasic patients (AA) and 14 normal controls (NC). Experiment 1 considered recognition memory for semantically unrelated items, whereas Experiments 2 and 3 assessed recognition memory for semantically related items. In Experiment 3, but not in Experiment 2, subjects were explicitly instructed to make a semantic association between the items. AA were impaired, compared to NC, only on the recognition memory performance of Experiment 1. The ability to make a semantic association between two items was significantly and positively correlated to the ability to recognise, in a subsequent test, those same items. A further analysis showed that patients who were impaired on the semantic association task did significantly worse on the recognition task of Experiment 3 than NC and than patients who were unimpaired on the semantic association task. These findings are discussed in the context of memory deficits in aphasia and interpreted as giving support to the view that episodic memory for an item is affected by the level of semantic awareness of that same item.

Aphasia↗

PubMed2006

Episodic memory impairment in Huntington's disease: a meta-analysis.

Memory dysfunction is an important feature in the clinical presentation of Huntington's disease (HD) and may precede the onset of motor symptoms. Although several studies have contributed to the quantitative and qualitative description of memory impairments in HD, the characterization of episodic memory impairments has varied considerably. Whereas most studies report significant impairments on free recall tests, performance on recognition tests has been considerably more variable, ranging from normal to markedly deficient. This absence of a well-established recognition memory deficit has led some investigators to attribute the memory deficits in HD to a retrieval-based episodic memory impairment. We felt that a quantitative review of the literature was needed to better characterize these episodic memory impairments. We conducted a meta-analysis to assess the magnitude of the recognition memory deficit in HD and to examine it in relation to the known deficit in recall. Memory data were provided by 544 symptomatic HD patients, 224 presymptomatic gene-carriers, and 963 control subjects. The overall group comparison between symptomatic patients and controls yielded effect sizes of d=1.95 for free recall and d=1.73 for recognition. We split the symptomatic group into two subgroups based on their mental status (mild and moderate/severe dementia) and both showed significant deficits in recall and recognition memory, though recall was more impaired than recognition in the mild dementia subgroup. Only slight memory impairment was observed in the presymptomatic subjects. The results show that deficits in recognition memory must be accounted for in future models of memory impairment in HD.

Adult↗

PubMed2006

Measurement of remote memory pre- and post-temporal lobectomy: a longitudinal case study.

There is evidence that remote memory is affected by temporal lobe epilepsy (TLE) and by temporal lobectomy (TL) for the relief of epilepsy. However, remote memory is not routinely assessed when patients with epilepsy undergo neuropsychological testing either pre- or postsurgery. We present a literature review and detailed longitudinal case study of a woman (A.Z.) who had right TLE and fears about deterioration of her remote memory following right TL. Remote memory was assessed by conventional methods (remote memory questionnaire for public events) and by a novel method of seeking vividness ratings for elicited autobiographical memories with A.Z.'s partner acting as the control. A.Z.'s level of memory for remote/recent public events and her rate of forgetting were the same as her partner's, both before and after surgery. A.Z.'s vividness ratings for her own autobiographical memories were similar to her partner's ratings for his memories. Her vividness ratings for her partner's memories that involved events common to both of them were slightly lower than his. A.Z.'s rate of forgetting of her own and her partner's memories was the same as that of her partner, both before and after surgery. There are two principal conclusions. First, this assessment method of measuring remote memory is easy to use and captured the patient's clinical concerns. Second, applying the methodology in this single case suggested that right-sided unilateral TLE and TL may pose no threat to remote memory.

Adult↗

PubMed2004

Autobiographical memories of anxiety-related experiences.

Ninety-nine undergraduate students retrieved three memories associated with each of the five emotional experiences: panic, trauma, worry, social anxiety, and feeling content. Subsequently, they answered 24 questions assessing properties of each memory, including the vividness and perceived accuracy of the memories and sensory, emotional, and anxiety-related experiences during retrieval. Memories were coded for affective tone and specificity. Results indicated that panic-related and trauma-related memories were rated similarly as content memories, but that they generally were associated with more imagery and emotional experiencing than worry-related or social anxiety-related memories. Participants experienced panic and worry symptoms to the greatest degree when they retrieved panic-related and trauma-related memories. All anxiety-related memories were characterized by more negative tone than content memories. Panic-related and trauma-related memories were more specific than worry-related, social anxiety-related, and content memories. These findings can explain partially why individuals with some, but not all, anxiety disorders experience enhanced memory for threatening material.

Adult↗

PubMed1997

Explicit and implicit memory bias in panic disorder with agoraphobia.

Thirty patients with a diagnosis of panic disorder with agoraphobia and 30 normal controls were compared on explicit memory (cued recall) and implicit memory (word stem completion) for positive, neutral, social threat, and physical threat words. The panic patients showed an explicit memory bias, but no implicit memory bias, for physical threat words. The index of explicit memory bias for physical threat words was found to correlate with anxiety sensitivity and degree of agoraphobic fear and avoidance. The index of baseline bias for threat words on the word completion task, on the other hand, correlated with trait anxiety. Although there were no correlations between explicit and implicit memory bias for physical threat words, explicit memory bias for physical threat words correlated with explicit memory bias indexes for positive words and social threat words. The results are discussed in terms of the functional role of an explicit memory bias for physically threatening events in panic disorder. The negative results on implicit memory bias are discussed in relation to earlier studies, the use of different implicit memory tasks, and the role of baseline bias on implicit memory tasks. Finally, the hypothesis is suggested that explicit and implicit memory bias for emotional information may represent two different styles of information processing, which serve as vulnerability factors for different emotional disorders.

Adult↗

PubMed2000

U-69,593 microinjection in the infralimbic cortex reduces anxiety and enhances spontaneous alternation memory in mice.

The present report investigated the contributions of the ventromedial prefrontal cortex to the control of spontaneous alternation/working memory and anxiety-related behaviour. In Experiment 1, we examined the effects of microinjections of the selective kappa(1) receptor agonist, U-69,593, in the infralimbic cortex (IL) of CD-1 mice on several ethologically-derived anxiety indices in the elevated plus-maze (EPM) and defensive/withdrawal (D/W) anxiety in the open field, as well as on memory in the EPM transfer-latency (T-L) test and implicit spontaneous alternation memory (SAP) in the Y-maze. In week 1, pretreatment with one injection of vehicle, 1, 10 or 25 nmol/1.0 microliter U-69,593 in the IL dose-dependently prolonged T-L and produced a dose-dependent anxiolytic behavioural profile in the first EPM trial. Following a 24-h delay, the same mice were given a drug-free second trial in the EPM tests of T-L memory and anxiety. Whereas T-L memory was not disturbed, small but detectable carry-over effects were observed in trial-2 EPM behaviour relative to vehicle-treated animals. In week 2, the same groups of mice were again pretreated with one injection of the same doses of U-69,593 in the IL and given a D/W test in an open field, followed immediately by an 8-min SAP trial in the Y-maze. The smallest U-69,593 dose was anxiolytic in the D/W test, and SAP/working memory was dose-dependently enhanced in the Y-maze. In Experiment 2, we evaluated whether 0.5 microliter volume microinjections would produce comparable behavioural and carry-over effects in the IL of three new groups of CD-1 mice, in the event that the 1.0 microl volume injections used in Experiment 1 diffused beyond the IL and therefore may have confounded some effects. Experiment 2 procedures were carried out in the same manner as in Experiment 1, except the animals were tested in reverse order. Thus in week 1, SAP memory was tested in the Y-maze followed by D/W anxiety in the open field for half of the animals in each group, and the other half was tested in reverse order. In week 2, T/L memory and anxiety were tested in the EPM in 2 trials as described in Experiment 1. Pretreatment with one injection of vehicle, 10 or 25 nmol/0.5 microliter U-69,593 in the IL reduced D/W anxiety and enhanced SAP memory regardless of testing order in week 1. In week 2, the same groups of mice were again pretreated with one injection of the same doses of U-69,593 in 0.5 microliter volumes in the IL and tested in the EPM. In a similar fashion to Experiment 1, U-69,593 dose-dependently prolonged T/L and produced an anxiolytic behavioural profile in the first EPM trial. Following a 24-h delay, T/L recall memory was again not significantly influenced, but a robust anxiolytic behavioural profile was observed in the second drug-free anxiety trial in the EPM relative to vehicle-treated animals. Results are discussed relative to a) injection volumes and testing order, b) the possible influence kappa receptors may exert on neurochemical responsivity to anxiety-provoking environments in the IL area of the mPFC, c) the possibility that kappa-mediated anxiolysis from the IL in CD-1 mice results from interactions with neurochemical systems involved in the blunting of incoming anxiety-provoking information, d) evidence that SAP memory may be an implicit subtype of working memory, and e) the possibility that IL implicit working memory processes may modulate the induction and expression of anxiety-related behaviour.

Animals↗

PubMed2002

Effects of chronic epilepsy on declarative memory systems.

Memory is systematically affected by temporal lobe epilepsy. Since surgery is a promising alternative to pharmacological treatment the questions which memory system is affected and what the long-term prognosis of memory is are more relevant than ever. We address these issues by cross-sectional and longitudinal analysis of memory performance in large series of patients with temporal lobe epilepsy (TLE). The findings indicate that episodic memory rather than semantic memory is impaired in TLE, in particular in TLE with mesial temporal pathology. With the exception that mesial functions appear increasingly affected by chronic non-mesial TLE, memory decline in TLE is not different from that observed in healthy control subjects. However, since patients perform poorer than controls at any age, normal senescence brings patients to mnesic disability at a younger age. Semantic memory seems unaffected by this process but early cortical lesions appear to interfere with knowledge acquisition. Longitudinal data come to a different conclusion regarding the contribution of epilepsy/seizures to memory decline. Conservative treatment is associated with significant decline in figural memory and 37% of the patients experience some memory decline in the long run. Surgery partly anticipates the decline observed with conservative treatment, but losses are most marked after left temporal lobe surgery. After surgery, quite stable memory or even late recovery from surgery is indicated. Leaving aside the surgical intervention, the data provide evidence that the longitudinal memory outcome in TLE is determined by seizure control, seizure severity, mental reserve capacities, and the retest interval. Thus early and efficient seizure control and the prevention of any cerebral damage from the beginning of epilepsy are demanded.

Epilepsy↗

PubMed2003

Memory impairment suggests hippocampal dysfunction in abstinent ecstasy users.

Previous studies have consistently shown impairments of memory and learning in regular users of the neurotoxic drug ecstasy (3,4-methylenedioxymethamphetamine [MDMA]). In addition, deficits in working memory, planning ability and central executive control, as well as high cognitive impulsivity, were also reported in some studies. Hence, the memory decrements may be secondary due to other cognitive failures. The purpose of this study was to analyze the nature of the cognitive deficits of ecstasy users. Tests of memory, working memory, central executive function and cognitive impulsivity were administered to 60 currently abstinent ecstasy users and to 30 nonusers. Heavy ecstasy users (n=30, lifetime dose > or =80 ecstasy tablets) had lower memory performance than both nonusers and moderate users (n=30, lifetime dose <80 ecstasy tablets). In contrast, we found no group differences in central executive function, working memory, planning ability and cognitive impulsivity between ecstasy users and controls. Poorer memory and working memory performance was associated with a heavier pattern of ecstasy use. Low working memory, planning ability and central executive control and high cognitive impulsivity did not predict poor memory performance. Our results indicate primary memory dysfunction in heavy ecstasy users, which may be related to a particularly high vulnerability of the hippocampus to the neurotoxic effects of MDMA. Hippocampal dysfunction after ecstasy use may be a risk factor for earlier onset and/or more severe age-related memory decline in later years.

Adult↗

PubMed2000

Chronicity of memory impairment in long-term out-of-hospital cardiac arrest survivors.

As a result of out-of-hospital defibrillation initiatives, many cities have an increasing population of out-of-hospital cardiac arrest survivors. We previously identified that one third of these patients suffer memory problems in the months after resuscitation. The pattern of memory impairment (impaired recall memory and intact recognition memory) is suggestive of hippocampal damage. In this study we followed up ten subjects who had previously been found to have memory impairment after their cardiac arrest. To assess the chronicity of this memory impairment, we re-tested memory function approximately 3 years after the index events. These subjects were compared with age and sex matched control subjects with previous myocardial infarction and no cardiac arrest. Memory was assessed using the Rivermead Behavioural Memory test (RBMT). To further assess recall and recognition memory we used the Doors and People test (DPT), which is specifically designed to identify deficits in these functions. RBMT scores declined significantly in both groups compared with the original assessment 8 months after cardiac arrest, possibly an effect of ageing-control group: mean (S.D.) 22.2 (1. 4)-18.4 (2.9); cardiac arrest group: 16.1 (2.7)-14.6 (4.4). The inter-group difference in RBMT score remained significant (P=0.001). DPT scores were poor in the cardiac arrest group (mean (S.D.) total 5.8 (2.8)), compared with the control group (10.8 (3.4)) who scored normally. Both recall and recognition memory were poor in the cardiac arrest group. We conclude that the memory deficits that we previously observed in cardiac arrest victims are persistent. Both recall and recognition memory are affected, implying that non-selective brain injury may be the mechanism.

Aged↗

PubMed2001

A comparison of memory for verbal and non-verbal material in schizophrenia.

Verbal memory impairment has been well explored in schizophrenia, but it is unclear whether findings relate to the type of material to be learned or the component process required by the memory task. Also, sparse data on non-verbal memory also open the question of how well schizophrenia patients encode this material. We tested whether episodic memory performance in schizophrenia varies as a function of stimulus material (verbal/non-verbal) and determined the integrity of various component memory processes. Memory tests that differ in stimulus material (words, California Verbal Learning Test, CVLT; designs, Biber Figure Learning Test-Extended, BFLT-E) yet produce similar memory component measures were used. Subjects were 28 neuroleptic-medicated inpatients with a diagnosis of chronic schizophrenia. Results showed that both verbal and non-verbal memory performance was impaired relative to age-matched controls. Learning and recall measures were most severely impaired, with memory storage problems and impairment in recognition memory evident. On the verbal task, the relative sparing of recognition memory suggested retrieval processes, in addition to encoding processes, were disrupted. On the non-verbal task, the deficits appeared more limited to encoding. Therefore, while the operational integrity of components such as encoding were compromised regardless of material, retrieval processes showed material-specific effects. To the degree verbal and non-verbal memory functions can be lateralized in the brain, these data support the possibility of deficits in both right and left hemisphere declarative memory systems in schizophrenia.

Adult↗

PubMed1999

Episodic memory and learning in patients with chronic schizophrenia.

This study explored the pattern of memory functioning in 58 patients with chronic schizophrenia and compared their performance with 53 normal controls. Multiple domains of memory were assessed, including verbal and non-verbal memory span, verbal and non-verbal paired associate learning, verbal and visual long-term memory, spatial and non-spatial conditional associative learning, recognition memory and memory for temporal order. Consistent with previous studies, substantial deficits in long-term memory were observed, with relative preservation of memory span. Memory for temporal order and recognition memory was intact, although significant deficits were observed on the conditional associative learning tasks. There was no evidence of lateralized memory impairment. In these respects, the pattern of memory impairment in schizophrenia is more similar in nature to that found in patients with memory dysfunction following mesiotemporal lobe lesions, rather than that associated with focal frontal lobe damage.

Adult↗