Differential spatial memory impairment after right temporal lobectomy demonstrated using temporal titration.
In this study a temporal titration method to explore the extent to which spatial memory is differentially impaired following right temporal lobectomy was employed. The spatial and non-spatial memory of 19 left and 19 right temporal lobectomy (TL) patients was compared with that of 16 normal controls. The subjects studied an array of 16 toy objects and were subsequently tested for object recall, object recognition and memory for the location of the objects. By systematically varying the retention intervals for each group, it was possible to match all three groups on object recall at sub-ceiling levels. When memory for the position of the objects was assessed at equivalent delays, the right TL group revealed disrupted spatial memory, compared with both left TL and control groups (P < 0.05). MRI was used to quantify the extent of temporal lobe resection in the two groups and a significant correlation between hippocampal removal and both recall of spatial location and object name recall in the right TL group only was shown. These data support the notion of a selective (but not exclusive) spatial memory impairment associated with right temporal lobe damage that is related to the integrity of the hippocampal functioning. (+info)
Disrupted temporal lobe connections in semantic dementia.
Semantic dementia refers to the variant of frontotemporal dementia in which there is progressive semantic deterioration and anomia in the face of relative preservation of other language and cognitive functions. Structural imaging and SPECT studies of such patients have suggested that the site of damage, and by inference the region critical to semantic processing, is the anterolateral temporal lobe, especially on the left. Recent functional imaging studies of normal participants have revealed a network of areas involved in semantic tasks. The present study used PET to examine the consequences of focal damage to the anterolateral temporal cortex for the operation of this semantic network. We measured PET activation associated with a semantic decision task relative to a visual decision task in four patients with semantic dementia compared with six age-matched normal controls. Normals activated a network of regions consistent with previous studies. The patients activated some areas consistently with the normals, including some regions of significant atrophy, but showed substantially reduced activity particularly in the left posterior inferior temporal gyrus (iTG) (Brodmann area 37/19). Voxel-based morphometry, used to identify the regions of structural deficit, revealed significant anterolateral temporal atrophy (especially on the left), but no significant structural damage to the posterior inferior temporal lobe. Other evidence suggests that the left posterior iTG is critically involved in lexical-phonological retrieval: the lack of activation here is consistent with the observation that these patients are all anomic. We conclude that changes in activity in regions distant from the patients' structural damage support the argument that their prominent anomia is due to disrupted temporal lobe connections. (+info)
The predictive value of changes in effective connectivity for human learning.
During learning, neural responses decrease over repeated exposure to identical stimuli. This repetition suppression is thought to reflect a progressive optimization of neuronal responses elicited by the task. Functional magnetic resonance imaging was used to study the neural basis of associative learning of visual objects and their locations. As expected, activation in specialized cortical areas decreased with time. However, with path analysis it was shown that, in parallel to this adaptation, increases in effective connectivity occurred between distinct cortical systems specialized for spatial and object processing. The time course of these plastic changes was highly correlated with individual learning performance, suggesting that interactions between brain areas underlie associative learning. (+info)
Kleine-Levin and Munchausen syndromes in a patient with recurrent acromegaly.
Hypothalamic disease often affects the patients' personality and this also applies to pituitary tumors with suprasellar extension. We report on a patient with a 12-year history of recurrent acromegaly, treated with three transphenoidal operations, single field radiation therapy and bromocriptine/octreotide administration. During the course of follow-up she presented with self-inflicted anemia and Kleine-Levin syndrome (hypersomnia, hyperphagia and hypersexuality). Furthermore, she developed post-radiation necrosis within the right temporal lobe. Whether her neurological and personality disorders result - at least partially - from the acromegaly or the temporal lobe necrosis remains unclear. (+info)
Increased poly(ADP-ribosyl)ation of nuclear proteins in Alzheimer's disease.
Experimental studies indicate that overactivation of the DNA repair protein poly(ADP-ribose) polymerase (PARP) in response to oxidative damage to DNA can cause cell death due to depletion of NAD+. Oxidative damage to DNA and other macromolecules has been reported to be increased in the brains of patients with Alzheimer's disease. In the present study we sought evidence of PARP activation in Alzheimer's disease by immunostaining sections of frontal and temporal lobe from autopsy material of 20 patients and 10 controls, both for PARP itself and for its end-product, poly(ADP-ribose). All of the brains had previously been subjected to detailed neuropathological examination to confirm the diagnosis of Alzheimer's disease or, in the controls, to exclude Alzheimer's disease-type pathology. Double immunolabelling for poly(ADP-ribose) and microtubule-associated protein 2 (MAP2), glial fibrillary-acidic protein (GFAP), CD68, A beta-protein or tau was used to assess the identity of the cells with poly(ADP-ribose) accumulation and their relationship to plaques and neurofibrillary tangles. Both PARP- and poly(ADP-ribose)-immunolabelled cells were detected in a much higher proportion of Alzheimer's disease (20 out of 20) brains than of control brains (5 out of 10) (P = 0.0018). Double-immunolabelling for poly(ADP-ribose) and markers of neuronal, astrocytic and microglial differentiation (MAP2, GFAP and CD68, respectively) showed many of the cells containing poly(ADP-ribose) to be neurons. Most of these were small pyramidal neurons in cortical laminae 3 and 5. A few of the cells containing poly(ADP-ribose) were astrocytes. No poly(ADP-ribose) accumulation was detected in microglia. Double-immunolabelling for poly(ADP-ribose) and tau or A beta-protein indicated that the cells with accumulation of poly(ADP-ribose) did not contain tangles and relatively few occurred within plaques. Our findings indicate that there is enhanced PARP activity in Alzheimer's disease and suggest that pharmacological interventions aimed at inhibiting PARP may have a role in slowing the progression of the disease. (+info)
Evaluation of the NINCDS-ADRDA criteria in the differentiation of Alzheimer's disease and frontotemporal dementia.
OBJECTIVES: The diagnosis of Alzheimer's disease (AD) is now reliant on the use of NINCDS-ADRDA criteria. Other diseases causing dementia are being increasingly recognised--for example, frontotemporal dementia (FTD). Historically, these disorders have not been clearly demarcated from AD. This study assesses the capability of the NINCDS-ADRDA criteria to accurately distinguish AD from FTD in a series of pathologically proved cases. METHODS: The case records of 56 patients (30 with AD, 26 with FTD) who had undergone neuropsychological evaluation, brain imaging, and ultimately postmortem, were assessed in terms of whether at initial diagnosis the NINCDS-ADRDA criteria were successful in diagnosing those patients who had AD and excluding those who did not. RESULTS: (1) The overall sensitivity of the NINCDS-ADRDA criteria in diagnosing "probable" AD from 56 patients with cortical dementia (AD and FTD) was 0.93. However, the specificity was only 0.23; most patients with FTD also fulfilled NINCDS-ADRDA criteria for AD. (2) Cognitive deficits in the realms of orientation and praxis significantly increased the odds of a patient having AD compared with FTD, whereas deficits in problem solving significantly decreased the odds. Neuropsychological impairments in the domains of attention, language, perception, and memory as defined in the NINCDS-ADRDA statement did not contribute to the clinical differentiation of AD and FTD. CONCLUSION: NINCDS-ADRDA criteria fail accurately to differentiate AD from FTD. Suggestions to improve the diagnostic specificity of the current criteria are made. (+info)
Structural maturation of neural pathways in children and adolescents: in vivo study.
Structural maturation of fiber tracts in the human brain, including an increase in the diameter and myelination of axons, may play a role in cognitive development during childhood and adolescence. A computational analysis of structural magnetic resonance images obtained in 111 children and adolescents revealed age-related increases in white matter density in fiber tracts constituting putative corticospinal and frontotemporal pathways. The maturation of the corticospinal tract was bilateral, whereas that of the frontotemporal pathway was found predominantly in the left (speech-dominant) hemisphere. These findings provide evidence for a gradual maturation, during late childhood and adolescence, of fiber pathways presumably supporting motor and speech functions. (+info)
Conduction aphasia elicited by stimulation of the left posterior superior temporal gyrus.
OBJECTIVE: Disruption of fascicular tracts that connect Wernicke's to Broca's areas is the classic mechanism of conduction aphasia. Later work has emphasised cortical mechanisms. METHODS: To determine the distribution of language on dominant cortex, electrical cortical stimulation was performed using implanted subdural electrodes during brain mapping before epilepsy surgery. RESULTS: A transient, isolated deficit in repetition was elicited with stimulation of the posterior portion of the dominant superior temporal gyrus. CONCLUSION: This finding suggests that cortical dysfunction, not just white matter disruption, can induce conduction aphasia. (+info)