This study aimed at investigating the clinical usefulness of the Mental Deterioration Battery (MDB) in the neuropsychological diagnosis and characterization of the dementia syndrome. In this paper, we report: (a) normative data for various test scores derived from the analysis of performance of 340 normal subjects living in urban areas; (b) an evaluation of the reliability of the single tests and of the battery as a whole in differentiating normal subjects from patients affected by cognitive deterioration derived from the analysis of performance of 130 normal subjects living in rural areas and 134 patients affected by probable Alzheimer’s dementia; (c) a cluster analysis of performances of the 340 normal subjects in the standardization group to evaluate possible criteria of homogeneity according to which the various MDB scores tend to aggregate; (d) an analysis of performance profiles of 183 patients with right monohemispheric focal lesions, 159 patients with left unilateral lesions with aphasia and 131 left-lesioned nonaphasic patients to evaluate the specificity of the single tests of the battery in documenting a selective impairment of one of the two cerebral hemispheres. Results confirm the reliability of the MBD in discriminating between normal and demented patients and provide indications for use of the battery in differentiating qualitative patterns of cognitive impairment.

Background: A recently devised test of motor cortex excitability (short latency afferent inhibition) was shown to be sensitive to the blockade of muscarinic acetylcholine receptors in healthy subjects. The authors used this test to assess cholinergic transmission in the motor cortex of patients with AD. Methods: The authors evaluated short latency afferent inhibition in 15 patients with AD and compared the data with those of 12 age-matched healthy controls. Results: Afferent inhibition was reduced in the patients (mean responses ± SD reduced to 85.7% ± 15.8% of the test size) compared with controls (mean responses ± SD reduced to 45.3% ± 16.2% of the test size; p < 0.001, unpaired t-test). Administration of a single oral dose of rivastigmine improved afferent inhibition in a subgroup of six patients. Conclusions: The findings suggest that this method can be used as a noninvasive test of cholinergic pathways in AD. Future studies are required to evaluate whether short latency afferent inhibition measurements have any consistent clinical correlates.

Objectives: Recent transcranial magnetic stimulation (TMS) studies demonstrate that motor cortex excitability is increased in Alzheimer’s disease (AD) and that intracortical inhibitory phenomena are impaired. The aim of the present study was to determine whether hyperexcitability is due to the impairment of intracortical inhibitory circuits or to an independent abnormality of excitatory circuits. Methods: We assessed the excitability of the motor cortex with TMS in 28 patients with AD using several TMS paradigms and compared the data of cortical excitability (evaluated by measuring resting motor threshold) with the amount of motor cortex disinhibition as evaluated using the test for motor cortex cholinergic inhibition (short latency afferent inhibition) and GABAergic inhibition (short latency intracortical inhibition). The data in AD patients were also compared with that from 12 age matched healthy individuals. Results: The mean resting motor threshold was significantly lower in AD patients than in controls. The amount of short latency afferent inhibition was significantly smaller in AD patients than in normal controls. There was also a tendency for AD patients to have less pronounced short latency intracortical inhibition than controls, but this difference was not significant. There was no correlation between resting motor threshold and measures of either short latency afferent or intracortical inhibition (r = −0.19 and 0.18 respectively, NS). In 14 AD patients the electrophysiological study was repeated after a single oral dose of the cholinesterase inhibitor rivastigmine. Resting motor threshold was not significantly modified by the administration of rivastigmine. In contrast, short latency afferent inhibition from the median nerve was significantly increased by the administration of rivastigmine. Conclusions: The change in threshold did not seem to correlate with dysfunction of inhibitory intracortical cholinergic and GABAergic circuits, nor with the central cholinergic activity. We propose that the hyperexcitability of the motor cortex is caused by an abnormality of intracortical excitatory circuits.

We report the case of a patient (C.O.) who showed a selective defect in the recognition of familiar people, with very mild disease progression during a period of 30 months resulting from focal atrophy of the right temporal lobe. On formal neuropsychological testing, C.O. obtained high scores on tests of general intelligence, episodic memory, language, executive functions, selective attention, visual recognition and visual–spatial abilities. On more specific tasks of familiar and unfamiliar face recognition, C.O. scored above the controls’ means on perceptual tests, but obtained highly pathological results on mnesic–associative tests. His disorder of recognition of familiar people was not due to loss of person‐specific information, since he obtained highly abnormal naming scores when presented with photographs of famous people but borderline or mildly abnormal scores in a tasks in which he had to name celebrities from verbal definitions. On the other hand, C.O.’s recognition disorder could not be considered to be a form of ‘associative prosopagnosia’ since a similar defect was observed when he was requested to access information about famous persons through their voice rather than their face. Two alternative interpretations are advanced to explain C.O.’s inability to access his relatively spared person‐specific knowledge not only through the person’s face but also through the person’s voice. The first hypothesis is that, before accessing the person‐specific information, unimodal recognition channels must converge into a multimodal, non‐verbal person‐recognition system and that the right anterior temporal cortices play a crucial role in this integrative activity. The second hypothesis is that the face‐recognition units have privileged access to person‐specific semantic knowledge and that other recognition subsystems require coactivation of the face‐recognition units in order to access person‐specific semantic information.

The aim was to evaluate the effects of poststroke depression and antidepressant therapy on the improvement of motor scores and disability, to verify if the negative effects of poststroke depression on functional recovery could be counterbalanced by taking antidepressant drugs. RESULTS OBTAINED BEFORE, DURING, AND AFTER REHABILITATION on the Barthel index, Canadian neurological scale, and Rivermead mobility index—by 49 depressed patients with stroke, who had been treated (n=25) or not treated (n=24) according to the different therapeutic approaches of their physicians, were compared with results similarly obtained by 15 non-depressed patients with stroke. Analysis was by multivariate analysis of variance for repeated measures There was a non-significant difference between the groups in their motor and functional scores, and a significant improvement on time. A significant interaction between group and time was seen. This interaction was particularly significant on the Rivermead mobility index, and was due to the fact that the recovery of non-treated depressed patients with stroke was less than the non-depressed and the depressed but treated patients with stroke. Furthermore, recovery from depression was significantly greater in treated than in non-treated depressed patients with stroke. In conclusion, poststroke depression has negative effects on functional recovery, and a pharmacological treatment of depression can counterbalance this effect.

The construct of mild cognitive impairment (MCI) has been proposed to identify patients at risk of developing Alzheimer's disease (AD) in the pre-clinical stage. Although subjects with MCI have an increased risk of progressing to dementia, most remai