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Memory Loss from a Subcortical White Matter Infarct

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Memory Loss from a Subcortical White Matter Infarct J Neurol Neurosurg Psychiatry: first published as 10.1136/jnnp.51.6.866 on 1 June 1988. Downloaded from 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 ofFlorida, 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 cerebro- vascular 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. Protected by copyright. Memory loss is currently believed to reflect grey day of his illness the patient was transferred to Shands matter damage of either the mesial temporal lobe,' -4 Teaching Hospital at the University of Florida for further the mesial or the basal forebrain.'0 l evaluation. thalamus,5-9 Examination at that time showed the patient to be awake, Cerebrovascular accidents resulting in memory dys- alert, attentive and fully oriented. He was able to repeat four function may occur in any of these three numbers forward, could not recall any of three objects after regions.3 79 12 13 In contrast, amnesia from white 3 minutes, but was able to remember recent presidents. matter damage is unusual and when present is usually Spontaneous speech was grammatically correct with mild related to fornix lesions. 14 - 19 hesitancy on initiation of sentences and a tendency towards We observed a patient, however, who developed a echolalia. Repetition, naming, reading and writing were all severe verbal amnesia from an infarct of the posterior preserved. Verbal comprehension was mildly impaired only limb of the internal capsule. Aside from its obvious when dependent upon understanding complex syntactic structures involved in relationships. Finger naming, right/left orientation and sparing of the usual memory, calculations were normal. Visual-spatial testing of spontane- the lesion was also atypical by its apparent limitation ously drawn and copied figures was normal. There was no http://jnnp.bmj.com/ to the white matter pathways of the diencephalon. neglect and no difficulty with either graphaesthesia or stereo- gnosia. The remainder of his neurological examination dem- Case report onstrated a moderate right hemiparesis in a pyramidal distri- bution with concomitant hyperreflexia and extensor plantar A 69 year old, right-handed, high school educated gas sta- response. Neuropsychological assessment included Form I tion supervisor was in good health until the acute onset of a of the Wechsler Memory Scale. Despite scoring nearly right hemiparesis associated with dysarthria and mild flawlessly on the personal information (6/6) and orientation expressive difficulties. His symptoms improved after 2 hours, (4/5) subtests, the patient only recalled 4/24 and 2/22 memo- only to recur 30 minutes later, at which time continuous ries from the logical memory subtest (about 2 SD below that on September 24, 2021 by guest. intravenous heparin was begun. His deficits fluctuated over expected for his intelligence and age).20 Paired associate the next 36 hours before becoming permanent. On the 10th testing yielded a score of 4/21 (all easy associations), which falls more than 3 SD below the mean.20 In contrast, non- Address for reprint requests: Carol A. Kooistra, M.D., 145 Dillon verbal memory function was less affected, as shown by his Drive, Spartanburg, S.C. 29302, USA visual reproduction subtest score (4/14), only 1 SD below mean. His memory quotient was calculated as 79. Received 20 February 1987 and in revised form 21 September 1987. A computed tomography (CT) scan of the head 14 days Accepted 22 September 1987 after onset of symptoms revealed an area of lucency 866 J Neurol Neurosurg Psychiatry: first published as 10.1136/jnnp.51.6.866 on 1 June 1988. Downloaded from Memory loss from a subcortical white matter infarct 867 _ w~~oo ML,&v t I ...F.. i N Fig (a) CT scan showing lucency in left posterior internal capsule. (b) coronal CT scan, reconstructed, showing lucency in internal capsule. Protected by copyright. occupying the posterior limb and genu of the left internal projects to the cingulate gyrus through the lateral capsule (fig). Coronal reconstruction demonstrated the in- thalamic radiations and post-commissural ferior aspect of the lesion to extend within the white matter fornix.22 24 to just above the suprasellar cistern (fig). The arterial distri- The amygdaloid system was delineated by bution of the presumed thrombotic infarct was felt to best fit and brought to prominence by Horel's that of the anterior choroidal artery.21 Yakovlev23 Over the following weeks, the patient demonstrated mild temporal stem theory of amnesia.24 This system's improvement in motor deficits; however, two years after targets again lie within the diencephalon and are discharge he remains significantly amnestic, incapable of reached by either the stria terminalis or ventral recalling any of three objects after three minutes. 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 Discussion cross the anterior limb of the internal capsule and anterior commissure and connecting with the hypo- Amnesia has not been previously recognised as a thamalus, nucleus accumbens and anterior pole of the http://jnnp.bmj.com/ sequela of damage to the internal capsule. Therefore, thalamus.25 26 the presence of severe memory deficits in this case The ventral amygdalofugal pathway consists of may be related to damage to some additional two components. Both originate from the basolateral diencephalic structure(s), with sparing of the dorsal amygdala and travel anteriorly and medially through medial thalamus, hippocampal formation, and basal the albal stalk of the temporal lobe to enter the forebrain. inferior diencephalon. One component continues Recent experimental work in memory has empha- rostrally to the septal region as the diagonal band of sised two separate but parallel anatomic systems: the Broca, additionally sending some fibres to the dorsal on September 24, 2021 by guest. hippocampal and the amygdaloid. The former is medial thalamus via the inferior thalamic peduncle.25 essentially composed of those pathways described by The second component forms the ansa peduncularis, Papez22 in which hippocampal efferents travel which courses medially, lying ventral to the ansa len- through the fornix to reach directly (post- ticularis and posterior limb of the internal capsule, commissurally)23 and indirectly (via the mammillary and ultimately reaches the hypothalamus, whereupon bodies and mammillothalamic tract) the anterior the fibres turn superiorly and posteriorly to terminate nucleus of the thalamus, which then subsequently in the magnocellular portion of the dorsal medial J Neurol Neurosurg Psychiatry: first published as 10.1136/jnnp.51.6.866 on 1 June 1988. Downloaded from 868 Kooistra, Heitman nucleus, again entering by way of the inferior the ventral amygdalofugal pathways and the dorsal thalamic peduncle. medial thalamus-frontal fibres as they course in the The principal dorsal medial nucleus' efferent path- vicinity of the genu and the posterior limb of the ways project to the prefrontal cortex, exiting through internal capsule, thereby effectively disconnecting the inferior thalamic peduncle to head rostrally in the dorsal medial thalamus from prefrontal and lateral anterior internal capsule.27 28 Thus, the amyg- amygdaloid areas. Additionally, the medial forebrain daloid system interconnects the anterior inferior tem- bundle, portions of the basal nucleus of Meynert, and poral cortex, the basolateral amygdala, the dorsal anterior thalamic nucleus efferents may be affected. medial nucleus and the prefrontal cortex with the var- The severity of the patient's memory loss would sug- ious diencephalic pathways travelling in the region of gest that more than one structure or system is both the anterior and posterior limbs of the internal involved. Despite the problems inherent in defining capsule and either entering or exiting the thalamus via the extent of ischaemia by CT scanning, there appears the inferior thalamic peduncle. to be no radiological involvement of the mammillary Mishkin demonstrated the parallel nature of bodies, the medial thalamus, the fornix, or the hippo- the hippocampal and amygdaloid systems through campus. The possibility of diaschisis initially causing selective cortical and subcortical lesions. His animals functional disturbances in areas remote from the demonstrated a more severe recognition memory infarct seems unlikely owing to the persistence of the deficit with combined destruction of amygdala and memory
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