Role of acetyl-L-carnitine in the treatment of cognitive deficit in chronic alcoholism.

Preliminary data are reported from a multicentred double-blind placebo-controlled study concerned with the effects of acetyl-L-carnitine (LAC) on some cognitive deficits of at least one month-abstinent alcoholics. Fifty-five patients, showing impaired performance in at least two out of six mnemonic, praxic and verbal tasks, were randomly assigned to either LAC 2 g/day or a placebo group. They were tested by means of a neuropsychological battery exploring the areas of memory, constructional praxia, deductive-logical functions and language. Testing time was on baseline (T0), after 45 (T45) and 90 (T90) days. On the Rey's 15 word memory test (long-term), the Wechsler memory scale (logical memory), and the Similarities WAIS subtest, the T90 difference between LAC and the placebo was significant in favour of the former treatment. On the copying drawing test (simple copy), the placebo group did not show any T0-T90 variation, while significant improvement in the LAC group was greater than in the placebo group. As LAC has proved to ameliorate the performance or to accelerate the recovery on tests representative of all cognitive areas explored, it is conceivable that the drug acts diffusely, either at the cholinergic transmission or at the neuronal metabolism level. It is concluded that acetyl-L-carnitine can be a useful and safe therapeutic agent in the subtle cognitive disturbances of chronic alcoholics.

[Disorders of autonomic responses to emotional stimuli in patients with unilateral hemispherical lesions]. / Perturbation des réponses végétatives aux stimuli émotionnels au cours des lésions hémisphériques unilatérales.

The authors have studied in 31 patients affected by right (N = 12) or left (N = 19) hemispheric lesions and in 10 normal controls the autonomous response to emotional stimuli. Stimuli consisted of 3 short films, aiming to provoke respectively a negative emotional reaction, a positive emotional response or a non-emotional reaction. Galvanic skin response and heart rate were considered as the dependent variables of our research. Both normal controls and left brain-damaged patients were very influenced by the emotional nature of the stimuli and showed clear signs of activation of the sympathetic and para-sympathetic systems in front of emotional films. By contrast, right brain-damaged patients were not influenced by the emotional or non-emotional nature of the stimuli and showed neither a clear galvanic skin response nor a significant decrease of heart rate in front of emotional films.

Cognitive improvement in clinical trials with nootropic drugs: when can it be expected and how to clarify its meaning.

In order to have a correct evaluation of the activity of a nootropic drug, the criteria adopted for the choice of patients to be included in the clinical trials and the methods used to clarify the meaning of changes observed on cognitive tasks are reported. The results of a clinical trial with the nootropic oxiracetam carried out in line with the above-mentioned criteria and methods are related.

Dementia in Parkinson's disease: possible specific involvement of the frontal lobes.

We carried out a neuropsychological study on cognitive impairment in 57 subjects affected by idiopathic Parkinson's Disease (PD) and 32 subjects affected by Alzheimer's Disease (AD). First, we found two different subgroups of Parkinsonian patients, the first one with and the second without dementia. We clearly identified these two distinct subclinical entities regardless of mean age, age of onset, duration of treatment; on the contrary, the type of treatment seems to play a specific role in the appearance of dementia in PD, anticholinergics being assumed almost exclusively by demented Parkinsonian patients. Second, we observed two main differences for cognitive impairment between PD with dementia and AD. In fact, cognitive impairment is consistently more evident in Alzheimer patients than in Parkinsonian ones with dementia; in addition, demented Parkinsonians show a pattern of impairment similar to that exhibited by patients affected by frontal lobe lesions. This result supports neuroanatomical and neurochemical data on the involvement of the whole dopaminergic system in PD and the role played by the ventromedial tegmental area projecting to the frontal cortex in causing cognitive dysfunction in this disease.

[The pattern of neuropsychologic compromise in patients with Parkinson disease]. / Profilo di compromissione neuropsicologica in pazienti affetti da morbo di Parkinson.

We carried out a neuropsychological study on cognitive impairment in 57 subjects affected by idiopathic Parkinson's Disease (P.D.) and 32 subjects affected by Alzheimer's Disease (A.D.). First, we found two different subgroups of parkinsonian patients, the first one with dementia and the second one without dementia. We clearly identified these two distinct subclinical entities regardless of mean age, age of onset, duration of treatment; on the contrary, the type of treatment seems to play a specific role on the appearance of dementia in P.D., anticholinergics being assumed almost exclusively by demented parkinsonian patients (chi square c. Yates = 422; p less than 0.05). Second, we showed two distinct patterns of cognitive impairment between P.D. with dementia and A.D. In fact, cognitive impairment is consistently more evident in Alzheimer patients than in parkinsonian ones with dementia; in addition, demented parkinsonians show a pattern of impairment similar to that exhibited by patients affected by frontal lobe lesions. This result supports neuroanatomical and neurochemical data on the involvement of the whole dopaminergic system in P.D. and the role played by the ventro-medial tegmental area projecting to the frontal cortex. In conclusion, our study, identifying a specific pattern of cognitive impairment in P.D., well-differenciated from demented patients of different aetiology, suggests beneficial effects with dopaminergic agonists in these patients; in fact, these agents, acting on the second neuron, may stimulate the prefrontal region that is probably involved in the cognitive impairment of parkinsonian patients.