Journal of Neurology, Neurosurgery, and Psychiatry 1988;51:866-869

Short report

Memory loss from a subcortical white matter infarct
CAROL A KOOISTRA, KENNETH M HEILMAN
From the Department ofNeurology, College ofMedicine, University of Florida, and the Research Service,
Veterans Administration Medical Center, Gainesville, FL, USA

SUMMARY Clinical disorders of memory are believed to occur from the dysfunction of either the
mesial temporal lobe, the mesial thalamus, or the basal forebrain. Fibre tract damage at the level of
the fornix has only inconsistently produced amnesia. A patient is reported who suffered a cerebrovascular accident involving the posterior limb of the left internal capsule that resulted in a persistent
and severe disorder of verbal memory. The inferior extent of the lesion effectively disconnected the
mesial thalamus from the amygdala and the frontal cortex by disrupting the ventral amygdalofugal
and thalamic-frontal pathways as they course through the diencephalon. This case demonstrates
that an isolated lesion may cause memory loss without involvement of traditional structures
associated with memory and may explain memory disturbances in other white matter disease such
as multiple sclerosis and lacunar state.
Memory loss is currently believed to reflect grey
matter damage of either the mesial temporal lobe,' -4
the mesial thalamus,5-9 or the basal forebrain.'0 l
Cerebrovascular accidents resulting in memory dysfunction may occur in any of these three
regions.3 79 12 13 In contrast, amnesia from white
matter damage is unusual and when present is usually
related to fornix lesions. 14 - 19
We observed a patient, however, who developed a
severe verbal amnesia from an infarct of the posterior
limb of the internal capsule. Aside from its obvious
sparing of the usual structures involved in memory,
the lesion was also atypical by its apparent limitation
to the white matter pathways of the diencephalon.
Case report
A 69 year old, right-handed, high school educated gas station supervisor was in good health until the acute onset of a
right hemiparesis associated with dysarthria and mild
expressive difficulties. His symptoms improved after 2 hours,
only to recur 30 minutes later, at which time continuous
intravenous heparin was begun. His deficits fluctuated over
the next 36 hours before becoming permanent. On the 10th
Address for reprint requests: Carol A. Kooistra, M.D., 145 Dillon
Drive, Spartanburg, S.C. 29302, USA

Received 20 February 1987 and in revised form 21 September 1987.
Accepted 22 September 1987

day of his illness the patient was transferred to Shands
Teaching Hospital at the University of Florida for further
evaluation.
Examination at that time showed the patient to be awake,
alert, attentive and fully oriented. He was able to repeat four
numbers forward, could not recall any of three objects after
3 minutes, but was able to remember recent presidents.
Spontaneous speech was grammatically correct with mild
hesitancy on initiation of sentences and a tendency towards
echolalia. Repetition, naming, reading and writing were all
preserved. Verbal comprehension was mildly impaired only
when dependent upon understanding complex syntactic
relationships. Finger naming, right/left orientation and
calculations were normal. Visual-spatial testing of spontaneously drawn and copied figures was normal. There was no
neglect and no difficulty with either graphaesthesia or stereognosia. The remainder of his neurological examination demonstrated a moderate right hemiparesis in a pyramidal distribution with concomitant hyperreflexia and extensor plantar
response. Neuropsychological assessment included Form I
of the Wechsler Memory Scale. Despite scoring nearly
flawlessly on the personal information (6/6) and orientation
(4/5) subtests, the patient only recalled 4/24 and 2/22 memories from the logical memory subtest (about 2 SD below that
expected for his intelligence and age).20 Paired associate
testing yielded a score of 4/21 (all easy associations), which
falls more than 3 SD below the mean.20 In contrast, nonverbal memory function was less affected, as shown by his
visual reproduction subtest score (4/14), only 1 SD below
mean. His memory quotient was calculated as 79.
A computed tomography (CT) scan of the head 14 days
after onset of symptoms revealed an area of lucency

866

Memory loss from a subcortical white matter infarct
_

w~~oo

867

v
ML,&

I

t
...F..

i

N

Fig (a) CT scan showing lucency in left posterior internal
capsule. (b) coronal CT scan, reconstructed, showing
lucency in internal capsule.

occupying the posterior limb and genu of the left internal

capsule (fig). Coronal reconstruction demonstrated the inferior aspect of the lesion to extend within the white matter
to just above the suprasellar cistern (fig). The arterial distribution of the presumed thrombotic infarct was felt to best fit
that of the anterior choroidal artery.21
Over the following weeks, the patient demonstrated mild
improvement in motor deficits; however, two years after
discharge he remains significantly amnestic, incapable of
recalling any of three objects after three minutes.

Discussion
Amnesia has not been previously recognised as a
sequela of damage to the internal capsule. Therefore,
the presence of severe memory deficits in this case
may be related to damage to some additional
diencephalic structure(s), with sparing of the dorsal
medial thalamus, hippocampal formation, and basal
forebrain.
Recent experimental work in memory has emphasised two separate but parallel anatomic systems: the
hippocampal and the amygdaloid. The former is
essentially composed of those pathways described by
Papez22 in which hippocampal efferents travel
through the fornix to reach directly (postcommissurally)23 and indirectly (via the mammillary
bodies and mammillothalamic tract) the anterior
nucleus of the thalamus, which then subsequently

projects to the cingulate gyrus through the lateral
post-commissural
and
radiations
thalamic

fornix.22 24
The amygdaloid system was delineated by
Yakovlev23 and brought to prominence by Horel's
temporal stem theory of amnesia.24 This system's
targets again lie within the diencephalon and are
reached by either the stria terminalis or ventral
amygdalofugal pathways. The stria terminalis lies in
the lateral wall of the temporal horn and body of the
lateral ventricle, arching superiorly and anteriorly to
cross the anterior limb of the internal capsule and
anterior commissure and connecting with the hypothamalus, nucleus accumbens and anterior pole of the
thalamus.25 26
The ventral amygdalofugal pathway consists of
two components. Both originate from the basolateral
amygdala and travel anteriorly and medially through
the albal stalk of the temporal lobe to enter the
inferior diencephalon. One component continues
rostrally to the septal region as the diagonal band of
Broca, additionally sending some fibres to the dorsal
medial thalamus via the inferior thalamic peduncle.25
The second component forms the ansa peduncularis,
which courses medially, lying ventral to the ansa lenticularis and posterior limb of the internal capsule,
and ultimately reaches the hypothalamus, whereupon
the fibres turn superiorly and posteriorly to terminate
in the magnocellular portion of the dorsal medial

868
nucleus, again entering by way of the inferior
thalamic peduncle.
The principal dorsal medial nucleus' efferent pathways project to the prefrontal cortex, exiting through
the inferior thalamic peduncle to head rostrally in the
lateral anterior internal capsule.27 28 Thus, the amygdaloid system interconnects the anterior inferior temporal cortex, the basolateral amygdala, the dorsal
medial nucleus and the prefrontal cortex with the various diencephalic pathways travelling in the region of
both the anterior and posterior limbs of the internal
capsule and either entering or exiting the thalamus via
the inferior thalamic peduncle.
Mishkin demonstrated the parallel nature of
the hippocampal and amygdaloid systems through
selective cortical and subcortical lesions. His animals
demonstrated a more severe recognition memory
deficit with combined destruction of amygdala and
hippocampus than with an isolated lesion of either
structure.29 Similar results were obtained with single
and combined lesions of the anterior and dorsal
medial nuclei of the thalamus,301 the fornix and
stria terminalis,32 the hippocampus and stria terminalis,"8 and the fornix and amygdala.33
Recently, the basal nucleus of Meynert has
emerged as a contributor to mnemonic function. The
cells of the basal nucleus do not occupy a discrete area
of the substantia innominata, but rather can be found
adjacent to the septal region, as well as within the
ansa lenticularis, the ansa peduncularis, the inferior
thalamic peduncle, the internal capsule, the medial
forebrain bundle, the anterior commissure and the
medullary lamina of the globus pallidus.34 Afferents
originate predominantly from the allocortex, the
septal region, the nucleus accumbens and the hypothalamus,35 with anterior nucleus projecting to mesial
cortex via the fornix and the cingulum and the posterior nucleus projecting to the dorsolateral cortex.36
Aside from Mishkin's work involving fibre tract
lesions, other experimental support exists for
diencephalic white matter damage causing memory
deficits. Skinner and Lindsley placed cryogenic
probes within the inferior thalamic peduncle of cats
and produced deficits in tasks of bar pressing and
single alternation.37 Additionally, Mair, Warrington,
and Weiskrantz38 identified a small zone of damaged
diencephalon in patients with Korsakoff's disease,
which they felt disconnected structures in the temporal lobe from areas in the frontal cortex. Considering
the extensive network of pathways needed to coordinate mnemonic function, a variety of white matter
lesions could potentially produce amnesia and may
form the basis of memory loss associated with both
multiple sclerosis and multi-infarct dementia.
The infarct reported here appears to extend
sufficiently inferiorly and anteriorly to have damaged

Kooistra, Heitman
the ventral amygdalofugal pathways and the dorsal

medial thalamus-frontal fibres as they course in the
vicinity of the genu and the posterior limb of the
internal capsule, thereby effectively disconnecting
dorsal medial thalamus from prefrontal and
amygdaloid areas. Additionally, the medial forebrain
bundle, portions of the basal nucleus of Meynert, and
anterior thalamic nucleus efferents may be affected.
The severity of the patient's memory loss would suggest that more than one structure or system is
involved. Despite the problems inherent in defining
the extent of ischaemia by CT scanning, there appears
to be no radiological involvement of the mammillary
bodies, the medial thalamus, the fornix, or the hippocampus. The possibility of diaschisis initially causing
functional disturbances in areas remote from the
infarct seems unlikely owing to the persistence of the
memory disorder.

This study was supported by the Medical Research
Service of Veterans Administration and the State of
Florida Memory Disorders Clinic.
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