Jeri S. Janowsky

Source memory impairment in patients with frontal lobe lesions

In two experiments, we investigated memory for recently learned facts and memory for the source of the facts (i.e. where and when the facts were learned) in patients with frontal lobe lesions, age-matched elderly control subjects, and younger subjects. In both experiments, patients with frontal lobe lesions recalled as many facts as their age-matched subjects and the younger subjects, but they frequently attributed facts to incorrect sources. In the second experiment, both patients with frontal lobe lesions and their age-matched subjects committed more source errors than younger subjects. These findings suggest that the frontal lobes may play a special role in associating facts to the context in which they were learned. The results are also discussed in the light of the source memory impairment that occurs in amnesic patients.

Cognitive Impairment Following Frontal Lobe Damage and Its Relevance to Human Amnesia

Whether frontal lobe pathology can account for some of the cognitive impairment observed in amnesic patients with Korsakoffs syndrome was investigated. Various cognitive and memory tests were given to patients with circumscribed frontal lobe lesions, patients with Korsakoffs syndrome, non-Korsakoff amnesic patients, and control Ss. Patients with frontal lobe lesions were not amnesic. Nevertheless they exhibited 2 deficits that were also exhibited by patients with Korsakoffs syndrome but not by other amnesic patients: (a) impairment on the Wisconsin Card Sorting Test and (b) impairment on the Initiation and Preservation subscale of the Dementia Rating Scale. Thus, frontal lobe pathology can explain some of the cognitive deficits observed in patients with Korsakoffs syndrome.

Memory for the temporal order of events in patients with frontal lobe lesions and amnesic patients

Patients with frontal lobe lesions, amnesic patients with Korsakoffs syndrome, other (non-Korsakoff) amnesic patients, and control subjects were given tests of memory for temporal order. In the first experiment, subjects were presented with a list of 15 words and then asked to reproduce the list order from a random array of the words. In the second experiment, they were asked to arrange in chronological order a random display of 15 factual events that occurred between 1941 and 1985. In both experiments, patients with frontal lobe lesions were impaired in placing the items in the correct temporal order, despite normal item memory (i.e. normal recall and recognition memory for the words and facts). The two groups of amnesic patients exhibited impaired memory for temporal order as well as impaired item memory. Patients with Korsakoffs syndrome exhibited poorer temporal order memory than the other amnesic patients, despite similar levels of item memory. These findings demonstrate that patients with frontal lobe lesions have difficulty organizing information temporally. Patients with Korsakoffs syndrome, who have both diencephalic and frontal damage, have memory impairment together with a disproportionate deficit in memory for temporal order.

Memory and metamemory: Comparisons between patients with frontal lobe lesions and amnesic patients

Metamemory refers to knowledge about one’s own memory capabilities. The accuracy of metamemory judgments (i.e., feeling of knowing) was tested in patients with frontal lobe lesions and control subjects. Their performance was compared to other findings for 6 patients with Korsakoff s syndrome and 5 other patients with amnesia. In Experiment 1, subjects were presented sentences and then asked to recall key words from each sentence. They then judged their feeling of knowing for nonrecalled items in terms of how likely they thought they would be to recognize the key words on a subsequent recognition test. Patients with frontal lobe lesions exhibited impaired feeling of knowing when memory was weakened by imposing a 1–3-day delay between sentence presentation and recall. Experiment 2 tested feeling-of-knowing accuracy for nonrecalled general-information questions. On this test, patients with frontal lobe lesions performed normally. The metamemory deficit observed in Experiment 1 suggests that the frontal lobes contribute, at least in part, to metamemory judgments. The 5 (non-Korsakoff) amnesic patients had intact metamemory functions, but patients with Korsakoff’s syndrome did not. These findings suggest that the metamemory impairment in patients with Korsakoff’s syndrome is due, in part, to frontal lobe pathology.

Early Language Development in Infants with Cortical and Subcortical Perinatal Brain Injury

To understand better the cognitive sequelae of mild perinatal brain injury, we studied three groups of high-risk infants, using the Early Language Milestone Scale (ELM Scale). Premature infants with Grades I and II intraventricular hemorrhages (IVH) were delayed on the expressive but not the receptive subscale of the ELM Scale. Mildly asphyxiated full-term infants were slightly delayed on both the expressive and receptive subscales. Premature infants without IVH performed the same as the normal sample on which the scale was based. Although normal intellectual functioning has been reported in infants with Grade I-II IVH, this study demonstrates early specific deficits in expressive language in these children. These results are discussed in relation to localization of language in the adult brain, and the influence of subcortical structures on development and maturation of the cortex. J Dev Behav Pediatr 8:3–7, 1987. Index terms: intraventricular hemorrhage, language, cognitive development.

Initial sensitivity and tolerance to ethanol in mice: correlations among open field activity, hypothermia, and loss of righting reflex

The sensitivity of male Swiss albino mice to the effects of ethanol was successively tested using measures of open field activity (OFA), hypothermia (HT), and duration of loss of righting reflex (LORR). Doses used were 1, 3, and 4.5 g/kg (ip) ethanol. Tests were conducted 1 week apart and were counterbalanced for order. HT was positively correlated with baseline temperature. This could represent a “normalizing” effect of ethanol, or an undetermined common mechanism. HT and degree of subsequent tolerance to HT were highly positively correlated. Baseline OFA was positively correlated with ethanol-induced LORR. LORR also correlated positively with HT, but neither baseline nor ethanol-stimulated OFA were significantly associated with HT.

THE OUTCOME OF PERINATAL BRAIN DAMAGE: THE RÔLE OF NORMAL NEURON LOSS AND AXON RETRACTION

The consequences of brain damage depend on the capacity of the brain to reorganize at the time of the damage. Until recently, early brain development had been thought of principally in terms of kinds of growth: cell proliferation, migration, establishment of connections, and elaboration of dendritic and axonal arbors. The effects of early brain damage, in addition to the direct tissue-loss, were thought of in terms of alterations of growth: failure of cells to proliferate and establish connections, or compensatory axonal stunting or sprouting. However, it has become clear that subtractive and degenerative processes are as much a part of normal brain development as generative and additive ones. Neurons are produced in excess and many die in early development; axons spread diffusely and later retract. These phenomena are of particular interest to those concerned with understanding the effects of early brain damage in humans because many of the degenerative events occur around birth and in the early postnatal period when the probability of injury is highest. This paper will review these subtractive events as they have been described in the experimental literature, and explore their potential r6le in alterations of brain organization after early brain damage in human infants. The types of perinatal brain damage we will be considering include intraventricular hemorrhage (IVH) as a complication of premature delivery, which results in focal damage to germinal zones adjoining the basal ganglia, as well as diffuse loss elsewhere due to secondary hydrocephalus, and localized cerebral infarcts. In both cases we will explore by reference to the experimental literature what secondary brain reorganizations are likely to occur due to alterations of normal neuron loss and axon retraction. These effects are likely to be major: in the majority of brain structures studied to date it has been shown that close to 50 per cent of neurons generated normally die in the process of establishing their connectivity in early development, and that this process is directly altered by damage. Similarly, almost every developing neuron that has been described has been shown to have a more extensive axonal arbor early in development than at maturity, and this developmental change can be altered by both mechanical disruption like early brain injury and deviations in early ch 00 m

Drawing ability in four young children with congenital unilateral brain lesions.

The drawings of four 5-yr-old children, two with left and two right hemisphere congenital brain injury, were compared with those of 20 normal 3.5-5 yr-olds. Two types of drawings were evaluated: copied geometric forms and free drawings. The children with left hemisphere injury showed normal development in both copying and free drawing. The children with right hemisphere injury were developmentally impaired in the copying task. In addition, their free drawings lacked configurational coherence; they included the elements of the figures but failed to arrange them in spatially organized ways. This failure to organize spatially elements is consistent with the descriptions of spatial cognitive disorders found in the drawings of adults with right parietal brain lesions.

Pyrazole exacerbates handling-induced convulsions in mice

Abstract Severity of handling-induced convulsions was reduced in mice in comparison to the scores on an initial test administered 4 days earlier. Daily injections of pyrazole, an inhibitor of alcohol dehydrogenase, prevented the reduction of convulsions in handled mice and exacerbated convulsions in mice tested for the first time after injection. The effects of pyrazole were dose-related.