The Syndrome of Functional Memory Disorder: Definition, Etiology, and Natural Course

The Syndrome of Functional MemoryDisorder: Definition, Etiology, and Natural

Course

Klaus Schmidtke, M.D., Susanne Pohlmann, M.D.,Birgitta Metternich, Diplom-Psychologin

Objectives: Nonorganic, functional memory disorder (FMD) is frequent in memoryclinic patients, and is an important differential diagnosis to prodromal dementia.The authors propose a definition of FMD as an acquired medical and psychologicalcondition that is closely related to psychosocial burden and distress. Design: Pro-spective follow-up study, aimed to evaluate the natural course of FMD. Setting:University hospital memory clinic. Participants: Seventy-three patients who sufferedmemory deficits and psychological distress and had normal test results. Forty-sixattended a follow-up examination after a mean delay of 20.1 months. Measure-ments: FMD severity was assessed with a structured inventory and an overallself-rating scale. Objective performance was assessed by standardized tests of memoryand attention. Results: Identified causes of distress were overwork, interpersonalconflicts, somatic illness, adjustment disorder, dysthymia, and Alzheimer phobia. Atfollow-up, FMD had resolved in only six patients, and persisted in 39. Averagesymptom severity showed only a minor reduction. Conclusion: FMD is, in manyinstances, a long-term rather than transient problem. Possible reasons include thepersistence of burden factors and the failure to evade the “stress spiral” of mutualreinforcement of distress and cognitive dysfunction. (Am J Geriatr Psychiatry 2008; 16:981–988)

Key Words: Memory, subjective cognitive impairment, mild cognitive impairment,somatoform disorders

Nonorganic memory disorders represent alarge but under-researched diagnostic sub-

group among patients attending memory clinics, andan important differential diagnosis to mild cognitiveimpairment and early dementia. The percentage ofmemory-clinic patients without organic or major

psychiatric disorders has been reported to vary be-tween 6% and up to 31% of referrals.1,2

According to patients’ account, nonorganic mem-ory disorder encompasses credible, frequent, andsignificant mnestic and attentional deficits in dailyliving. Typical symptoms include forgetting chores

Received March 27, 2008; revised July 11, 2008; accepted July 13, 2008. From the Memory Clinic, Center for Geriatric Medicine and GerontologyFreiburg, University Hospital Freiburg, Freiburg, Germany. Send correspondence and reprint requests to Klaus Schmidtke, M.D., Center forGeriatric Medicine and Gerontology Freiburg, Lehener Str. 88, 79106 Freiburg, Germany. e-mail: [email protected]

© 2008 American Association for Geriatric Psychiatry

Am J Geriatr Psychiatry 16:12, December 2008 981

while walking to some place to dispatch them, tem-porary block of overlearnt memory contents, disrup-tion of the coherence of thoughts and conversations,prospective memory failures, and absent-minded-ness.3–6 The lapses of memory and attention thatthese patients experience may precipitate anxiety,embarrassment, and fear of dementia. Nonorganicmemory disorder can cause disruption of routineactivity, namely underperformance in private andprofessional chores, and thus itself become an impor-tant secondary stress factor. Patients’ educational,professional, and socioeconomic attainment level isoften above-average.3,5 One reason may be that non-manual workers are more disturbed by impairmentsof memory and concentration.

Subjective cognitive (or memory) impairment (SCI) is adescriptive term that has recently raised interest asthe earliest clinically tangible state preceding demen-tia. Studies indicate that SCI in older adults can beassociated with a decrease in mediotemporal andneocortical gray matter density7,8 and may confer anelevated risk for future cognitive decline.9–11 How-ever, many older patients with SCI do not progressto dementia, and SCI is also seen in younger patientsin whom the likelihood of incipient dementia is verylow. To date, there is no concept on the etiology ofSCI, and its clinical presentation has not been sys-tematically studied. SCI patients with nonorganicbackground are not distinguished from those whohave not-yet-measurable organic disease.

We suggest the term functional memory disorder(FMD) for persistent and credible, but presumablynonorganic deficits of memory in daily life. “Func-tional” is given preference over “subjective,” and“disorder” is given preference over “complaint,” be-cause patients do not merely complain, but experi-ence credible memory deficits in their daily life, andtheir problem is not merely subjective, but real. Wepropose an etiological model and a set of diagnosticcriteria for FMD, and report findings on its clinicalcourse.

Definition of FMD

It is warranted to define a syndrome of FMD, be-cause the condition is not a residual category butfrequent and presents with a recognizable spectrumof signs and symptoms. We define FMD as an ac-quired medical and psychological condition with sig-

nificant failure of memory and concentration thatoccurs in daily living, is unrelated to organic factors,and is assumed to be caused by distress and psycho-logical dysfunction.12–14 Although FMD does not, inthe strict sense, present on the physical plane, thesymptomatology of intellectual impairment can beconceptualized as a sign of physical, i.e., brain dys-function. It therefore seems justified to assign FMDto the group of somatoform disorders.13

Notably, the concept of FMD, as applied here, doesnot encompass cognitive deficits in the context of majorpsychiatric illness. Also, due to the presence of regularand significant instances of memory failure in dailyliving, FMD is not to be mistaken for hypochondriaand does not refer to patients whose complaints merelyreflect exaggerated worries about minor and age-re-lated decrease of cognitive performance. Accordingly,in a study by Ponds et al.,4 patients with similarlydefined nonorganic memory disorder did not attainpathological scores on a hypochondria question-naire.

Depression is another recognized cause of nonor-ganic cognitive disorder. Unlike FMD, it is com-monly associated with neuropsychological deficits.11

FMD can be associated with depression in variousways: a) both can be caused by third factors, b) FMDcan cause or promote depression, c) depression cancause cognitive deficits. Elevated depression scoresin the absence of clinically relevant depressive dis-order have been found in patients with nonorganicmemory disorder.5,6,13 However, it needs to be em-phasized that FMD is not typically caused by depres-sion. Patients with depression typically complain ofcognitive impairment, but most FMD patients are notclinically depressed. The crucial point is that perceiveddistress, rather than clinically relevant depression orother forms of major psychiatric illness, is postulatedto be at the core of FMD. Nonetheless, FMD is com-patible with dysthymia or subclinical depressivesymptomatology, which is common among sufferersfrom psychosocial distress.

FMD patients’ typically normal neuropsychologicaltest results could be related to the special situation ofa testing session, which enables patients to mobilizeattention and to suppress internal distraction. It isdebatable whether patients with subnormal normaltest results should be excluded from the diagnosis ofFMD. We suggest that patients with results in the

Syndrome of Functional Memory Disorder

Am J Geriatr Psychiatry 16:12, December 2008982

borderline performance range from �1 to �1.5 stan-dard deviations (SD) should not be excluded.

Hypotheses on the Etiology of FMD

The following hypotheses are the basis of a pro-posed etiological framework for the developmentand maintenance of FMD:

1. Life events or circumstances elicit long-term psy-chological and emotional distress, e.g., interper-sonal conflicts at home or at work, exhaustion oroverwork, biographical crises, pain, illness andhandicap, maladjustment to changed living con-ditions. Preexisting external and internal factorsmay contribute to mounting psychological dis-tress or reduced capacity to compensate, e.g., per-sonality traits.

2. Continuous distress causes a state of internal dis-tractedness, reduced ability to focus, to maintainattention, and slowing of thought processes.These deficits interfere with long-term memory atthe stages of registration and retrieval. This canalso lead to temporary blocking of well-estab-lished contents of memory such as numbers,names, words, or routine activities.Reduced attention and distractability can also leadto decreased short-term memory performance, caus-ing instances of rapid forgetting, disruption of thecoherence of thoughts, and failure to retain a task orerrand while being on one’s way to dispatch it.

3. Deficits of memory and concentration can elicitobjective problems in daily living, rumination,self-accusation, and fear of organic disease.Such objective and subjective consequences canamount to significant secondary stress factors.Thereby, a vicious circle of distress, cognitivedysfunction, anxiety, and frustration may be setin motion that contributes to the enhancementof FMD. Where present, personality traits likeproneness to distress, high achievement motiva-tion, memory-related perfectionism, and a ten-dency toward self-criticism may make patientsmore susceptible to such positive feedback.6,14

4. Inasmuch as the sources of distress are variable intime, their consequences on cognitive perfor-mance can be expected to vary as well, with wors-ening of FMD in periods of particular strain andemotional discomfort.

Objectives of the Present Study

The objective of the present investigation was toprospectively examine the course of FMD in a natu-ralistic setting. To this end, we conducted a fol-low-up study of a group of patients with a clinicaldiagnosis of FMD.

METHODS

Subjects and Study Design

Consecutive patients were included who were pre-sented at a university hospital memory clinic withrecent memory deficits. History-taking included de-tails on the symptoms of memory and concentrationfailure in daily living, and on external and psycho-logical stress factors. Patients were considered forinclusion if a diagnosis of nonorganic memory im-pairment was made according to a set of five FMDcriteria (Panel 1, Appendix).

Baseline assessment also included the applicationof the tests and scores listed below. On the same day,patients received individual counseling. They werereassured that test performances were within thenormal range. The model of stress-induced cognitiveimpairment was explained and psychosocial burdenfactors were discussed. In some instances, psycho-therapy was recommended.

One to 3 years later, the same patients were invitedto a follow-up visit. Those patients who attendedwere reexamined using the same procedure, plustwo Likert scales to assess change of the levels ofmemory dysfunction and psychosocial burden. Anew diagnosis was then made based on the currentprofile of symptoms and scores.

Severity of FMD Symptomatology

A validated FMD inventory was applied to assessthe severity of FMD symptomatology (Panel 2, Appen-dix). It assesses 10 symptoms that were identified asindicators of nonorganic cognitive deficits and has beenshown to differentiate between FMD patients and con-trol subjects with high accuracy.14 The score equals tothe number of yes-answers to the 10 questions.

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Neuropsychological Testing

Verbal memory was assessed with the auditoryverbal learning test (immediate free recall of a 15-word-list, sum of five trials). For patients over age 60,the 10-word-list of the Consortium to Establish aRegistry for Alzheimer’s Disease (CERAD) serieswas applied (sum of three trials; Ref. 15).

Attention and concentration were assessed with thedigit connection test.16 It involves connecting the num-bers 1 to 90 with a continuous line at maximum speedacross four trials. For patients over age 60, the shorter,geriatric version of the same test was applied.

Age-corrected z-scores were taken from tablespublished with the digit connection test and theCERAD test series and from a standardization sam-ple published by Helmstaedter et al.17 for the audi-tory verbal learning test.

Additional Variables

The following symptoms were assessed, and thenumber of yes-answers was added to form an ap-proximate measure of vegetative, presumably psy-chosomatic symptoms: 1) lightheadedness or sensa-tion of cranial pressure, 2) numbness or dizziness, 3)tiredness and increased need for sleep, 4) decline ofgeneral level of performance by �50%.

Only at follow-up, two Likert scales of changewere applied to assess:

Overall change of subjective memory impairmentin daily living, as reported by patients.

Overall change of psychosocial burden, as ex-plored by the examiner.

(Scores: 1 � much better, 2 � somewhat better, 3 �unchanged, 4 � somewhat worse, 5 � muchworse.)

At follow-up, patients were also asked to rate theeffect of counseling at baseline as either helpful or nothelpful. Lastly, it was assessed whether patients hadreceived psychotherapeutic or psychiatric therapy.

RESULTS

One hundred thirty-two consecutive memory clinicpatients with a diagnosis of probable nonorganiccognitive impairment were considered for inclusion.

Fifty-nine did not meet inclusion criteria due to de-pression (N � 48), bipolar affective disorder (N � 1),adult attention deficit disorder (N � 3), personalitydisorder (N � 1), coinciding significant organic dis-ease (N � 1), and test performances below �1.5 SD(N � 5).

Of the remaining 73 patients who were included,46 patients did, and 27 did not attend the follow-upvisit. A statistical comparison of patients who didand who did not attend revealed no significant dif-ference, or trend for a difference, of group means forage (55.2 � 10.6 versus 53.4 � 8.2), FMD inventoryscore (7.6 � 2.3 versus 8.0 � 1.8), auditory verballearning test (55.7 � 8.7 versus 53.6 � 8.2), CERADword list learning (20.8 � 1.9 versus 20.5 � 2.6), digitconnection test (81.3 � 20.9 versus 86.8 � 16.9), anddigit connection test/short version (32.4 � 15.5 ver-sus 27.7 � 3.2) (two-sided t tests).

The mean delay to follow-up for the 46 patientswho attended was 20.1 � 6.3 months. In one patient,early stage dementia was diagnosed at follow-up.She was excluded from further analyses. The remain-ing 45 patients consisted of 24 men and 21 women.

At baseline, these causes of burden and distresswere identified in an anamnestic interview (casenumber/mean age): adjustment disorder (8/45years), overwork in job or family (12/56 years), in-terpersonal conflict in job or family (6/60 years),somatic illness (5/58 years), dysthymia (8/58 years),and Alzheimer phobia (2/59 years). Test scores aregiven in Table 1.

At follow-up, FMD was found to have resolved insix patients (normal subjective memory function). In39, FMD was found to be still present. All patientsattained digit connection test performances ��1.5SD. One patient attained a verbal memory perfor-mance of �1.3 SD, all others attained performances��1 SD.

The FMD inventory showed a small reduction ofmean symptom severity (Table 1, Wilcoxon signed-rank test, z � �4.33, p �0.001). On the Likert scale ofmemory dysfunction, 9 patients rated themselvessomewhat or much improved at follow-up, 28 asunchanged, and 8 as somewhat worsened (mean,2.9 � 0.72). On the Likert scale of psychosocial bur-den, 23 patients were rated somewhat or much im-proved at follow-up, 16 as unchanged, and 6 assomewhat or much worsened (mean, 2.4 � 1.0).The two Likert scales were significantly correlated



(Spearman-correlation, r � 0.43, p � 0.003, N � 45).The Likert scale of change in memory dysfunction wascorrelated with the change of the FMD inventory scores(baseline minus follow-up; Spearman-correlation, r ��0.44, p � 0.002, N � 45), but it was not correlatedwith the differences in memory and digit connectiontest scores between baseline and follow-up scores.

FMD severity also was significantly correlatedwith vegetative complaints at baseline (r � 0.45) andat follow-up (r � 0.44) (Spearman-correlations,p �0.005, N � 45), but not with neuropsychologicaltest scores at baseline and at follow-up.

Twenty-one patients stated that the counseling atbaseline had been helpful, 18 said it was not helpful,and 6 were undecided. Twelve patients had receivedpsychotherapeutic or psychiatric therapy. There wasa minimal difference of outcome of subjective mem-ory function between patients who received therapyand those who had not (mean Likert score, 2.8 � 0.56versus 3.0 � 0.76).

A comparison of the mean values of some keyvariables between the younger (�56 years, N � 23)and the older subgroup (�57 years, N � 22) showedonly minor differences, which were not statisticallysignificant, for FMD inventory scores at baseline(7.9 � 2.2 versus 7.4 � 2.3) and at follow-up (5.8 �2.9 versus 5.9 � 2.9) (two-sided t tests), and for Likertscores of psychosocial burden (2.7 � 1.1 versus 2.2 �1.0) and memory dysfunction (2.9 � 0.76 versus3.0 � 0.69) at follow-up (Mann-Whitney tests).

DISCUSSION

These psychological or social burden factors wereidentified as follows: dysthymia, adjustment disor-der, overwork, interpersonal conflicts, somatic dis-ease, and fear of developing Alzheimer disease.Corresponding subgroups exhibited only minor dif-ferences of symptom severity and outcome (data notshown). Our findings suggest that FMD can be theconsequence of a spectrum of untoward circum-stances and burden factors, ranging from physical topsychological, private to work-related, and dysthy-mic to affectively neutral. Age ranged from 34 to 78years (mean, 55.2), showing that FMD is more prev-alent in the second half of life, but not limited toelderly people. A comparison between the youngerand the older half of the present patient sampleshowed only minor and nonsignificant differencesfor a set of key variables.

FMD severity was significantly correlated with afour-item scale of vegetative, and presumably psy-chosomatic, complaints, presumably due a commonrelationship with the level of psychosocial distress.The observed lack of an association between subjec-tive impairment and test results is a known findingin nonorganic memory impairment.18

A comparison of patients who did and who didnot attend the follow-up examination showed nosignificant between-group differences. Thus, there isno indication for a systematic bias toward a loss offollow-up data of older or more impaired patients.However, a bias due to preferential attrition of pa-tients with undetected prodromal organic diseasecannot be ruled out.

In addition to 73 patients who were eligible forinclusion into the present study, further 59 patientswith probable nonorganic impairment were screenedand excluded. Of these, a majority had depression,emphasizing the importance of depression as an-other cause of nonorganic cognitive impairment in amemory clinic environment.

Outcome

Only one patient had deteriorated clinically andneuropsychologically by the time of follow-up andreceived a new diagnosis of early dementia. In theother 45 patients, verbal memory scores ��1 SD atfollow-up, except for one patient who scored at �1.3

TABLE 1. Means and Standard Deviations of Age and TestScores of FMD Patients Who Attended BothExaminations (n � 45)

Baseline Follow-Up

Age 55.2 � 10.6 (34–78) 56.9 � 10.6 (36–80)Auditory verballearning test(n � 33)

55.7 � 8.7 (32–67) 61.5 � 9.4 (44–74)

CERAD verballearning test(n � 12)

20.8 � 1.9 (17–23) 22.1 � 1.9 (19–25)

Digit connection test(s) (n � 33)

81.3 � 20.9 (54–127) 83.3 � 23.0 (50–135)

Digit connection test,short version (n �12)

32.4 � 15.5 (20–55) 25.3 � 8.0 (17–45)

FMD inventory score(0–10)

7.6 � 2.6 (1–10) 5.8 � 2.9 (0–10)

Vegetative complaints(0–4)

1.70 � 1.3 (0–4) 1.18 � 1.3 (0–4)

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SD, provided no indication of impending dementiaor mild cognitive impairment. Other studies withlonger follow-up periods have observed progressionto dementia in subgroups of unselected, cognitivelynormal patients with “subjective memory com-plaint” (e.g., Ref. 10). Incipient organic disease de-spite normal test results could be explained by highpremorbid levels of functioning and by limited va-lidity of cognitive tests. Hence, it remains possiblethat some of our patients will eventually developorganic disease. Three points that argue against alarge proportion of incipient dementia cases are thepresence of an alternative explanation for cognitiveimpairment, the low mean age, and the stability ofmemory and attentional test scores from baseline tofollow-up (Table 1).

Another principle finding is that, after a meandelay of 20.1 months, FMD had essentially resolvedin only six patients. A post-hoc evaluation showsthat psychosocial burden was rated better (N � 1) or“much better” (N � 5) in these six patients. How-ever, in the large majority, FMD persisted. The aver-age Likert score of subjective memory function was“unchanged” across all subjects. Symptom severity,as assessed by the FMD inventory, showed a signif-icant but small decrease. Thus, FMD was largelystable, with the exception of the minority of patientswho recovered. It thus appears that, within the limitsof the applied follow-up interval, FMD is often along-term rather than a transient problem, as it is thecase in other somatoform disorders.

It is logical to assume that lack of improvementwas, to some degree, due to persistence of psychos-ocial burden factors and distress. The significant cor-relation between the Likert scores of change of psy-chosocial burden and the change of subjectivememory function supports the hypothesis that bur-den factors play an important role in the etiology ofFMD. However, we assume that, to some degree,lack of improvement was also due to the continuouseffect of a mutual reinforcement between distressand cognitive failure.

CONCLUSION

The coherent pattern of correlations between base-line and follow-up measures of cognitive impair-

ment in daily living, psychosocial burden, and veg-etative complaints supports the proposed etiologicalmodel. Whether psychosocial burden and distressare indeed causal for FMD in each case is, however,uncertain.

The concept of FMD can assist in identifying sub-groups of subjective memory impairment patientswho do or do not require intervention, and thosewho are at low versus high risk of median-termcognitive decline. With regard to trials in mild cog-nitive impairment, it is important to subdivide pa-tients with memory complaints into probable FMD-and probable pre-Alzheimer cases, namely thosewith test results in the border zone between �1 and�1.5 SD.

Unless FMD is recognized and diagnosed as asyndrome in its own right, underlying psychologi-cal factors may remain undetected and untreated.Timely diagnosis of FMD may help to avoid re-peated medical investigations, relieve the fear oforganic disease, and break the spiral of psycholog-ical distress and underperformance. In the presentstudy, one-time counseling was mostly not suffi-cient to resolve FMD. A directed therapeutic ap-proach may therefore be needed. Ponds et al.4 haveevaluated a three- to five-session therapy program.At follow-up, patients rated themselves less for-getful, less anxious, and less perfectionist in regardto memory performance. Our research group hasrecently evaluated a novel group therapy programinvolving 13 sessions of psychoeducation, cogni-tive restructuring, stress management and relax-ation techniques, and mindfulness exercises.14 Thetreated group showed a significantly higher improve-ment than a wait-list control group on the memoryself-efficacy measure of the Metamemory in Adulthoodquestionnaire.19 A multimodal group-therapy ap-proach thus seems to be helpful in alleviating FMDsymptomatology.

APPENDIX

Panel 1: Clinical FMD Criteria

1. Complaint of acquired (�6 months) dysfunctionof memory that, as perceived by patients, signif-



icantly affects their level of functioning in pro-fessional and/or private life.

2. Presence of external and/or subjective factors,addressed as psychosocial burden factors, thatcause significant psychological stress.

3. Verbal memory and attentional capacity above�1.5 SD (age-corrected), as assessed by stan-dardized tests.

4. Absence of a recognizable organic cause of cog-nitive impairment. A physical examination, notincluding imaging, was routinely performed.

5. Absence of major psychiatric disease, e.g., psycho-sis, major depression, dissociative disorder, obses-sive-compulsive disease, etc. (previous or present).Patients with dysthymia or adjustment disorderwith depressed mood were included if the BeckDepression Inventory score was �15.

Panel 2: The FMD Inventory

Items related to a deficit of working memory andconcentration:

1. Do your forget errands on the way to their exe-cution?

2. Do you rapidly forget essential parts of a per-sonal or telephone conversation?

3. Do you experience disruptions of the thread ofthoughts in conversations?

4. Do you experience absent-mindedness and day-dreaming during conversations?

Items related to a deficit of the registration of newcontents:

5. Do you forget important contents of conversa-tions, appointments, and errands (time scale ofdays)?

6. Do you experience difficulties understandingand registering the contents of news, reading,and lectures?

Items related to a deficit of retrieval:

7. Do you experience blocks of retrieval of well-known names, phone numbers, PIN codes, etc.(but typically recall them later)?

8. Do you commit errors, or experience “blackouts”during routine activities at work, at home, whiledriving, etc.?

9. Do you experience difficulties finding words?

Item related to the variability of symptom sever-ity:

10. Is your memory impairment subject to variations,namely less marked during times of relaxation?

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The Syndrome of Functional Memory Disorder: Definition, Etiology, and Natural Course