Tau and Abeta42 protein in CSF of patients with frontotemporal degeneration.

BACKGROUND: CSF concentrations of tau and beta-amyloid protein-42 (Abeta42) have been extensively studied in AD. Few data are available concerning CSF levels of both proteins in patients with frontotemporal degeneration (FTD). METHODS: The authors investigated CSF tau and Abeta42 concentrations in 34 patients with FTD, 74 patients with AD, and 40 cognitively healthy control subjects. CSF levels of tau and Abeta42 were measured by ELISA. With use of receiver operating characteristic-derived cutoff points and linear discrimination lines, the diagnostic sensitivity and specificity of both markers were determined. RESULTS: CSF tau concentrations were significantly higher in FTD than in control subjects but were significantly lower than in AD. CSF Abeta42 levels were significantly lower in FTD than in control subjects but were significantly higher than in AD. In subjects with FTD, neither tau nor Abeta42 levels correlated with the severity of dementia. The best discrimination between the diagnostic groups was obtained by simultaneous measurement of tau and Abeta42, yielding a sensitivity of 90% at a specificity of 77% (FTD vs controls) and a sensitivity of 85% at a specificity of 85% (FTD vs AD). CONCLUSIONS: In FTD, CSF levels of tau are elevated and Abeta42 levels are decreased. With use of these markers, subjects with FTD can be distinguished from control subjects and from patients with AD with reasonable accuracy.

[Brain stem and cerebellar atrophy in neurosyphilis]. / Hirnstamm- und Kleinhirnatrophie bei Neurosyphilis.

A 54-year-old man suffered from serologically proven neurosyphilis with tetraspastic syndrome and bladder dysfunction. He showed a pronounced psychopathy with cognitive decline and attention/concentration deficits. MRI showed slowly progressive cerebellar and brainstem atrophy, which has rarely been described over the past decades. During times of higher incidence and prevalence of neurosyphilis, infratentorial atrophy had been described occasionally, but today this clinical manifestation has been all but forgotten.

Repetitive peripheral magnetic stimulation alleviates tactile extinction.

Despite its frequency in right brain damaged patients crucial mechanisms of tactile extinction are still obscure and treatments are unavailable. Recent PET observations suggest a hypometabolism in the primary and secondary somatosensory cortex of the lesioned hemisphere in patients with tactile extinction. Functional and morphological investigations have shown that the sensorimotor cortex has a remarkable capability of reorganization when the sensory inflow is changed. Repetitive peripheral magnetic stimulation (RPMS) applied in patients suffering from central paresis alleviates sensorimotor as well as cognitive deficits by the induction of proprioceptive inflow, thereby activating plasticity in the CNS. Based on the observation of reduced metabolic activity in patients suffering from tactile extinction we applied RPMS to explore the effects of peripheral sensory stimulation on tactile extinction. Fourteen right-hemisphere lesioned patients with tactile extinction were randomly allocated to an experimental and a control group. The experimental group received one single RPMS treatment of the left forearm as well as a condition of attentional cueing known to improve visual extinction. The control group, with comparable tactile extinction scores, neither received RPMS nor verbal cueing, but was tested twice to evaluate possible learning or test repetition effects. In the experimental group RPMS led to a significant reduction of left-sided extinctions in the recognition of different tactual surfaces, but had no effect on ipsilesional errors. In contrast, attentional cueing had no significant effect on left-sided extinction errors but unexpectedly increased right-hand extinction errors slightly but significantly. The control group showed stable extinction scores of the left- and right-hand stimulus across two measurements, thus ruling out learning or test repetition effects. These results show that sensory inflow is an important modulatory factor in tactile extinction. Furthermore, multiple RPMS may prove a promising way for the rehabilitation of patients with this disorder.

[Balint syndrome and associated disorders. Anamnesis--diagnosis--approaches to treatment]. / Balint-Syndrom und assoziierte Störungen. Anamnese--Diagnostik--Behandlungsansätze.

Balint syndrome is a combination of symptoms including simultanagnosia, a disorder of spatial and object-based attention, disturbed spatial perception and representation, and optic ataxia resulting from bilateral parieto-occipital lesions. Fixation and ocular exploration of space are severely impaired, as are reading, writing, drawing and orientation as well as movement in space. Low-level visual impairments may be associated and difficult to evaluate but are not a necessary element of Balint syndrome. This review summarizes the relevant facts of the etiology, localization of lesions, and the core features as well as frequently associated disorders of the syndrome. Instructions for the examination of patients are given and approaches for the management and treatment outlined. Models of attention and space representation are described for the explanation of this multifaceted and exciting syndrome. Finally the key features of the syndrome are summarized in a table at the end of the paper.