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Neurocase (2001) Vol. 7, pp. 269–282
© Oxford University Press 2001
PREVIOUS CASES
Isolated Retrograde Amnesia
Kristina Fast and Esther Fujiwara
Department of Physiological Psychology, University of Bielefeld, PO Box 100131, D-33501 Bielefeld, Germany
The syndrome of isolated retrograde amnesia refers to a
neuropathological state of impaired memory for information
acquired prior to the onset of brain damage (retrograde
memory) contrasted with normal or near-normal learning of
new information after the onset of the disease (anterograde
memory). Whereas a more extensive impairment of
anterograde memory together with minimal retrograde
amnesia is often described in patients with (medial) temporal
lobe damage or diencephalic lesions (e.g. Alvarez and Squire,
1995), disproportionate retrograde memory impairment can
be found less frequently in patients with more heterogeneous
lesions. Isolated retrograde amnesia is also known as ‘focal
retrograde amnesia’ (e.g. Kapur, 1993, 2000; Evans et al.,
1996; Carlesimo et al., 1998a, b; Kopelman, 2000a), ‘pure
retrograde amnesia’ (e.g. Lucchelli et al., 1998), or ‘selective
retrograde amnesia’ (e.g. Andrews et al., 1982).
Although the aetiology and even the existence of the
syndrome of retrograde amnesia is controversial [see Kapur
(2000), Kopelman (2000a, b)], the principal symptom is
consistently described as a severe loss of (mainly and
mostly episodic) retrograde memory, combined with largely
preserved anterograde memory ability. [See Tulving and
Markowitsch (1998) for a recent definition of episodic
memory.]
A wide variety of aetiologies has been observed in different
cases suffering from disproportionate retrograde amnesia. As
organic aetiologies, the following were noted most consistently: mild brain injury (Stracciari et al., 1994; De Renzi
et al., 1995; Starkstein et al., 1997), severe traumatic brain
injury (Goldberg et al., 1981; Rousseaux et al., 1984; Kapur
et al., 1992; Markowitsch et al., 1993a, b; Hunkin et al.,
1995; Kapur et al., 1996), encephalitis (Eslinger and Cermak,
1988; Stuss and Guzman, 1988; O’Connor et al., 1992, 1997;
Yoneda et al., 1992; Eslinger et al., 1993, 1996; Hokkanen
et al., 1995; Calabrese et al., 1996; Carlesimo et al., 1998a;
Levine et al., 1998), hypoxia (De Renzi and Lucchelli, 1993),
vascular pathology (Andrews et al., 1982; Evans et al., 1996;
Reinvang and Gjerstad, 1998), epilepsy (transient epileptic
amnesia; TEA) (Kapur et al., 1989) and transient global
amnesia (TGA) (Roman-Campos et al., 1980; Evans et al.,
1993), suggesting that multifocal lesions produce isolated
retrograde amnesia. Patients with more restricted organic
brain damage most commonly demonstrate combined
bilateral temporal lobe and pre-frontal damage (Damasio,
1989; Markowitsch et al., 1993a, b; Markowitsch, 1995;
Kapur, 1997; Kroll et al., 1997; Markowitsch and Ewald,
1997; Levine et al., 1998). Sometimes damage is centred at
both anterior temporal lobes (Tanaka et al., 1999), the medial
temporal lobe structures of both hemispheres (including parts
of the hippocampus and amygdala) (Fujii et al., 1999), or
right parieto-occipital and left occipital regions (Hunkin et al.,
1995). A patient with isolated retrograde amnesia and organic
pathology was described by Tanaka et al. (1999). Following
herpes simplex encephalitis, patient HK suffered from a
persistent isolated retrograde amnesia after damage to the
bilateral temporal poles and anterior parts of the inferotemporal lobes with some extensions to anterior parts of the
medial temporal lobes as revealed by magnetic resonance
imaging (MRI). The lesions were more severe on the left
hemisphere, and no pathology was found in the frontal
lobes. Standard neuropsychological assessment revealed no
impairments in anterograde memory and other cognitive
domains. The patient’s low verbal IQ was attributed to
reduced performance in the information subtest of the
Wechsler Adult Intelligence Scale (WAIS; Wechsler, 1981)
and was explained by a general semantic knowledge deficit.
Her remote memory was severely deteriorated and affected
mainly autobiographical events, while both personal and
impersonal semantic memories were less impaired. An
advantage of recognition performance over performance in
free recall was observed in tests of impersonal semantic
memory, while retrieval mode had no effect on autobiographical memory. It was suggested that the anterior temporal
poles play a critical role in evoking remote memories and
Correspondence to: Kristina Fast, Department of Physiological Psychology, University of Bielefeld, P.O. Box 100131, D-33501 Bielefeld, Germany.
Tel: ⫹49 521 1064484; Fax: ⫹49 521 1066049; e-mail: [email protected]
270 Previous cases: Isolated retrograde amnesia
possibly contain codes necessary for retrieval processes.
Alternatively, Markowitsch (1995) suggested the anterior
temporal lobes as a critical relay between the pre-frontal lobes
and the posterior association cortices. Retrieval processes,
therefore, are assigned to pre-frontal regions. These then are
connected via anterior temporal lobes with formerly stored
information, situated in posterior association areas.
Predominantly frontal lesions were described in patient
ML (Levine et al., 1998). He sustained a severe head injury
with small right frontal lobe and left inferior posterior
temporal contusions, a mild diffuse oedema and small
bifrontal subdural hygromas [computer tomographic (CT)
results 6 days post-trauma]. More than 1 year later, a MRI
scan revealed damage in the right ventral frontal cortex, the
underlying white matter, as well as in a few other smaller
foci. Neuropsychological deficits included minor visuomotor
and visuoperceptual problems, possibly caused by a subtle
right upper quadrant anopsia, and a low score on an
experimental task of strategy application. His disproportionate
retrograde amnesia included a general retrieval deficit for
semantic knowledge (personal and impersonal) and autobiographical episodes. Additionally, in an experimental task
series, the ‘remember–know paradigm’ (Tulving, 1985) was
applied to test different levels of consciousness according to
two memory systems: episodic and semantic memory. Levine
et al. (1998) suggested the remember–know technique as a
sensitive indicator for different memory qualities in patients
with (isolated) retrograde amnesia. It is hypothesized that
episodic information is processed autonoetically (being
aware of one’s self across time) and can be measured
by ‘remember’ judgements, while semantic information is
processed noetically (being aware of more general,
impersonal facts) and can be assessed by ‘know’ judgements.
A clear dissociation of remember and know judgements was
found in ML, indicating preserved noetic awareness while
autonoetic consciousness, on the other hand, was extremely
poor. With regard to prior event-related potential and positron
emission tomography (PET) findings, Levine et al. (1998)
explained ML’s impairment in remember responses and
autonoetic awareness by his right frontotemporal disconnection.
More posterior lesions were observed in patient DH
(Hunkin et al., 1995) following a closed head injury. Structural
MRI revealed lesions in the right parieto-occipital and left
occipital lobes. Temporal, frontal or diencephalic lesions
could not be identified. Neuropsychological assessment indicated a severe loss of personal and public remote memory
accompanied by visual anterograde memory impairments.
DH’s pattern of deficits can be explained by a model of
Damasio (1989). He proposed that episodic memory is
represented in a multimodal fashion, and assumed that
different aspects of an episode are stored unimodally in the
sensory cortices in which they were originally registered.
Recalling of an episode therefore requires similar neural
activity patterns to those which occurred when the event was
initially perceived. It is suggested that DH’s lesions disrupted
transmission of information either from visual activity in the
posterior cortex to multimodal convergence zones or vice
versa, resulting in a change in neural activity patterns and
exacerbating recall.
As exemplified above, multiple lesions are associated with
isolated retrograde amnesia. Accordingly, it is possible that
different brain regions contribute to different aspects of
remote memory processes resulting in similar observable
deterioration.
From a theoretical point of view, bilateral hippocampal
lesions are also considered likely to evoke autobiographical
memory loss. In the multiple trace model of Nadel and
Moscovitch (1997) [see also Moscovitch and Nadel (1999)] it
is assumed that, through close interaction of the hippocampal
complex with other cortical structures, the experience of an
event is mediated and by this process multiple traces are
formed over time. Nadel and Moscovitch (1997) proposed
that older memories require more memory traces compared
with recent memories and that successful retrieval is facilitated
by a higher quantity of memory traces. Moreover, they assumed
that episodic memories remain dependent upon continuing
interactions between the hippocampal complex and
neocortex.
Long-term consolidation processes depend on the
hippocampal complex. Therefore, Moscovitch and Nadel
(1998) supposed extensive bilateral hippocampal lesions
to be necessary to evoke dense autobiographical amnesia.
However, as shown above, in some cases with isolated
retrograde amnesia, various lesion sites could not be entirely
explained by this model. Another hypothesis centres on
frontotemporal networks sparing medial temporal regions as
critical for remote memory access (e.g. Kroll et al., 1997).
In comparing the neuropsychological performance of two
patients with combined bilateral temporopolar and pre-frontal
damage with a patient suffering solely from bilateral prefrontal damage, Kroll et al. (1997) observed disproportionate
retrograde memory deficits only in the patients with combined
lesions. Emphasizing this regional combination (Kapur et al.,
1992; Markowitsch et al., 1993a, b; Markowitsch and Ewald,
1997), in light of corresponding results of functional neuroimaging studies in non-brain-damaged subjects (Fink et al.,
1996), the authors considered the temporofrontal junction
area (e.g. fasciculus uncinatus) to be critical for retrieving
old memories.
The syndrome of isolated retrograde amnesia can also be
caused by psychogenic factors, such as psychic traumata
and stress, and becomes even more complex when these
psychological factors are considered. Within this group of
patients, those with a clear psychogenic causation (Schacter
et al., 1982; Bremner et al., 1995; Campodonico and
Rediess, 1996; Markowitsch et al., 1997a, b; Costello et al.,
1998) can be differentiated from others with possible or
likely psychological aetiologies, combined with additional
(manifest) organic brain injury. If neither psychogenic causation nor organic causation can be clearly identified or separated, the term ‘functional retrograde amnesia’ is often used
Previous cases: Isolated retrograde amnesia 271
to indicate metabolic changes in brain regions contributing
to memory processes [see also De Renzi et al. (1997) and
Markowitsch (1999)]. A frequently observed combination of
psychogenic and organic aetiologies for isolated retrograde
amnesia is represented by patients with initial brain pathology
but without enduring organic lesions (Stuss, 1993; Binder,
1994; Kopelman et al., 1994; Lucchelli et al., 1995). Disproportionate and lasting retrograde amnesia is frequently
described in mild head trauma patients without pathological
signs in static neuroimaging (Barbarotto et al., 1996;
De Renzi et al., 1997; Lucchelli et al., 1998; Mackenzie
Ross, 2000).
For instance, patient PA (Barbarotto et al., 1996) sustained
a minor head trauma followed by isolated retrograde amnesia.
Psychogenic and organic causation as well as deliberate
simulation were discussed by the authors. CT and single
photon emission computer tomography revealed no pathological signs and psychiatric evaluation gave no evidence of
present or previous psychiatric disorders. Post-incidental
clinical observations led to the assumption of a histrionic
personality disorder and hysterical personality structures.
Besides her retrograde amnesia, only multimodal short-term
memory deficits were reported, accompanied by an intact
anterograde long-term memory. PA complained of a loss of
both semantic and episodic memories. However, neuropsychological assessment only revealed evidence of a severe
loss of autobiographical memories. Semantic memory was
also very poor, but indications for an implicit use of semantic
knowledge were observed. The authors concluded that the
presence of minor brain damage together with several psychogenic factors, a hysterical personality profile, emotional
stress, possible secondary gain deriving from disease and
intact implicit metamemory may all have contributed to the
isolated retrograde amnesia.
A case with a more transient isolated retrograde amnesia
was described by Papagno (1998). Patient CL sustained a
minor head injury caused by falling from a scaffold. CT and
MRI were normal, EEG data showed irritative components
in the left temporal region. Psychiatric evaluation revealed
no psychiatric diagnoses, whereas in a clinical interview
several episodes of emotional stress, including separation
from his girlfriend 6 months prior to the accident, were
ascertained. Besides his profound retrograde amnesia, his
neuropsychological deficits included category-specific
naming difficulties (living versus non-living things) and
impaired verbal fluency. Learning ability, retrieval of postincident learned information, and the ability to relearn autobiographical data, were spared. The transient retrograde
amnesia was defined by a total loss of semantic and autobiographical memories characterized by an absence of a clearcut temporal gradient. All aspects of retrograde amnesia
and language impairment recovered spontaneously 10 days
after the incident. Psychogenic and organic aetiology were
discussed with respect to the idea of a mnestic block
syndrome, proposed by Markowitsch (1996).
In his revised model of psychogenic and organic amnesia,
Kopelman (2000a) described the contributions of organic
and psychogenic/functional factors to cognitive disorders as
interactive and of considerable variation.
Additional external and internal influencing factors acting
on memory-relevant brain systems were established. These
factors are comprised of learning experiences, current
emotional state, personal semantic belief system, severe
precipitating stress and ‘normal’ environmental input. The
importance of careful assessment of all these factors is
emphasized to provide a more comprehensive classification
of patients with isolated retrograde amnesia on the continuum
of organic and psychogenic/functional (namely hysterical/
unconscious and malingering/simulation) amnesia.
In conclusion, the nature of the syndrome of isolated
retrograde amnesia has to be considered as multifaceted and
heterogeneous in aetiology, brain lesion or pathology, and
neuropsychological impairment. These conditions lead to
marked difficulties in differentiating aetiologies, structural
and functional neuropathologies, as well as in specifying a
theoretical model capable of elucidating all contributing
aspects.
References
Alvarez P, Squire LR. Memory consolidation and the medial temporal lobe:
a simple network model. Proceedings of the National Academy of Sciences
1995; 91: 7041–5.
Andrews E, Poser CM, Kessler M. Retrograde amnesia for forty years. Cortex
1982; 18: 441–58.
Barbarotto R, Laiacona M, Cocchini G. A case of simulated, psychogenic or
focal pure retrograde amnesia: did an entire life become unconscious?
Neuropsychologia 1996; 34: 575–85.
Binder LM. Psychogenic mechanisms of prolonged autobiographical retrograde
amnesia. Clinical Neuropsychologist 1994; 8: 439–50.
Bremner JD, Krystal JH, Southwick SM, Charney DS. Functional
neuroanatomical correlates of the effects of stress on memory. Journal of
Traumatic Stress 1995; 8: 527–53.
Calabrese P, Markowitsch HJ, Durwen HF, Widlitzek H, Haupts M, Holinka
B et al. Right fronto-temporal cortex as a critical locus for the ecphory of
old episodic memories. Journal of Neurology, Neurosurgery and Psychiatry
1996; 61: 304–10.
Campodonico JR, Rediess S. Dissociation of implicit and explicit knowledge
in a case of psychogenic retrograde amnesia. Journal of the International
Neuropsychological Society 1996; 2: 146–58.
Carlesimo GA, Sabbadini M, Loasses A, Caltagirone C. Analysis of the
memory impairment in a post-encephalitic patient with focal retrograde
amnesia. Cortex 1998a; 34: 449–60.
Carlesimo GA, Sabbadini M, Bombardi P, Di Porto E, Loasses A, Caltagirone
C. Retrograde memory deficits in severe closed-head injury patients. Cortex
1998b; 34: 1–23.
Costello A, Fletcher PC, Dolan RJ, Frith CD, Shallice T. The origins of
forgetting in a case of isolated retrograde amnesia following a hemorrhage:
evidence from functional imaging. Neurocase 1998; 4: 437–46.
Damasio AR. Time-locked multiregional retroactivation: a systems level
proposal for the neural substrates of recall and recognition. Cognition 1989;
33: 25–62.
De Renzi E, Lucchelli F. Dense retrograde amnesia, intact learning capability
and abnormal forgetting rate: a consolidation deficit? Cortex 1993; 29:
449–66.
De Renzi E, Lucchelli F, Muggia S, Spinnler H. Persistent retrograde amnesia
following a minor trauma. Cortex 1995; 31: 531–42.
De Renzi E, Lucchelli F, Muggia S, Spinnler H. Is memory loss without
anatomical damage tantamount to a psychogenic deficit? The case of pure
retrograde amnesia. Neuropsychologia 1997; 35: 781–94.
Eslinger PJ, Cermak LS. Anatomic correlates of retrograde amnesia. Social
Neuroscience Abstracts 1988; 14: 1289.
272 Previous cases: Isolated retrograde amnesia
Eslinger PJ, Damasio H, Damasio AR, Butters N. Nonverbal amnesia and
asymmetric cerebral lesions following encephalitis. Brain and Cognition
1993; 21: 140–52.
Eslinger PJ, Easton A, Grattan LM, Van Hoesen GW. Distinct forms of partial
retrograde amnesia after asymmetric temporal lobe lesions: possible role of
the occipitotemporal gyri in memory. Cerebral Cortex 1996; 6: 530–9.
Evans JJ, Wilson BA, Wraight EP, Hodges JR. Neuropsychological and
SPECT scan findings during and after transient global amnesia: evidence
for the differential assessment of remote episodic memory. Journal of
Neurology, Neurosurgery and Psychiatry 1993; 56: 1227–30.
Evans JJ, Breen EK, Antoun N, Hodges JR. Focal retrograde amnesia
for autobiographical events following cerebral vasculitis: a connectionist
account. Neurocase 1996; 2: 1–11.
Fink G, Markowitsch HJ, Reinkemeier M, Bruckbauer T, Kessler J, Heiss
WD. A PET-study of autobiographical memory recognition. Journal of
Neuroscience 1996; 16: 4275–82.
Fujii T, Yamadori A, Endo K, Suzuki K, Fukatsu R. Disproportionate
retrograde amnesia in a patient with herpes simplex encephalitis. Cortex
1999; 35: 599–614.
Goldberg E, Antin SP, Bilder RM, Gerstman LJ, Hughes JEO, Mattis S.
Retrograde amnesia: possible role of mesencephalic reticular activation in
long-term memory. Science 1981; 213: 1392–4.
Hokkanen L, Launes R, Vataja R, Vallanne L, Iivanainen M. Isolated retrograde
amnesia for autobiographical material associated with acute left temporal
lobe encephalitis. Psychological Medicine 1995; 25: 203–8.
Hunkin NM, Parkin AJ, Bradley VA, Burrows EH, Aldrich FK, Jansari A
et al. Focal retrograde amnesia following closed head injury: a case study
and theoretical account. Neuropsychologia 1995; 33: 509–23.
Kapur N. Focal retrograde amnesia: a critical review. Cortex 1993; 29: 217–34.
Kapur N. How can we best explain retrograde amnesia in human memory
disorder. Memory 1997; 5: 115–29.
Kapur N. Focal retrograde amnesia and the attribution of causality: an
exceptionally benign commentary. Cognitive Neuropsychology 2000; 17:
623–37.
Kapur N, Young A, Bateman D, Kennedy P. Focal retrograde amnesia: a long
term clinical and neuropsychological follow-up. Cortex 1989; 25: 387–402.
Kapur N, Ellison D, Smith M, McLellan L, Burrows EH. Focal retrograde
amnesia following bilateral temporal lobe pathology: a neuropsychological
and magnetic resonance study. Brain 1992; 116: 73–86.
Kapur N, Scholey K, Moore E, Barker S, Brice J, Thompson S et al. Longterm retention deficits in two cases of disproportionate retrograde amnesia.
Journal of Cognitive Neuroscience 1996; 8: 416–34.
Kopelman MD. Focal retrograde amnesia and the attribution of causality:
an exceptionally critical review. Cognitive Neuropsychology 2000a; 17:
585–621.
Kopelman MD. Comments on focal retrograde amnesia and the attribution of
causality: an exceptionally benign commentary by Narinder Kapur.
Cognitive Neuropsychology 2000b; 17: 639–40.
Kopelman MD, Christensen H, Puffett A, Stanhope N. The great escape: a
neuropsychological study of psychogenic amnesia. Neuropsychologia 1994;
32: 675–91.
Kroll NEA, Markowitsch HJ, Knight RT, von Cramon DY. Retrieval of old
memories: The temporo-frontal hypothesis. Brain 1997; 120: 1377–99.
Levine B, Black SE, Cabeza R, Sinden M, Mcintosh AR, Toth JP et al.
Episodic memory and the self in a case of isolated retrograde amnesia.
Brain 1998; 121: 1951–73.
Lucchelli F, Muggia S, Spinnler H. The ‘Petites Madeleines’ phenomenon in
two amnesic patients. Sudden recovery of forgotten memories. Brain 1995;
118: 167–83.
Lucchelli F, Muggia S, Spinnler H. The syndrome of pure retrograde amnesia.
Cognitive Neuropsychiatry 1998; 3: 91–118.
Mackenzie Ross S. Profound retrograde amnesia following mild head injury:
organic or functional? Cortex 2000; 36: 521–37.
Markowitsch HJ. Which brain regions are critically involved in the retrieval
of old episodic memory? Brain Research Reviews 1995; 21: 117–27.
Markowitsch HJ. Organic and psychogenic retrograde amnesia: two sides of
the same coin? Neurocase 1996; 2: 357–71.
Markowitsch HJ. Gedächtnisstörungen. Stuttgart: Kohlhammer. 1999.
Markowitsch HJ, Ewald K. Right-hemispheric fronto-temporal injury leading
to severe autobiographical retrograde and moderate anterograde episodic
amnesia. Neurology, Psychiatry and Brain Research 1997; 5: 71–8.
Markowitsch HJ, Calabrese P, Haupts M, Durwen HF, Liess J, Gehlen W.
Searching for the anatomical basis of retrograde amnesia. Journal of Clinical
and Experimental Neuropsychology 1993a; 15: 947–67.
Markowitsch HJ, Calabrese P, Haupts M, Durwen HF, Niess J, Gehlen W.
Retrograde amnesia after traumatic injury of the fronto-temporal cortex.
Journal of Neurology, Neurosurgery and Psychiatry 1993b; 56: 988–92.
Markowitsch HJ, Calabrese P, Fink GR, Durwen HF, Kessler J, Härting C
et al. Impaired episodic memory retrieval in a case of probable psychogenic
amnesia. Psychiatry Research 1997a; 74: 119–26.
Markowitsch HJ, Fink GR, Thöne A, Kessler J, Heiss WD. A PET-study of
persistent psychogenic amnesia covering the whole life span. Cognitive
Neuropsychiatry 1997b; 2: 135–58.
Moscovitch M, Nadel L. Consolidation and the hippocampal complex revisited:
In defense of the multple-trace model. Current Opinion in Neurobiology
1998; 8: 297–300.
Moscovitch M, Nadel L. Multiple-trace theory and semantic dementa: A reply
to K.S. Graham. Trends in Cognitive Sciences 1999; 3: 87–9.
Nadel L, Moscovitch M. Memory consolidation, retrograde amnesia and the
hippocampal complex. Current Opinion in Neurobiology 1997; 7: 217–27.
O’Connor M, Butters N, Miliotis P, Eslinger P, Cermak LS. The dissociation
of anterograde and retrograde amnesia in a patient with herpes encephalitis.
Journal of Clinical and Experimental Neuropsychology 1992; 14: 159–78.
O’Connor M, Sieggreen MA, Ahern G, Schomer D, Mesulam M. Accelerated
forgetting in association with temporal lobe epilepsy and paraneoplastic
encephalitis. Brain and Cognition 1997; 35: 71–84.
Papagno C. Transient retrograde amnesia associated with impaired naming of
living categories. Cortex 1998; 34: 111–21.
Reinvang I, Gjerstad L. Focal retrograde amnesia associated with vascular
headache. Neuropsychologia 1998; 36: 1335–41.
Roman-Campos G, Poser CM, Wood FB. Persistent retrograde memory deficit
after transient global amnesia. Cortex 1980; 16: 509–18.
Rousseaux M, Delafosse A, Cabaret M, Lesoin F, Jomin M. Amnésie retrograde
post traumatique. Cortex 1984; 20: 575–93.
Schacter DL, Wang PL, Tulving E, Freedman M. Functional retrograde
amnesia: a quantitative case study. Neuropsychologia 1982; 20: 523–32.
Squire LR, Alvarez P. Retrograde amnesia and memory consolidation:
A neurobiological perspective. Current Opinion in Neurobiology 1995; 5:
169–77.
Starkstein SE, Sabe L, Dorrego MF. Severe retrograde amnesia after a mild
injury. Neurocase 1997; 3: 105–9.
Stracciari A, Ghidoni E, Guarino M, Poletti M, Pazzaglia P. Post-traumatic
retrograde amnesia with selective impairment of autobiographical memory.
Cortex 1994; 30: 459–68.
Stuss DT. An unusual case of retrograde amnesia: fact or fake? Journal of
Clinical and Experimental Neuropsychology 1993; 15: 389.
Stuss DT, Guzman DA. Severe remote memory loss with minimal anterograde
amnesia: a clinical note. Brain and Cognition 1988; 8: 21–30.
Tanaka Y, Miyazawa Y, Hashimoto R, Nakano I, Obayashi T. Postencephalitic
focal retrograde amnesia after bilateral anterior temporal lobe damage.
Neurology 1999; 53: 344–50.
Tulving E. Memory and consciousness. Canadian Psychology 1985; 26: 1–12.
Tulving E, Markowitsch HJ. Episodic and declarative memory: role of the
hippocampus. Hippocampus 1998; 8: 198–204.
Wechsler D. Wechsler Adult Intelligence Scale-Revised. New York:
Psychological Corporation, 1981.
Yoneda Y, Yamadori A, Mori E, Yamashita H. Isolated prolonged retrograde
amnesia. European Neurology 1992; 32: 340–2.
Received on 26 March, 2001; accepted on 12 April, 2001
Previous cases: Isolated retrograde amnesia 273
A traumatic temporal lobe pathology
and autobiographical memory
A case of simulated, psychogenic or focal
pure retrograde amnesia: did the entire
life become unconscious?
R. Babinsky, B. Maier, P. Calabrese,
H. J. Markowitsch and W. Gehlen
R. Barbarotto, M. Laiacona and G. Cochini
Abstract
Abstract
A patient with isolated autobiographical episodic memory is presented. The
patient (male; 64 years old) was admitted to hospital suffering from double
images and headache. CT examination revealed an arachnoid cyst at the
anterior part of the left temporal lobe. In neuropsychological examination, a
clear dissociation between subnormal autobiographical episodic memory and
intact anterograde memory as well as unimpaired remote memory for personal
and public facts was found. Regarding limited lesion sites in this patient, it
is hypothesized that left anterior temporal lobe regions may play a critical
role in effortful processing of episodic autobiographical memories.
A patient (PA; female; 38 years old) developed a pure retrograde amnesia
covering her whole life-span following a mild head injury. CT and SPECT
gave no evidence for brain pathology. Psychogenic and organic aspects of the
amnesia were taken into account to explain the patient’s profile as well as the
possibility of simulated amnesia. Her implicit use of remote information was
not impaired, supporting the interpretation of a psychogenic block in a person
with a hysterical personality structure instead of deliberate simulation.
Journal
European Neurology 1994; 34: 290–1
Neurocase Reference Number:
P814
Primary diagnosis of interest
Isolated (focal) autobiographical retrograde amnesia
Author’s designation of case
Not stated
Key theoretical issue
d
Journal
Neuropsychologia 1996; 34: 575–85
Neurocase Reference Number:
P815
Primary diagnosis of interest
Isolated (focal) retrograde amnesia
Author’s designation of case
PA
Key theoretical issue
d
In a patient a dissociation between unimpaired anterograde memory
performance and retrograde autobiographical amnesia is attributed to a
selective left temporal pole lesion
A patient developed a pure retrograde amnesia without temporal gradient
following a mild head trauma with no persistent brain pathology. Postmorbid information was normally learned and retrieved. The case was
discussed as a form of psychogenic amnesia caused by mnestic block or
by unconscious simulation
Key words: amnesia; retrograde; arachnoid cysts; anterior temporal lobe
Key words: retrograde amnesia; psychogenic amnesia
Scan, EEG and related measures
Scan, EEG and related measures
EEG, CT
1993: CT
1994: SPECT
Standardized assessment
Wechsler Adult Intelligence Scale (modified version: Reduzierter WechslerIntelligenztest WIP), Concept Comprehension Task, Concentration Endurance
Test d2, Zahlen-Verbindungs-Test (German version of Trail Making Test),
Wechsler Memory Scale-Revised, Aachener Aphasie Test (German language
test), Word Stem Completion Tasks, Famous Events Test, Autobiographical
Memory Interview, German personality questionnaire
Other assessment
None
Lesion location
d
d
EEG: normal
CT: arachnoid cyst at the left temporal pole filled with fluid, possibly
cerebrospinal fluid
Standardized assessment
Mini-Mental-Status Test, Raven’s Progressive Matrices, Token Test, Naming
of Objects and Details, Behavioural Memory Rivermead Test, Digit Span,
Disyllable Word Span, Spatial Span, Verbal Learning, Story Recall, Spatial
Learning, Semantic Memory Questionnaire, Public Events and Famous People
Questionnaires, Fame Decision Task, Autobiographical Memory
Questionnaire, Procedural Memory Task
Other assessment
Psychodiagnostic evaluation: clinical interview, Rorschach Test, Blacky Test
Lesion location
d
d
CT: normal
SPECT: normal
Lesion type
Lesion type
Arachnoid cyst
Mild head injury
Language
Language
English
English
274 Previous cases: Isolated retrograde amnesia
Analysis of the memory impairment in a
post-encephalitic patient with focal
retrograde amnesia
G. A. Carlesimo, M. Sabbadini, A. Loasses and
C. Caltagirone
Abstract
Data from a post-encephalitic patient (AV; female; 29 years old) with focal
retrograde amnesia is presented. MRI demonstrated widespread abnormal
intensity areas encroaching upon the white matter of temporal, parietal and
occipital lobes but sparing temporal poles and orbito-frontal cortex. The
quality of her memory impairment is extensively studied. AV’s memory deficit
encompassed autobiographical data, public events and famous people. In a
public events questionnaire, a negative temporal gradient with good recollection
of events that occurred about 15 years before the disease, but poor memory
of more recent events was found. Lexicality judgement for words and
familiarity judgement for proper names was normal, but she was poor in
familiarity judgement for famous faces (prosopagnosia) and in accessing the
meaning of words or specific information about people. Visual input lexicon
and semantic description system are supposed to normally function through
close associations between the two systems, e.g. by means of corresponding
nodes. Diffuse damage of associative areas of posterior-temporal and parietal
lobes in patient AV is assumed to account for her remote memory deficits.
Journal
Remembering and knowing the past: a
case study of isolated retrograde amnesia
G. Dalla Barba, M. C. Mantovan, E. Ferruza
and G. Denes
Abstract
A patient (RM; female; 17 years old) suffered from a sudden selective
retrograde amnesia for personal episodes with mostly spared retrograde
memory for semantics. General intellectual and learning abilities were normal.
Neuroimaging data gave no hints for brain damage. Although the patient
complained of occipital headache, back pain and nausea, these signs were too
unspecific and gave no sufficient support for an organic pathogenesis.
Psychogenic aetiology could not be excluded, but history and clinical
observations did not fit with known cases of psychogenic amnesia. There was
no evidence for simulation. The dissociation between episodic and semantic
memory in RM gave support for the distinction between remembering
and knowing.
Journal
Cortex 1997; 33: 143–54
Neurocase Reference Number:
P817
Cortex 1998; 34: 449–60
Primary diagnosis of interest
Neurocase Reference Number:
Isolated (focal) retrograde amnesia
P816
Author’s designation of case
Primary diagnosis of interest
RM
Isolated (focal) retrograde amnesia
Author’s designation of case
AV
Key theoretical issue
d
Key theoretical issue
d
In this patient diffuse bilateral damage of associative areas in the posteriortemporal and parietal lobes led to isolated retrograde amnesia. On the
neuropsychological level, dissociation across different pre-semantic
structural description systems and between the visuo-verbal description
system and the semantic system were observed
A case of spontaneously developed retrograde amnesia involving solely
personal memory was described. No clear evidence for organic brain
damage, psychogenic aetiology or simulation was found. The case gave
additional support for the distinction between episodic and semantic memory
Key words: amnesia; retrograde amnesia
Scan, EEG and related measures
Key words: memory disorders; retrograde amnesia; herpes virus encephalitis
CT, MRI, PET
Scan, EEG and related measures
Standardized assessment
MRI, CSF examination, visual field testing
Standardized assessment
Token Test, Boston Naming Test, Wechsler Adult Intelligence Scale, Raven’s
Progressive Matrices, Wechsler Memory Scale-Revised, Corsi Span, Rey–
Osterrieth Complex Figure Test B, semantically related word list, semantically
unrelated word list, short story, supraspan, copying line drawings, test for
prosopagnosia, Famous Events Recognition Test, Lexical Decision Task,
Semantic Decision Task, Famous Faces Test, Famous Names Test
Other assessment
Verbal autobiographical memory testing (main life episodes derived by AV’s
mother), visual autobiographical memory testing (photographs provided by
AV’s mother)
Lesion location
d
Widespread abnormal intensity areas diffusing to the white matter of
temporal, parietal and occipital lobes and periventricular regions of both
hemispheres, predominantly on the left side
Lesion type
(Presumed) herpes encephalitis
Language
English
Wechsler Adult Intelligence Scale-Revised, Wechsler Memory Scale, Crovitz
Cueing Procedure, Warrington Recognition Memory Test, Verbal Fluency,
Famous Faces Test, Famous Person Test, Famous Events Questionnaire,
Semantic Association Test based on items adapted from the Pyramid and
Palm Tree Test, unspecified tests on perception, language, praxis, visual
attention and ‘frontal’ functions
Other assessment
Rorschach Test, Persons and Places Sorting Out Test (based on items given
by the parents), recognition of personal past episodes (remember/knowing
paradigm), recognition of personal photographs (based on photographs given by
the parents), name–activity incongruous association (paired-associate learning)
Lesion location
d
CT, MRI, PET: normal
Lesion type
None
Language
English
Previous cases: Isolated retrograde amnesia 275
Is memory loss without anatomical
damage tantamount to a psychogenic
deficit? The case of pure retrograde
amnesia
Other assessment
Tests of writing, computational abilities and motor skills
Lesion location
d
CT, EEG, MRI, SPECT: normal
Lesion type
Presumed mild head trauma
E. De Renzi, F. Lucchelli, S. Muggia and
H. Spinnler
Abstract
Following a car accident, a patient (Andrea; male; 58 years old) remained
unconscious for approximately 20 min and confused for a few hours.
After the incident he developed a retrograde amnesia, whereby organic or
psychological aetiology remained unclear. Neither signs of brain damage were
detectable in the neurological examination and on CT, MRI and SPECT, nor
evidence for psychiatric history, psychological stress or emotional precipitants
was found. The retrograde amnesia covered his whole life and affected
autobiographical events as well as famous facts and encyclopaedic knowledge.
It also partially involved the verbal and visual lexicon in a way that reading,
writing and counting were no longer possible. The retrograde amnesia
contrasted with the preservation of anterograde memory which permitted the
patient to reacquire some autobiographical information, but in a detached
manner. In a 4 year follow-up, retrograde amnesia persisted. The authors
propose that cases of focal retrograde amnesia, similar to the present one,
might be classified separately from organic and psychogenic forms under the
label of ‘functional’ retrograde amnesia. In functional retrograde amnesia
the threshold of activation of pre-morbid memories is assumed to be abnormally
raised by the trauma, leaving the encoding and retrieval of new memories
unaffected.
Journal
Neuropsychologia 1997; 35: 781–94
Neurocase Reference Number:
P818
Primary diagnosis of interest
Isolated (focal) retrograde amnesia
Author’s designation of case
Andrea
Key theoretical issue
d
A dissociation between partially preserved anterograde memory and
profound retrograde memory loss in combination with additional
neuropsychological impairments was observed in a patient without
neurological pathology. Despite successfully reacquiring autobiographical
and contextual information, the patient remained impaired in several
procedural domains for at least 2 years. The amnesic profile is interpreted
by a trauma-raised threshold of patterned matrices of facilitation and
inhibition allocated to pre-incidentally encoded engrams, leaving the
engrams themselves and storage/retrieval processes undamaged
Key words: memory disorders; retrograde amnesia; functional amnesia
Scan, EEG and related measures
CT, ECG, EEG, MRI, SPECT
Standardized assessment
Raven’s Progressive Matrices, Weigl Colour Form Sorting Test, Wisconsin
Card Sorting Test, Visual Form Discrimination, Unknown Face Recognition,
Token Test, Peabody Picture Vocabulary Test, Boston Naming Test, Verbal
Fluency, Semantic Fluency (colours, animals, fruits, cities), Word Repetition,
Lexical Decision (auditory), Famous Face Recognition Tests, Autobiographical
Memory Questionnaire, Story Recall, Paired Associate Learning, BuschkeFuld 10-word Learning (selective reminding), Corsi Supra-Span Spatial
Learning, Rey–Osterrieth Complex Figure Test, Name–Activity Association
Learning Test
Language
English
276 Previous cases: Isolated retrograde amnesia
Disproportionate retrograde amnesia in
a patient with herpes simplex
encephalitis
Focal retrograde amnesia following
closed head injury: a case study and
theoretical account
T. Fujii, A. Yamadori, K. Endo, K. Suzuki and
R. Fukatsu
N. M. Hunkin, A. J. Parkin, V. A. Bradley,
E. H. Burrows, F. K. Aldrich, A. Jansari and
C. Burdon-Cooper
Abstract
A patient (female; 51 years old) developed a severe retrograde amnesia
extending back for about 10 years associated with a relatively mild anterograde
amnesia following herpes simplex encephalitis. Neuroimaging revealed a
bilateral medial temporal lobe pathology. The retrograde amnesia included
autobiographical memory as well as knowledge about famous people and
public events.
Abstract
Not stated
Data from a closed head injury patient (DH; male; 40 years old) are presented
who suffered from focal retrograde amnesia. Structural MRI revealed posterior
brain lesions in parietal and occipital regions. The patient was unable to
recollect any autobiographical incidents from the pre-morbid period, although
he provided personal and public information from this period. The data are
discussed in relation to other reported instances of focal retrograde amnesia
and a theoretical account is considered. The systems-level model of recall
and recognition is applied to the patient’s neuropsychological impairments. The
model proposes that episodic memory comprises multimodal representation and
it assumes that different aspects of episodes are stored unimodally in the
sensory cortices in which they were originally registered. Recalling an episode
is supposed to require similar neural activity patterns compared to those
occurred, when the event was initially perceived. It is suggested by the authors
that DH’s lesions disrupted transmission of information either from visual
activity in the posterior cortex to multimodal convergence zones or vice versa,
thus resulting in changed neural activity patterns and deteriorated recall.
Key theoretical issue
Journal
Journal
Cortex 1999; 35: 599–614
Neurocase Reference Number:
P819
Primary diagnosis of interest
Isolated (focal) retrograde amnesia
Author’s designation of case
d
A patient suffered from a severe but temporally limited retrograde amnesia
coupled with a relatively mild anterograde amnesia following herpes
simplex encephalitis
Neuropsychologia 1995; 33: 509–23
Neurocase Reference Number:
P820
Key words: retrograde amnesia; herpes simplex encephalitis; herpes virus
Primary diagnosis of interest
Scan, EEG and related measures
Isolated (focal) retrograde amnesia
MRI, SPECT
Author’s designation of case
Standardized assessment
DH
Wechsler Adult Intelligence Scale, Mini-Mental-State Test, Token Test,
Raven’s Progressive Matrices, Wisconsin Card Sorting Test, Verbal Fluency,
Wechsler Memory Scale-Revised, Rey Auditory Verbal Learning Test, Rey–
Osterrieth Complex Figure Test, Kohs Cube Test, Memory for Public Events,
Dead or Alive Test
Key theoretical issue
Other assessment
Clinical assessment of anterograde autobiographical memory, structured
interview of autobiographical memory based on information of the patient’s
closest sister
Lesion location
d
d
MRI: abnormal high intensity areas in bilateral medial temporal lobes
(including two thirds of the hippocampal formation, hippocampus, dendate
gyrus, subiculum) and the posterior part of the amygdala
SPECT: diminution of regional blood flow in bilateral anterior medial
temporal lobe regions
Lesion type
Herpes simplex encephalitis
Language
English
d
The dissociation between preserved anterograde memory functioning and
impaired remote memory access is explained by means of disrupted
transmission between unimodal sensory cortices and multimodal
convergence zones. According to the occipital lesions in the patient,
impaired visual processing might account for the inability to evoke similar
visual activity patterns compared with those of initially experienced
episodes, thus leading to a recall deficit of remote memories
Key words: memory; amnesia; retrograde
Scan, EEG and related measures
MRI
Standardized assessment
Wechsler Adult Intelligence Scale-Revised, National Adult Reading Test,
Wechsler Memory Scale-Revised, Rey Auditory Verbal Learning Test, Rey–
Osterrieth Complex Figure Test, Warrington Recognition Memory Test,
Cognitive Estimation, Wisconsin Card Sorting Test, Verbal Fluency, Public
Events Test, Famous Faces Test, Famous Names Test, Autobiographical
Memory Interview, autobiographical cueing procedure
Other assessment
None
Previous cases: Isolated retrograde amnesia 277
Lesion location
d
Structural lesions in the right parieto-occipital and left occipital lobes. The
right hemispheric lesions were associated with focal atrophy of cortex and
underlying white matter, the left occipital lesion involved damage to a
discrete area of grey matter on the inferior surface of the occipital lobe.
Additional damage involved the medial surface of both occipital lobes
associated with some enlargement of the body of the right lateral ventricle
and gross enlargement of the posterior horns bilaterally
Amnesia can facilitate memory
performance: evidence from a patient
with dissociated retrograde amnesia
N. Kapur, P. Heath, P. Meudell and P. Kennedy
Lesion type
Abstract
Closed head injury
A patient (ED; male; 70 years old) suffered from transient attacks of retrograde
amnesia lasting 15 min to several hours during the last 6 years. No precipitating
factors were revealed. The attacks produced an impairment in the ability to
recall past events and facts especially for verbal material without corresponding
anterograde impairments. The findings gave support for fractionation of
memory in different components of a single aspect of memory and indicated
that in certain situations specific types of amnesia can produce a facilitation
effect compared to the performance of healthy controls.
Language
English
Journal
Neuropsychologia 1986; 24: 215–21
Neurocase Reference Number:
P821
Primary diagnosis of interest
Isolated (focal) retrograde amnesia
Author’s designation of case
ED
Key theoretical issue
d
A case of dissociation in memory was presented which indicated that a
‘functional facilitation paradigm’ might be useful to explore the scope of
facilitation effects in amnesic patients
Key words: retrograde amnesia; memory
Scan, EEG and related measures
CT, EEG
Standardized assessment
Wechsler Adult Intelligence Scale, National Adult Reading Test, Wechsler
Memory Scale, Benton Visual Retention Test, Faces Matching Task, Wisconsin
Card Sorting Test, Verbal Fluency, Famous Personalities Test, Public Events
Test of Retrograde Amnesia, Voices Recognition Test of Famous Personalities
Other assessment
Paired Associate Learning Test
Lesion location
d
d
CT: normal
EEG: normal
Lesion type
Not stated
Language
English
278 Previous cases: Isolated retrograde amnesia
Long-term retention deficits in two cases
of disproportionate retrograde amnesia
N. Kapur, K. Sholey, E. Moore, S. Barker,
J. Brice, S. Thompson, A. Shiel, R. Carn,
P. Abbott and J. Fleming
Other assessment
2. Long-term retention test of stimuli used in the Wechsler Memory ScaleRevised (recall and recognition versions), retention test of events recorded
from the patient’s diary by using graded retention intervals (1–5 weeks)
Lesion location
d
Abstract
Data from two patients with disproportionate retrograde amnesia are presented.
Both patients suffered from severe closed head injury. The first patient (GR;
female; 40 years old) had residual autobiographical amnesia for pre-incidental
events, mild anterograde memory deficits and significantly impaired longterm knowledge acquisition. The second patient (SP; female; 50 years old)
was left with marked retrograde amnesia for events, mild anterograde memory
deficits and faster rate of forgetting over a period of 6 weeks compared to
control subjects. In both cases there was major pathology in the region of the
left temporal lobe, with lateral structures being more affected than medial
structures. Evidence for the independence of certain anterograde and retrograde
memory mechanisms is provided and a link of retrograde amnesia to
impairments in very long-term retention is assumed. It is hypothesized that
lesions to intrahemispheric fasciculi or similar association fibres in combination
with lesions to critical anterior or posterior cerebral structures may lead
to disconnection of visual–semantic and other associations from verbal
representations of such associations, resulting in the observed
neuropsychological impairment.
Journal
Journal of Cognitive Neuroscience 1996; 8: 416–34
Neurocase Reference Number:
P822
Primary diagnosis of interest
Disproportionate retrograde amnesia
Author’s designation of case
1. GR
2. SP
Key theoretical issue
d
In two patients a relationship between retrograde amnesia and long-term
retention deficits is found. The possibility is raised that some forms of
disproportionate retrograde amnesia might result from more than one site
of brain pathology with intrahemispheric connections of anterior temporal
lobes with posterior brain regions being critically involved in remote
memory access
Key words: closed head injury; autobiographical memory; retrograde amnesia;
long-term follow-up; consolidation; medial temporal lobe
Scan, EEG and related measures
1. EEG, MRI, PET
2. MRI
Standardized assessment
1. National Adult Reading Test, Wechsler Adult Intelligence Scale-Revised,
modified Wisconsin Card Sorting Test, Verbal Fluency, Graded Naming
Test, Facial Recognition Test, Wechsler Memory Scale-Revised, Recognition
Memory Test, Autobiographical Memory Interview, structured interview of
autobiographical memory, Dead-or-Alive-Test, Famous Faces Test, Famous
Names Test, Knowledge of Terms Test, Knowledge of Abbreviations Test
2. National Adult Reading Test, Wechsler Adult Intelligence Scale-Revised,
modified Wisconsin Card Sorting Test, Verbal Fluency, Graded Naming Test,
Facial Recognition Test, Rey–Osterrieth Complex Figure Test, Wechsler
Memory Scale-Revised, Recognition Memory Test, Autobiographical Memory
Interview, structured interview of autobiographical memory, Public Events Test
d
d
d
1. MRI: marked abnormality of the left inferolateral temporal lobe with
gliosis in the remaining parenchyma and some involvement of the left
parietal lobe. Focal dilatation of the left temporal horn. The right temporal
lobe showed a discrete area of gliosis in the inferior temporal gyrus.
Additionally, atrophy of the left posterior hippocampus, marked atrophy of
the posterolateral aspect of the left frontal lobe, mild atrophy of the left
fornix, marked atrophy of the left anterior perforated substance were
shown and dilatation of the lateral and third ventricles reflected mild
generalized atrophy.
PET: area of abnormality in the left temporoparietal region.
EEG: focal transient abnormality around the right mid-temporal and right
parietal electrodes.
2. Major atrophy of the left temporal lobe, particularly involving the
temporal pole and the anterior portions of the three temporal gyri. Dilatation
of the left temporal horn. Some involvement of the left hippocampus,
especially in the anterior portion, and part of the right uncus/hippocampus.
Lesion type
Closed head injury
Language
English
Previous cases: Isolated retrograde amnesia 279
Episodic memory and the self in a case
of isolated retrograde amnesia
Lesion location
d
d
B. Levine, S. E. Black, R. Cabeza, M. Sinden,
A. R. Mcintosh, J. P. Toth, E. Tulving and
D. T. Stuss
Abstract
A patient (ML; male) suffered from isolated retrograde amnesia contrasting
with normal anterograde memory performance following a severe traumatic
head injury. MRI gave evidence for damage to the right frontal cortex and
underlying white matter. Initial SPECT showed left superior medial parietal
hypoperfusion which resolved 1 year later. The mnemonic deficits and
the impaired self-regulation measured by remember/know judgements were
discussed as produced by impaired autonoetic awareness affecting behaviour
across the time dimension. The findings suggest that the patient has impaired
autonoetic awareness attributable to the right ventral frontal lobe injury
including the right frontotemporal connections.
Journal
Brain 1998; 121: 1951–73
Neurocase Reference Number:
P823
Primary diagnosis of interest
Isolated (focal) retrograde amnesia
Author’s designation of case
ML
Key theoretical issue
d
Structural and functional neuroimaging as well as neuropsychological
findings converge on the hypothesis that the clinical syndrome of isolated
retrograde amnesia can be related to a right frontal lesion affecting the
ability to re-experience past experiences. This effect can also extend across
the time continuum into anterograde learning and self
Key words: functional reorganization; amnesia; autonoetic awareness; MRI;
PET
Scan, EEG and related measures
1993: CT, MRI
1994/1995: SPECT, PET
Standardized assessment
Galveston Orientation and Amnesia Test, Wechsler Adult Intelligence ScaleRevised, National Adult Reading Test-Revised, Wechsler Memory ScaleRevised, Trail Making Test, Stroop Task, Wisconsin Card Sorting Test,
Benton Visual Retention Test, Rivermead Behavioural Memory Test, Selective
Reminding Test, Autobiographical Memory Interview, Crovitz Cueing
Procedure, Six Elements Task, Boston Naming Test, Word List Learning, Verbal
Fluency, Procedural Learning, Conditional Associative Learning, Concept
Generation, Strategy Application
Other assessment
Anterograde cued recall and recognition/remember/knowing judgements,
amytal interview
d
d
d
CT/1993: subdural haematoma along the falx and right tentorium, small
left inferior posterior temporal contusions, small right frontal lobe
contusions, mild diffuse oedema, small bifrontal hygromas
MRI/1993: right ventral frontal cortex and underlying white matter (uncinate
fasciculus, a frontotemporal band of fibres)
SPECT/1994: left superior medial parietal hypoperfusion
SPECT/1995: resolved
PET/1994: normal
Lesion type
Severe closed head injury
Language
English
280 Previous cases: Isolated retrograde amnesia
The syndrome of pure retrograde
amnesia
Transient retrograde amnesia associated
with impaired naming of living
categories
F. Lucchelli, S. Muggia and H. Spinnler
Abstract
C. Papagno
Three cases of pure retrograde amnesia (PRA) are reported (CDA, AF, GC;
male; aged 15, 20, and 38 years old). The sudden onset of PRA occurred
after minor head trauma in two cases (CDA and AF) and after emotional
stress in one case (GC). Neuroimaging revealed no structural brain damage
in any of the three patients. Evidence of a temporal gradient was found. A
progressive recovery occurred in all cases. Issues concerning the definition of
PRA are addressed. A unitary, aetiology-independent mechanism linking of
heterogeneous triggering conditions to the isolated outcome of retrograde
amnesia is suggested. Neuropsychological aspects of such mechanisms are
envisaged.
Abstract
Journal
A patient (CL; male; 26 years old) suffered from a pure transient retrograde
amnesia for remembering personal and semantic memory contrasted with
normal learning ability following a mild head injury. The patient showed a
deficit in verbal fluency and naming with a living/non-living dissociation
during the amnesic period and recovered 10 days after the incident. CT and
MRI data gave no hints for brain damage, though EEG showed irritating
components in the left temporal region. The simultaneous presence of naming
impairment with living/non-living dissociation and impaired verbal fluency
was discussed as a functional inhibition which involves also less ‘psychogenic’
aspects of mind.
Cognitive Neuropsychiatry 1998; 3: 91–118
Journal
Neurocase Reference Number:
Cortex 1998; 34: 111–21
P824
Neurocase Reference Number:
Primary diagnosis of interest
P825
Isolated (focal) retrograde amnesia
Primary diagnosis of interest
Author’s designation of case
Isolated (focal) retrograde amnesia
CDA, AF, GC
Author’s designation of case
Key theoretical issue
CL
d
Pure retrograde amnesia after minor head trauma and emotional stress are
presented in three cases. The contributions of PRA to neuropsychological
research are discussed. In particular, the implicit versus explicit availability
of past information, the architecture of remote memory archives, and the
dissociation of anterograde and retrograde recall are considered
Key theoretical issue
d
Key words: pure retrograde amnesia
A case of transient retrograde amnesia following a mild head injury was
described. The simultaneous presence of a naming impairment with living/
non-living dissociation and impaired verbal fluency gave support for a
‘functional’ inhibition which also involves less ‘psychogenic’ but more
cognitive aspects of mind
Scan, EEG and related measures
Key words: retrograde amnesia; closed head injury
CDA: EEG, CT, MRI
GC: EEG, CT, MRI, SPECT
AF: EEG, CT
Scan, EEG and related measures
Standardized assessment
Standardized assessment
CT, MRI, EEG
CDA, CG, AF: Buschke Selective Reminding, Corsi Supra Span Learning,
Rey–Osterrieth Complex Figure Test, Verbal Span, Spatial Paired Associates
CDA: Famous Events Questionnaire
GC: Standardized Autobiographical Memory Questionnaire, Famous Events
Questionnaire
Raven’s Coloured Matrices, Token Test, Digit Span, Spatial Span, Story
Recall, Word List Learning, Supra Span Spatial Learning, Verbal Fluency
(phonological cues and categories), Picture Naming, Benton’s Line Orientation,
Digit Cancellation Test, Semantic Memory Battery (living/non-living
categories), Famous Faces Test, Famous Events Questionnaire
Other assessment
Other assessment
CDA: autobiographical memory interview provided with the help of relatives
and friends, psychiatric evaluation (several times)
GC: psychiatric evaluation (brief)
AF: informal assessment of autobiographical memory and semantic memory
Lesion location
Lesion location
d
d
d
CDA: EEG, CT, MRI: normal
GC: EEG, CT, MRI, SPECT: normal
AF: EEG, CT: normal
Lesion type
CDA: head trauma
GC: none
AF: head trauma
Language
English
Psychiatric evaluation, structured autobiographical interview based on
information provided by the mother
d
d
EEG: left temporal irritations
CT/MRI: normal
Lesion type
Mild head injury
Language
English
Previous cases: Isolated retrograde amnesia 281
Focal retrograde amnesia associated with
vascular headache
Post-encephalitic focal retrograde
amnesia after bilateral anterior temporal
lobe damage
I. Reinvang and L. Gjerstad
Abstract
A patient (DH; male; 42 years old) with repeated attacks of headache was
initially affected by a dense retrograde amnesia for public and private facts
and episodes comprising a period of 15–20 years. His anterograde memory
was spared and neuropsychological assessment showed only mild deficits of
other cognitive functions. There were hints for focal left frontotemporal
changes in EEG. CT, MRI and SPECT were normal. In a post-incidental
reassessment after 5 years he showed no neuropsychological deficits despite
his persisting dense retrograde amnesia with no abnormalities in PET.
Journal
Neuropsychologia 1998; 36: 1335–41
Neurocase Reference Number:
P826
Primary diagnosis of interest
Isolated (focal) retrograde amnesia
Author’s designation of case
DH
Abstract
A patient (HK; female; 43 years old) showed a severe, persistent retrograde
amnesia extending back to her childhood in contrast to very limited anterograde
deficits following a herpes simplex encephalitis. MRI revealed bilateral
damage of the temporal lobes and anterior inferotemporal lobes in the absence
of frontal lobe pathologies. The personal memory was more severely impaired
than the ability to recall factual knowledge about her past. Referring to
her impairments in recalling public memories, her scores in forced-choice
recognition tasks were nearly normal showing only mild impairment for the
last decade before the incident.
Journal
Neurology 1999; 53: 344–50
Neurocase Reference Number:
P827
Primary diagnosis of interest
Isolated (focal) retrograde amnesia
Key theoretical issue
d
Y. Tanaka, Y. Miyazawa, R. Hashimoto,
I. Nakano and T. Obayashi
A patient showed a persistent loss of retrograde memories for at least 15–
20 years following repeated attacks of headache. This was in contrast with
his anterograde memory and learning capability
Author’s designation of case
HK
Key theoretical issue
d
Key words: retrograde amnesia; vascular headache
Scan, EEG and related measures
1990:
1991:
1992:
1995:
1996:
1997:
EEG/CT
MRI/SPECT
EEG/MRI
SPECT
EEG/MRI
PET
Standardized assessment
Wechsler Adult Intelligence Scale, subtests of the Wechsler Memory Scale:
Designs, Paired Associate Learning, Paired Associate Recall; Digit Symbol
Incidental Memory, California Verbal Learning Test, Kimura Recurring
Figures, Trail Making Test, Verbal Fluency, Crovitz Cueing Procedure,
Autobiographical Memory Interview, Famous Events and Famous Names
Test, Grooved Pegs D/ND, Seashore Rhythm Test, Halstaed Category Test
Other assessment
A patient showed a persistent loss of retrograde memories extending back
to her childhood following probable herpes simplex encephalitis. This
profound retrograde amnesia in contrast with her anterograde memory was
produced by damage of bilateral temporal lobes and anterior inferotemporal
regions in the absence of frontal lobe pathology
Key words: retrograde amnesia; encephalitis; temporal lobe; magnetic
resonance imaging
Scan, EEG and related measures
EEG, CT, MRI
Standardized assessment
Wechsler Adult Intelligence Scale, Modified Card Sorting Test, Trail Making
Test, Wechsler Memory Scale-Revised, Rey Auditory Verbal Learning Test,
Rey–Osterrieth Complex Figure Test, Autobiographical Memory Interview,
Famous Faces Test, Public Events Test, TV Programs Test, Go/No Go Task,
Stroop Test, Token Test
Other assessment
Psychiatric examination
Personal photographs test (collection of private photographs with the help of
the patient’s mother and husband), assessment of perceptual-motor skills
Lesion location
Lesion location
d
d
EEG: focal theta activity in the left frontal temporal region
CT, MRI, SPECT; PET: normal
d
Lesion type
None
Language
English
d
d
MRI: bilateral lesions of temporal regions. Left hemispherical lesions:
temporal pole [Brodmann (BM) 38], part of anterior parahippocampal gyrus
(BM 28), anterior parts of the inferior and middle temporal gyri (BM 20,
21), parts of amygdala and hippocampus and left insular cortex (extreme
capsule, claustrum, external capsule, putamen, part of frontoparietal
operculum, anterior superior temporal gyrus (BM 22). Right hemispherical
lesions: less extensive damage of temporal pole (BM 38), part of anterior
parahippocampal gyrus
EEG: dysrhythmia with spikes in the left frontal and anterior temporal
regions
CT: normal
Lesion type
Herpes simplex encephalitis
Language
English
282 Previous cases: Isolated retrograde amnesia
Isolated prolonged retrograde amnesia
Y. Yoneda, A. Yamadori, E. Mori and
H. Yamashita
Abstract
A patient (male; 21 years old) with isolated retrograde amnesia following
encephalitis is reported. His memory deficit consisted of a loss of personal
and public events 1 year prior to the incident while sparing anterograde
memory performance. Functional neuroimaging (single-photon emission CT)
revealed a left temporal lobe pathology. The authors assumed that the
registration and storage of new information and the recall of events prior to
a brain damage might involve different neural structures. It is hypothesized
that recalling ability is mostly dependent on left temporal neocortical regions
while intact regions of the medial temporal lobe memory system, such as
hippocampal formation, and thalamic regions represent the anatomical basis
of learning ability for new information.
Journal
European Neurology 1992; 32: 340–2
Neurocase Reference Number:
P828
Primary diagnosis of interest
Isolated (focal) retrograde amnesia
Author’s designation of case
Not stated
Key theoretical issue
d
A dissociation between unimpaired anterograde memory performance and
dense retrograde amnesia for 1 year is attributed to left temporal lobe
dysfunction
Key words: amnesia; retrograde; temporal lobe; single-photon emission
computed tomography
Scan, EEG and related measures
EEG, CSF examination, CT, SPECT, MRI
Standardized assessment
Wechsler Adult Intelligence Scale, Mini-Mental Status Test, Raven’s
Progressive Matrices, Digit Span, Token Test, Miyake’s Retention Test,
Auditory Verbal Learning Test, Benton Visual Retention Test, Rey–Osterrieth
Complex Figure Test
Other assessment
Autobiographical memory testing with personal information collected from
family and colleagues, semantic remote memory testing with collected famous
events, amytal interview
Lesion location
d
d
CT, MRI: normal
SPECT: high tracer uptake in bilateral temporoparietal regions,
predominantly on the left side; a second SPECT scan (2 months later)
revealed low tracer uptake in the left posterior temporal lobe
Lesion type
Encephalitis
Language
English