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Many authors hypothesized a linkage between the anatomical region of damage and the nature of constructional apraxia. In particular, the functional impairment of right brain damaged patients should consist in a visuo-spatial defect. However a large amount of researches have showed impaired visuo-spatial abilities in apraxic subjects respect to non-apraxics, but independently by the side of brain damage. In these researches constructional and visuo-spatial abilities have been often evaluated by methods not comparable among them. Aim of this paper is to verify the constructional performances of left and right brain damaged patients, utilizing exclusively the copy of geometric figures and tasks considered specific in detecting visuo-spatial disabilities. The experimental results show that both left and right brain lesions produce impairments of visuo-spatial abilities. Lastly, the utility of a cognitive approach of study is discussed.

This study of a dyslexic patient supports the view that the level of impairment of the phonological route plays a role in the production of semantic paralexias. The patient's reading was based on a defective phoneme-to-grapheme transcoding, in spite of evidence that semantic information was available through non phonological routes. The hypothesis that the residual ability to carry out phonological recoding could block the production of semantic paralexias was confirmed by tachistoscopic reading, assumed to interfere with phonological recoding in this patient, that provoked a definite rise of this type of error. The relationship between the degree of damage of phonological route and the clinical expression of the syndromes of phonological dyslexia and deep dyslexia is also discussed.

This paper reports the clinical features of 2 patients affected by mixed transcortical aphasia. Both of them had extensive damage of the left hemisphere. Cerebral blood flow measurement showed a marked decrease in left-hemisphere flow. In particular, speech areas were found to be morphologically and functionally damaged. The present findings, together with a critical review of the literature, served as a starting point for a discussion of linguistic features, diagnostic criteria and classical neuroanatomical interpretation of mixed transcortical aphasia. The possible contribution of the right hemisphere in determining this aphasic syndrome is suggested.

Two hundred and seventy-nine consecutive patients referred for transient loss of consciousness, compatible with syncope, underwent head-up tilt to 70 degrees during polygraphic (EEG, ECG, pneumographic) and blood pressure monitorings. Vasovagal syncopes occurred in 28 patients with the following EEG changes: progressive slowing until the appearance of middle or high amplitude delta waves generalized and synchronous in 9 patients; delta waves suddenly followed by transient flattening of EEG activity in 16 patients. In 2 patients EEG could not be interpreted because of muscle and/or movement artifacts. Fifteen out of 28 patients exhibited a marked cardioinhibition, expressed by long-lasting cardiac pauses; a relationship between duration of EEG flat and duration of asystole was not found.

Spatial span (Corsi's block-tapping test) and verbal span (Wechsler's Digits Forward test) were measured in 651 normal subjects and in three groups of extrapyramidal patients (Progressive supranuclear palsy, Parkinson, and Huntington's Chorea). Analysis showed Huntington's Chorea patients scored lower on both tests than did controls and other groups.

Norms are provided for verbal and visuo-spatial immediate memory span, two tasks widely used in the clinical assessment of short-term memory and its neurological disorders. Data have been collected from 1355 male and female adult subjects, with various educational backgrounds and a 20-99 years age range. Span shows a major decrement after the late sixties and is affected by educational level. Male subjects score better on the spatial task. Data collected from 1112 male and female children, 4-to-10 year-old, show that span increases with age and boys score better on the spatial test.

The number of senile (neuritic) plaques (SP) and neurofibrillary tangles (NFT) in mamillary bodies (MB) and in the dorsomedial nucleus of the thalamus (DMNT) were assessed in 25 cases of definite Alzheimer's disease. In 20 cases with AD without other CNS disease the MB and DMNT showed SP and/or NFT in 19 (95%). No correlation was found between the number of SP and NFT and the duration or age of onset of the disease. In patients with AD plus another CNS disease, there were fewer SP and NFT regardless of duration and age at onset of the disease. AD is a diffuse disorder with cortical and subcortical changes. The involvement of MB and DMNT suggests that subcortical structures are also implicated in the memory disorder of AD. The association of AD with other diseases that can themselves cause dementia requires further studies, especially regarding the pattern of topographic distribution of the degenerative changes.

Memory coding processes can be divided according to their attentional requirement into "automatic" and "effortful". The aim of current research was to explore both automatic and effortful processes in early and late stages of Alzheimer type dementia. Patients were classified on the basis of restrictive clinical and neuropsychological criteria, in order to pinpoint possible specific impairments in the two patients' subgroups. The present paper reports preliminary data about 15 mildly and 15 severely demented patients. Statistical analysis showed that both the automatic and the effortful coding processes are impaired at the late but also at the early stages of dementia.

Two cases are described: one with left occipital lesion and the other one with bilateral occipital damage; the first showed deficit of Mental Imagery and preserved recognition of pictures in unusual perspective; the second, vice-versa, showed integrity of Mental Imagery and deficit in visual recognition. The relationship between Mental Imagery and recognition of pictures in unusual perspective is discussed.

Head-up tilt to 70 degrees lasting for 30 min is a further useful test for studying syncope. In 26.69% of 109 consecutive out-patients referred for loss of consciousness, it induced vasodepressor and/or cardioinhibitory reactions. All symptomatic patients had similar EEG changes and blood pressure fall during symptoms: by contrast, ECG features, due to vagal activation, were different. The pathogenetic mechanism of vasovagal or vasodepressor syncope is an abrupt sympathetic cardiovascular inhibition with more or less marked vagal cardiac activation. This cardiovascular pattern is due to a cardiac reflex in orthostatic syncope or, probably, to a central activation in emotional fainting.

We assessed neuropsychological performances of 22 patients affected by Autosomal Dominant Cerebellar Ataxia type 1. All subjects completed a comprehensive battery of standardized tests requiring a verbal response, without time constraints. In order to verify the hypothesis that disease severity is the major factor in determining the cognitive status in this syndrome, patients were divided into three groups according to the severity of the clinical picture, as evaluated by the Inherited Ataxias Progression Scale (IAPS). Statistical analysis of the three groups' raw scores showed a significant decrement in patients with more severe clinical pictures on verbal short-term memory tasks. A similar trend, but not significant, was seen for general intelligence tests and verbal learning tasks. The decrement of verbal short-term memory could be related to motor speech problems. On the other hand, the decline of cognitive abilities over the course of the Autosomal Dominant Cerebellar Ataxia type 1 was not homogeneous enough to ensure statistically reliable trends. Therefore, this cross-sectional study suggests that the progression of the disease is a necessary factor in determining cognitive decline, but it is not sufficient. Other disease-related factors (age at onset, genotypic variety) could play a critical role: among these, the size of the expanded CAG repeats is significantly related to a decline of verbal intelligence and short-term memory in SCA2 patients.