Brain

Grasby, P. M.; Frith, C. D.; Friston, K. J.; Bench, C.; Frackowiak, R. S. J.; Dolan, R. J.

doi: 10.1093/brain/116.1.1pmid: 8453452

Position emission tomography measurements of regional cerebral blood flow (rCBF) were performed in normal volunteers during two auditory—verbal memory tasks: a subspan and supraspan task. The difference in rCBF between tasks was used to identify brain areas/systems involved in auditory—verbal long-term memory. Increases in rCBF were observed in the left and right prefrontal cortex, precuneus and the retrosplenial area of the cingulate gyrus. Decreases in blood flow were centred in the superior temporal gyrus bilaterally. Separate comparisons were also made between each span task and a resting state. Brain regions showing increases in rCBF in these comparisons included the thalamus, left anterior cingulate, right parahippocampal gyrus, cerebellum and the superior temporal gyrus. The brain areas identified in these comparisons define a number of the neuroanatomical components of a distributed system for signal processing and storage relevant to auditory—verbal memory function.

Coslett, H. Branch; Saffran, Eleanor M.; Greenbaum, Sandy; Schwartz, Harry

doi: 10.1093/brain/116.1.21pmid: 8453458

A number of investigators have demonstrated that patients with pure alexia comprehend briefly presented words which they are unable to explicitly identify. We suggested previously that these patients may read by means of two distinct procedures: a laborious letter-by-letter method and a ‘whole-word’ procedure which, at least initially, does not support explicit word identification. We report a test of this proposal in a patient with pure alexia. We reasoned that if the patient had access to two distinct and incompatible procedures, he might be induced to switch from one to the other by changing task demands. We found that when instructed to name words, the patient employed a letter-by-letter strategy; in contrast, when instructed to make lexical decision or semantic judgements about rapidly presented words, he appeared to use a ‘whole-word’ strategy. These data support the hypothesis that two distinct procedures are available to this patient. We argue, further, that it is necessary to suppress use of the letter-by-letter strategy to demonstrate whole word reading capability in pure alexics, and that failure to do so may account for negative findings in other cases reported in the literature.

Pascual-Leone, Alvaro; Torres, Fernando

doi: 10.1093/brain/116.1.39pmid: 8453464

We studied the organization of the somatosensory cortex in proficient Braille readers, recording somatosensory evoked potentials (SEPs) in 10 subjects and using transcranial magnetic stimulation (TMS) in five subjects, and compared the results with those of 15 control subjects. Somatosensory evoked potentials were elicited by a focal electrical stimulus to the tip of the index finger and recorded from a contralateral 4×4 grid of scalp electrodes centred around C3' or C4'. Transcranial magnetic stimulation, with an 8-shaped coil centred over the same scalp positions, was delivered simultaneously with, and at different intervals after, the finger stimulus.The results of the right index (reading) finger in Braille readers were compared with those of their left index (non-reading) finger and of the right and left index fingers of the control subjects. The scalp areas from which we recorded N20 and P22 components of the SEP with an amplitude of at least 70% of the maximal amplitude recorded in each trial were significantly larger in SEPs evoked from the reading fingers. Detection of the stimulus applied to the reading finger was blocked by TMS delivered over a larger contralateral scalp area and during a longer time window after the stimulus.These experiments suggest that reading Braille is associated with expansion of the sensorimotor cortical representation of the reading finger.

Poirier, Pierre; Miljours, Sylvain; Lassonde, Maryse; Lepore, Franco

doi: 10.1093/brain/116.1.53pmid: 8453465

In order to evaluate the callosal and hemispheric involvement in sound localization, the present study examined response accuracy to auditory targets in acallosal subjects. The primary interest was to determine whether the congenital absence of the corpus callosum affects auditory localization, especially for sounds situated near the midline of auditory space or moving across it. A corollary objective was to examine the possible existence of an hemispheric asymmetry on audio-spatial localization tasks. Four subjects with callosal agenesis paired to four age and IQ-matched controls and 16 normal control subjects were asked to locate broad band noise bursts at fixed intensity (52 dB sound pressure level) in the horizontal plane in an anechoic chamber. Broad band noise bursts were delivered randomly through 16 loudspeakers, which were mounted at ∼10° intervals on a perimeter frame. Two conditions were tested: (i) localization of a fixed-sound source; (ii) localization of the beginning and the end of a simulated moving stimulus. Two response modes were used. Listeners reported the apparent stimulus location either (i) by pointing with the ipsilateral index finger or (ii) by calling out the estimated angles indicated on the calibrated sound perimeter. Aiming accuracy was assessed by calculating the mean deviation of the response from the objective target position. The results indicated that the responses of the acallosal subjects were less accurate than those of the controls. The deficit was observed not only at the midline but throughout the auditory field. This points to possible compensatory mechanisms following the early absence of the corpus callosum which are, however, limited. The results obtained with manual pointing were generally more precise than those obtained through oral responses. This difference suggests that the remapping of spatial positions onto a verbally based coordinate system involves a supplementary cognitive step which affects the precision of the response. Comparing the performance to stimulus presentation in the left and right fields indicated that no hemispheric asymmetry was apparent under any of the conditions for either the acallosal subjects or the IQ-matched and normal control subjects.

Vallar, Giuseppe; Bottini, Gabriella; Rusconi, Maria Luisa; Sterzi, Roberto

doi: 10.1093/brain/116.1.71pmid: 8453466

The effects of vestibular stimulation upon somatosensory deficits or tactile extinction contralateral to a hemispheric lesion were investigated in 20 right brain-damaged patients and 11 left brain-damaged patients. After stimulation, right brain-damaged patients showed a temporary partial recovery from left hemianaesthesia or extinction. Conversely, right somatosensory deficits associated with left brain damage were virtually unaffected by vestibular stimulation. Temporary recovery from somatosensory deficits was independent of the presence of visuo-spatial hemineglect. The suggestion is made that somatosensory deficits and extinction produced by right brain damage have an important non-sensory or perceptual component, that may be positively affected by vestibular stimulation. The mechanisms whereby this treatment may ameliorate somatosensory deficits may involve the restoration of the normal correspondence between somatotopic and egocentric representations of the body.

Töpper, R.; Schwarz, M.; Podoll, K.; Dömges, F.; Noth, J.

doi: 10.1093/brain/116.1.87pmid: 8453467

A fast route for transmission of deep and cutaneous afferent information to the frontal cortex is well established in non-human primates. Whether the incoming cortical information gives rise to early frontal somatosensory evoked potentials (SEPs) in humans is still a matter of contention. We attempted to solve this question by investigating the topography of SEP generators evoked by median nerve stimulation in 30 healthy subjects and in 30 patients suffering from Huntington's disease, who are known to have reduced SEP amplitudes. Using an earlobe reference, SEPs were recorded with an array of either five surface electrodes over the contralateral parietal cortex or 32 electrodes distributed over the whole scalp. In normal subjects analysis of frontal potentials revealed an early positive (P22) and negative (N30) component which could not be explained by generators located in the parietal cortex. Apart from the reduction of parietal components (N20, P25) frontal P22 and N30 were diminished or absent in Huntington's disease patients. Frontal potentials were even reduced in those patients who had parietal SEP amplitudes within the range of normal subjects. These frontal changes are similar to those reported in other basal ganglia disorders. Basal ganglia dysfunction might therefore be associated with changes of frontal SEP components.

van Nes, J. A. P. de; Kamphorst, W.; Ravid, R.; Swaab, D. F.

doi: 10.1093/brain/116.1.103pmid: 7680932

The monoclonal antibody Alz-50 is directed against modified forms of tau proteins. Various hypotheses have been put forward concerning the meaning of Alz-50 staining in Alzheimer's disease brains. Cytoskeletal alterations are reported to occur exclusively in the cortex and the subcortical nuclei directly connected with the contex. In addition, Alz-50 staining is presumed to be indicative of impending neuronal death. In order to test these hypotheses Alz-50 was applied to the hypothalamus and adjoining areas of five Alzheimer's disease patients of 40–90 years of age and five sex-and age-matched, non-demented controls. The results showed the following: (i) Alz-50 immunoreactivity is not restricted to Alzheimer's disease patients. Alz-50 immunoreactive beaded nerve fibres and patchy, granular cell bodies were observed in some hypothalamic nuclei of all controls with the exception of the youngest one. Dystrophic neurites were not only observed in all Alzheimer's disease hypothalami but also in that of the oldest control. (ii) In the hypothalamic area various nuclei had different Alz-50 staining patterns. Alz-50 staining could not, however, be related to neuronal death in the different nuclei. (iii) Histo-pathological changes in Alzheimer's disease patients are not restricted to the cortex or subcortical areas connected directly with the cortex. The present report indicates that the hypothalamus is considerably more affected in Alzheimer's disease than has often been assumed. However, these changes can also be found in non-demented old people.

Runmarker, Björn; Andersen, Oluf

doi: 10.1093/brain/116.1.117pmid: 8453453

An incidence cohort consisting of 308 multiple sclerosis patients was followed up repeatedly during at least 25 years of disease. A number of clinical factors were analysed with respect to their validity in assessing the long-term prognosis. Of the onset characteristics, the type of course was the most important, with primary progressive patients experiencing a much more severe course. In patients with an acute onset, low onset age, high degree of remission at first exacerbation, symptoms from afferent nerve fibres and onset symptoms from only one region (as compared with polyregional symptoms) of the central nervous system, were factors significantly associated with a favourable long-term prognosis. Of factors known 5 years after onset, a low number of affected neurological systems, a low neurological deficit score and a high degree of remission from the last bout were the most important favourable prognostic factors.

Morrissey, S. P.; Miller, D. H.; Kendall, B. E.; Kingsley, D. P. E.; Kelly, M. A.; Francis, D. A.; MacManus, D. G.; McDonald, W. I.

doi: 10.1093/brain/116.1.135pmid: 8453454

A 5-year follow-up study was performed on 89 patients who had undergone brain magnetic resonance imaging (MRI) at presentation with an acute clinically isolated syndrome of the optic nerves, brainstem or spinal cord of a type suggestive of multiple sclerosis. At presentation, MRI was abnormal, revealing one or more asymptomatic cerebral white matter lesions in 57 (64%), and was normal in 32 (36%). At follow-up, progression to clinically definite multiple sclerosis had occurred in 37 out of 57 (65%) with an abnormal MRI and one out of 32 (3%) with normal MRI. Human leucocyte antigen (HLA) typing was performed in 70 patients and cerebrospinal fluid (CSF) was examined at presentation in 36. The presence of HLA-DR2 antigen or cerebrospinal fluid oligoclonal IgG bands were both associated with a significantly increased risk of progression to multiple sclerosis, but MRI was much more powerful in predicting outcome. The presence of four or more MRI lesions at presentation was associated with a higher rate of progression to multiple sclerosis, more frequent development of moderate or severe disabilities and a greater number of new MRI lesions at follow-up.The results indicate that brain MRI at presentation with a clinically isolated syndrome suggestive of multiple sclerosis is a powerful predictor of the clinical course over the next 5 years. This observation, combined with an ability to detect other sometimes treatable disorders which can also cause such syndromes, suggests that MRI is the investigation of choice in evaluating this group of patients.

Namer, I. J.; Steibel, J.; Poulet, P.; Armspach, J. P.; Mohr, M.; Mauss, Y.; Chambron, J.

doi: 10.1093/brain/116.1.147pmid: 7680933

Blood—brain barrier permeability in myelin basic protein (MBP)-specific T cell induced experimental allergic encephalomyelitis (EAE) was studied by magnetic resonance imaging (MRI) in Lewis rats. Myelin basic protein-specific T cells of different specificity and/or purified protein derivative (PPD)-specific T cells were used. During the course of EAE, the volume of the lesions and the T1 and T2 relaxation times were recorded and evaluated with respect to the clinical signs.The results showed that the severity of abnormalities seen on MRI, corresponding to the blood-brain barrier breakdown and cerebral oedema depended on the following two factors: (i) the specificity of the MBP-specific T cells used; (ii) the number of MBP-specific T cells transferred. It was also shown that the more specific the cells were, the less severe the cerebral blood-brain barrier rupture. Moreover, the blood-brain barrier breakdown increased when the number of cells increased. Our results demonstrated that a synergy exists between MBP and PPD-specific T cells which seems to result in an increase in central nervous system inflammation. This helps to explain the role of Mycobacterium tuberculosis in the induction of EAE.