BackgroundBrain research has documented that the cortical mechanisms for language and action are tightly interwoven and, concurrently, new approaches to language therapy in neurological patients are being developed that implement language training in the context of relevant linguistic and non-linguistic actions, therefore taking advantage of the mutual connections of language and action systems in the brain. A further well-known neuroscience principle is that learning at the neuronal level is driven by correlation; consequently, new approaches to language therapy emphasise massed practice in a short time, thus maximising therapy quantity and frequency and, therefore, correlation at the behavioural and neuronal levels. Learned non-use of unsuccessful actions plays a major role in the chronification of neurological deficits, and behavioural approaches to therapy have therefore employed shaping and other learning techniques to counteract such non-use.AimsAdvances in theoretical and experimental neuroscience have important implications for clinical practice. We exemplify this in the domain of aphasia rehabilitation.Main ContributionWhereas classical wisdom had been that aphasia cannot be significantly improved at a chronic stage, we here review evidence that one type of intensive language-action therapy (ILAT)—constraint-induced aphasia therapy—led to significant improvement of language performance in patients with chronic aphasia. We discuss perspectives for further improving speech-language therapy, including drug treatment that may be particularly fruitful when applied in conjunction with behavioural treatment. In a final section we highlight intensive and rapid therapy studies in chronic aphasia as a unique tool for exploring the cortical reorganisation of language.ConclusionsWe conclude that intensive language action therapy is an efficient tool for improving language functions even at chronic stages of aphasia. Therapy studies using this technique can open new perspectives for research into the plasticity of human language circuits.

Three patients with PD developed manic behavior after bilateral implantation of electrodes for deep-brain stimulation (DBS). Common to all three patients were manic symptoms unremitting after levodopa reduction or stimulation "off," lower electrodes positioning caudal to the subthalamic nucleus area, postoperative DBS with the lower contacts (0) of the quadripolar electrodes, and resolution of the manic episodes coinciding with stimulation through higher contacts.

The treatment of aphasias-acquired language disorders-caused by stroke and other neurological conditions has benefitted from insights from neuroscience and neuropsychology. Hebbian mechanisms suggest that massed practice and exploitation of residual neurological capacities can aid neurorehabilitation of patients with poststroke aphasia, and progress in basic neuroscience research indicates that the language system of the human brain is functionally interwoven with perceptual and motor systems. Intensive speech and language therapies, including constraint-induced aphasia therapy, that activate both the linguistic and concordant motor circuits utilize the knowledge gained from these advances in neuroscience research and can lead to surprisingly rapid improvements in language performance, even in patients with chronic aphasia. Drug-based therapies alone and in conjunction with behavioral language therapies also increase language performance in patients with aphasia. Furthermore, noninvasive transcranial magnetic stimulation and electrical stimulation techniques that target neuronal activity within perilesional areas might help patients with aphasia to regain lost language functions. Intensive language-action therapies that lead to rapid improvements in language skills might provide a new opportunity for investigating fast plastic neuronal changes in the areas of the brain associated with language processing. Here, we review progress in basic neuroscience research and its translational impact on the neurorehabilitation of language disorders after stroke.

Neuropsychological deficits including cognitive impairment as well as depression are among the most frequent and important mental disorders found in patients with Parkinson's disease (PD). It has never been determined, however, whether there is a specific relationship between cognitive impairment and depression. A consecutive series of patients with PD was therefore examined for the presence of depression and neuropsychological deficits. Severity of depression was found to be the single most important factor associated with the severity of cognitive impairment. When PD patients with major depression were compared with an age and stage-matched group of nondepressed patients with PD using a neuropsychological battery, major depressed patients performed significantly worse than the nondepressed patients on all aspects of neuropsychological function tested. These impairments were most pronounced on frontal lobe tasks.

Both memantine and CIAT alone improved aphasia severity, but best outcomes were achieved combining memantine with CIAT. Beneficial effects of memantine and CIAT persisted on long-term follow-up.

The contribution of dopaminergic systems to cognitive defects in Parkinson's disease and the cognitive effects of levodopa remain controversial. The levodopa plasma levels and the neuropsychological performance of 10 parkinsonian patients with a stable motor response to the drug and 10 matched parkinsonian patients with a 'wearing-off' phenomenon were studied 12 h after levodopa was withdrawn (time zero), and at 1 h and 4 h after an oral dose of levodopa (i.e. at '+1H' and '+4H'), to investigate whether discrete cognitive domains are more sensitive to levodopa in parkinsonian patients with the wearing-off phenomenon. Considering the 20 patients as a whole, levodopa significantly diminished the response time in verbal and visuospatial memory tests, the extradimensional matching test and the Wisconsin card sorting test (WCST), without significantly improving or worsening the patient's accuracy. A significant group-by-time effect was only evident in the WCST; while in stable patients levodopa produced no changes, wearing-off patients significantly reduced the number of categories achieved and had more perseverative errors at +1H, recovering at +4H. These results confirm previous findings of selective adverse effects of levodopa on highly demanding executive tasks in Parkinson's disease and additionally suggest that some previous discrepancies between studies may be accounted for by lack of differentiation between stable and wearing-off conditions. 'Frontal' disturbances on neuropsychological tests with levodopa may become evident only after massive degeneration of the dopamine systems has occurred.

BACKGROUND: The cognitive effects of dopaminergic treatment in Parkinson's disease (PD) are still controversial.OBJECTIVE: To evaluate, in previously untreated patients with PD, whether chronic dopaminergic stimulation produces significant cognitive changes; whether they are sustained beyond the period of a few months; and whether the cognitive status of two motor-comparable groups is differently affected by levodopa and pergolide.DESIGN AND SUBJECTS: Parallel, randomized open study with blind neuropsychologic evaluation of 20 consecutive de novo patients with PD before and 3, 6, 12, 18, and 24 months after monotherapy with levodopa (n ‫ס‬ 10) or pergolide (n ‫ס‬ 10; 6-month monotherapy; pergolide + levodopa thereafter).RESULTS: Both treatments were associated with a signifi-cant improvement in motor scores and in tests assessing learning and long-term verbal and visual memory, visuospatial abilities, and various frontal tasks. While improvement in motor scores persisted, improvement in activities of daily living and in semantic fluency, Luria's rhythm and motor and long-term memory tests was not sustained at the 24-month examination. Further, performance on attentional, short-term memory, and the Stroop tests did not change over the course of the study. CONCLUSIONS: Both treatments were associated with incomplete but long-lasting (18 mos) improvement in many cognitive tasks which declined thereafter, suggesting that dopaminergic replacement is not enough to compensate for all cognitive deficits of PD.

We studied 26 patients in a randomized, placebo-controlled, double-blind parallel trial to evaluate the efficacy and safety of donepezil in chronic poststroke aphasia. Donepezil (10 mg/day) improved aphasia severity at endpoint (week 16) relative to placebo (p = 0.037).