Giancarlo Finali

L-deprenyl therapy improves verbal memory in amnesic Alzheimer patients.

Altered monoaminergic neurotransmission could play an important role in the cognitive dysfunctions typical of dementia of the Alzheimer type (DAT). DAT is not, however, a homogenous phenomenon inasmuch as two forms are distinguishable: early onset (EO) and late onset (LO). Moreover, focal patterns of neuropsychological deterioration fall into various subgroups. According to our hypothesis, DAT patients, who at the onset of the disease mainly manifest memory disorders, also represent a specific subgroup characterized by impaired cortically projecting catecholaminergic pathways. In a 6-month randomized, double-blind, cross-over study versus placebo we analysed the influence of L-deprenyl on the verbal memory of 19 amnesic EO-DAT patients. Verbal memory was assessed by means of the Rey Auditory Verbal Learning Test. The results obtained show significantly better performances for L-deprenyl treated patients in learning and long-term memory skills. We suggest that L-deprenyl, through selective inhibition of MAO-B and by increasing the activity of the catecholaminergic systems, positively influences cognitive functions and behaviour founded on memory efficiency.

Rapidly Progressive Aphasic Dementia with Motor Neuron Disease: A Distinctive Clinical Entity

The association of motor neuron disease (MND) with rapidly progressive aphasic dementia has been recognized as a distinct clinical syndrome within the group of frontotemporal dementias (FTDs). Although the clinical and neuropsychological features of this syndrome have been defined, a small number of post-mortem studies have been published with heterogeneous neuropathological findings. We performed cognitive, neuro-imaging and neuropathological studies on a 71-year-old male with rapidly progressive aphasic dementia and MND. We initially found a selective non-fluent aphasia associated with hypoperfusion of the left frontotemporal cortex. Proton magnetic resonance spectroscopy revealed an asymmetric change of brain metabolites, with greater changes in the left temporal lobe. The bulbar manifestations of MND occurred over the following 6 months, and the patient died of bronchopneumonia. The neuropathological examination revealed loss of neurons in the hypoglossal nucleus and anterior horns of the cervical spinal cord with microvacuolation and dot-like ubiquitin-positive deposits in the frontoparietotemporal cortex, but no changes suggestive of Alzheimer’s, Pick’s or Lewy body disease. These findings support the conclusion that MND with rapidly progressive aphasic dementia is a distinctive clinical entity within the group of FTD-MND.

Negative evidence of difference between right- and left-handers in interhemispheric transfer of information

The present study has been designed to investigate the relationship between handedness and callosal function. Based on the previous finding of a greater anatomical connection between the hemispheres in left-handers than in right-handers and in order to test the possibility of greater functional communication, the efficiency of interhemispheric transfer of information has been measured using a finger localization task. Comparison of two groups of male right-handed and left-handed subjects shows no difference in the efficiency of interhemispheric transfer of information.

Early frontal impairment as a predictor of dementia in Parkinson's disease

To the Editor: The very interesting article of Jacobs et al. [8] on Neuropsychological characteristics of dementia in Parkinsons disease (PD) suggests several ideas. A preclinical phase of parkinsonian dementia can be identified, and this preclinical phase presents a specific neuropsychological pattern that can be distinguished from the pattern seen in Alzheimers disease. Verbal fluency represents the type of cognitive performance that can best be correlated with subsequent development of dementia, and poor performance on these tests would reflect an executive dysfunction due to an involvement of the frontal-subcortical circuits. On the basis of our own results, an early frontal dysfunction can be considered the best predictive factor for the development of dementia in PD. [2] In particular, in an otherwise unselected sample of parkinsonian patients, we found that four different types of relationships can be observed between a frontal syndrome, dementia and PD: (1) no cognitive abnormalities are revealed by neuropsychological evaluation; (2) the frontal symptomatology is associated with a more generalized cognitive impairment; (3) signs of frontal dysfunction constitute the sole cognitive alteration that can be noted; and (4) the neuropsychological examination reveals abnormal cognitive functions that cannot be attributed to a frontal dysfunction. The first pattern can be …

Neuropsychological Follow-Up of Parkinsonian Patients with and without Cognitive Impairment

In order to evaluate possible progression in the severity of their cognitive impairment, 34 parkinsonians with intellectual impairment were followed longitudinally for 7 years. Each patient was matched for age, sex, severity and duration of illness, and pharmacological treatment, with a parkinsonian patient without cognitive impairment. Results suggest that cognitive deficits are not static but rather there is a progression in the severity. Furthermore, patients suffering from severe dementia are more likely to die during the follow-up period. The prognosis of Parkinsons disease seems to be changed substantially by the occurrence of dementia. The natural history of parkinsonian dementia does not seem to differ from the history of other forms of dementia with a progressively disabling course leading to a complete loss of autonomy.

Neuropsychological correlates of l-deprenyl therapy in idiopathic parkinsonism

1. Monoaminergic neurotransmitter systems are known to play an important role in neuropsychological functions and they are impaired in dementia of DAT and PD. 2. L-deprenyl is a monoamine-enhancing drug which at low doses selectively inhibits MAO-B, an enzyme whose brain activity has been reported to increase in normal aging and neurodegenerative dementing disorders. 3. The authors studied the effects of L-deprenyl, 10 mg/day, on several cognitive domains in idiopathic parkinsonians without dementia. Ten out-patients, treated with levodopa plus DDI, were tested before receiving L-deprenyl and retested six months after they had been treated with the drug. A control group of ten parkinsonian out-patients treated with only levodopa plus DDI, matched for age, educational level, severity and duration of extrapyramidal disease, was tested by the same neuropsychological battery and retested after a comparable time interval. 4. Statistically significant changes were noted in the verbal and visuospatial learning performances of PD patients treated with the combination of L-deprenyl and levodopa.

Superficial Siderosis of the Central Nervous System: A 70-Year-Old Man with Ataxia, Depression and Visual Deficits

Background: Superficial siderosis of the central nervous system (SSNS) is caused by cerebral, cerebellar and spinal cord tissue deposition of hemosiderin, often related to repeated episodes of subarachnoid hemorrhage. Typical symptoms include ataxia, sensorineural deafness and dementia. Methods and Results: An elderly patient with SSNS presenting with ataxia, depression and severe visual impairment was admitted to the Unit of Geriatrics of the University Hospital of Perugia, Italy. Late diagnosis and the association of symptoms with SSNS prevented the possible surgical treatment of the disease. Conclusions: Recognition of uncommon clinical variants may facilitate early diagnosis of SSNS and improve therapeutic results.

Verlagswechsel und Reduzierung des Abonnementspreises ab 2004

In der ersten Phase der Therapie ist es geglückt, der Patientin einen Raum zur Verfügung zu stellen, in der gerade in der Distanz der Phantasie eine therapeutische Kommunikation ermöglicht wurde. Diese Phantasie diente dazu, die negative Übertragung der Vater-Figur in der therapeutischen Situation mit mir abzuwehren. Durch die Anteilnahme am «symbolischen Raum» der Patientin wurde eine Annäherung an ihre innere Erlebniswelt möglich. Gleichzeitig konnte ich mir genügend Raum verschaffen – gerade vermittelt über das Verstehen der Figuren als dargestellte Teile ihres Selbst – um ihre Lage benennen und uns dem langsamen Verstehen annähern zu können. Dieser Verstehensprozess ermöglichte das allmähliche «Wissbar-Werden» ihrer inneren Verlassenheitsgefühle, gerade durch die in meiner Gegenübertragung immer wieder deutlich spürbaren und benennbaren Affekte. Diese «haltende Funktion» im Sinne des Containments hat zu einer Transformation emotionaler Inhalte beigetragen, wodurch sich die Patientin in unseren Stunden soweit von ihren frühen negativen Beziehungserfahrungen distanzieren konnte, dass sie mich in einem ersten Versuch als «den hilfreichen Dritten» in der Krisensituation nutzen konnte. Im Verlauf der Stunden und durch die sich abbildenden Prozesse der «Bewusstwerdung» in der Erzählung gelingt es A., die gegensätzlichen Strebungen aus ihrem Unbewussten in eine bewusstseinsnähere Form zu bringen. Ihr Ego-Komplex konnte dadurch an Kraft gewinnen und erlaubte es, sich dem «Undenkbaren» immer weiter anzunähern und schliesslich auszusprechen, wodurch es den Urteilsfunktionen der Patientin verfügbar gemacht werden konnte. Doch noch ist in der Erzählung der Patientin nicht entschieden, ob die Heldin nun von dieser Welt ist oder in das Reich der Götter gehört. Die Wirksamkeit des Unbewussten mit den noch inferioren Urteilsfunktionen wird gerade auf den ersten 62 Seiten, die sie vor der Therapie geschrieben hatte, in erstaunlicher Form sichtbar. Die Heldin muss einen «weiblichen Heldenkampf» um Bewusstheit führen, der im Fortsetzungsteil, der während unserer Therapie entstand, immer sichtbarer wurde. Doch so, wie der Mut der Heldin in der weiteren Entwicklung der Erzählung während unserer Therapiestunden zunimmt, sich ihrer Herkunft zu stellen, beginnt die Patientin auch ihre persönliche Konfliktsituation zu verstehen. Die dabei nun direkter erlebbaren Affekte von Trauer und Wut können nun ähnlich zur Matrix einer «Mutter-Kind-Interaktion» im therapeutischen Raum gehalten werden. Ich meine, dass gerade durch meine Akzeptanz der Abwehrmassnahmen der Patientin, die in dem Angebot der Erzählung verborgen waren, und die Nutzung dieser Erzählung als besondere Form eines Symbolisierungsprozesses, die Möglichkeiten der Patientin gewachsen sind, sich dem Risiko einer vertrauensvollen Beziehung zu stellen, was eben auch eine Modifikation der Komplexe durch neue Beziehungserfahrungen bedeutet. Zum Abschluss meiner Darstellung dieses ersten Therapieschrittes möchte ich noch einmal die junge Heldin der Erzählung (die inzwischen auf 104 Seiten gewachsen ist) zitieren, die folgendes mit ihrer Freundin bespricht und damit die Erweiterung des «Blickwinkels» der Patientin andeutet: «(...) – , wollte ihre Freundin wissen. , bestätigte sie (die Heldin). Plötzlich schaute sie ihre Freundin aufgeregt an. (...)»

Rapidly progressive aphasic dementia with motor neuron disease: A distinctive clinical entity?

The association of motor neuron disease (MND) with rapidly progressive aphasic dementia has been recognized as a distinct clinical syndrome within the group of frontotemporal dementias (FTDs). Although the clinical and neuropsychological features of this syndrome have been defined, a small number of post-mortem studies have been published with heterogeneous neuropathological findings. We performed cognitive, neuro-imaging and neuropathological studies on a 71-year-old male with rapidly progressive aphasic dementia and MND. We initially found a selective non-fluent aphasia associated with hypoperfusion of the left frontotemporal cortex. Proton magnetic resonance spectroscopy revealed an asymmetric change of brain metabolites, with greater changes in the left temporal lobe. The bulbar manifestations of MND occurred over the following 6 months, and the patient died of bronchopneumonia. The neuropathological examination revealed loss of neurons in the hypoglossal nucleus and anterior horns of the cervical spinal cord with microvacuolation and dot-like ubiquitin-positive deposits in the frontoparietotemporal cortex, but no changes suggestive of Alzheimers, Picks or Lewy body disease. These findings support the conclusion that MND with rapidly progressive aphasic dementia is a distinctive clinical entity within the group of FTD-MND.