Selective activation of human cortical area V5A by a rotating visual stimulus in fMRI; implication of attentional mechanisms.

The human homologue of area V5A of rotation-selective cells in the monkey medial superior temporal area (MST) was identified using functional magnetic resonance imaging (fMRI). It was located within the border region of occipito-temporo-parietal cortex, in four of 10 subjects on both sides, and on the right or left side in three subjects each. The stimulus was a black-and-white sine-modulated windmill presented either stationary or in rotation phases of 1 s duration. Areas V1-V3 did not show up with this paradigm. Focusing attention by mentally counting the number of rotation phases ensured high signal intensity in V5A, whereas moving attention away by counting electric stimuli to the wrist diminished it despite persistent fixation of gaze to the centre of the windmill.

Parallel increase of heterochromatic increment threshold and postadaptation thresholds in Parkinson's disease and in neuroleptic treatment.

Following reports on a predominant loss of blue/yellow contrast sensitivity in Parkinson's disease, we revisited the physiological phenomenon of transient tritanopia. Normative data were collected from 33 healthy individuals using different colour and time combinations. Stimuli of 440 nm wavelength (blue) proved optimal, if flashed for 50 msec within the early phase of a 2 sec pause in the 600 nm adaptation light. These conditions were then applied to 15 patients with Parkinson's disease. We found a parallel increase of increment threshold (P < 0.001) and postadaptation thresholds (P < 0.01), with little change in the extent of transient tritanopia. The same tendency at a lower significance level was found in 15 psychiatric patients under chronic treatment with depot neuroleptics.

Predominant affection of the blue cone pathway in Parkinson's disease.

Luminance contrast sensitivity and colour contrast thresholds were determined in 26 Parkinson patients and 17 normal controls of comparable age. They were psychophysically tested with a colour monitor system. Stimuli consisted of Gaussian enveloped luminance modulated or colour modulated (protan and tritan axis) vertical sine wave gratings with a spatial frequency of 1 cycle/degree. The stimuli subtended 4 degrees in diameter. Thresholds were determined using a two alternative forced choice method. Three different experimental conditions were explored: the detectability of stationary gratings, of moving gratings at velocities of 0, 2.5 and 5.0 cycles/s, and the detectability of horizontal square wave displacement at a frequency of 5 Hz for gratings of specified contrast levels. Intergroup differences were evaluated using two-tailed t tests with Satterthwaite corrections. Consistent and significant differences between normals and patients were found for tritan stimuli in the static and both dynamic conditions, and for luminance contrast stimuli in the displacement condition. Protan stimuli were much less apt to detect differences between the groups. We conclude that the retinal deficit of dopamine in Parkinson's disease is reflected in diminished centre/surround inhibition and that these changes are primarily apparent when vision is tested along the tritan axis, because blue cones are sparsely distributed.

Visual thresholds to low-contrast pattern displacement, color contrast, and luminance contrast stimuli in Parkinson's disease.

We used the computerized Moorfield Vision System to demonstrate specific increases in various perceptual visual thresholds in idiopathic Parkinson's syndrome. Fifteen patients were compared to 13 age-matched normals. Motion detection was impaired maximally (2 p < 0.01 and better in two-tailed t test) at luminance contrasts of 3-7%. Stimulus was an achromatic vertical 4 cycles/degrees sine wave grating subtending 3 degrees x 2 degrees, centered 5 degrees in the nasal field and oscillating at 5 Hz. In addition, stationary color and luminance contrast thresholds were tested with flashed display of 5 degrees x 6 degrees random letters, which were presented for 200 ms (color) and 50 ms (achromatic). Color discrimination was impaired in the tritan axis only (2 p < 0.05 in two-tailed t test). All achromatic stimuli--luminance increments, decrements, and phase reversing stimuli--were equally well seen by patients and controls. We conclude that the dopaminergic deficit of retinal amacrine cells in Parkinson patients can be monitored by combined low-contrast and motion (displacement) stimuli. Future studies will determine if moving colored targets are more effective in discriminating patients from controls than are the achromatic gratings used in this work.

Malignant gliomas--ploidy and DNA-content before and after therapy.

DNA ploidy and S-phase percentage from nine malignant gliomas (four glioblastomas, four anaplastic astrocytomas grade 3 and one anaplastic oligoastrocytoma grade 3) have been estimated by single cell cytophotometry on biopsy and necropsy specimens. All gliomas from biopsy material showed, with the exception of two diploid tumours, a polyploid-aneuploid DNA-pattern and stem-lines of different ploidy. The most frequent stem-lines were diploid and hyperdiploid. In necropsy material, following treatment i.e. operation and combined drug and radiation therapy, the heterogeneous nature of all malignant gliomas persisted. From seven aneuploid-polyploid gliomas four showed an elevation and three of them a decrease of DI values. Diploid tumors remained diploid. Because of marked heterogeneity of ploidy patterns and the small number of tumors investigated, ploidy changes could not be used for estimation of therapy efficacy and prognosis. Further studies will be necessary to answer this question.

Latency and duration of the muscle silent period following transcranial magnetic stimulation in multiple sclerosis, cerebral ischemia, and other upper motoneuron lesions.

In muscles with sustained voluntary contraction, EMG activity is transiently inhibited after transcranial magnetic stimulation. We recorded this postexcitatory silent period (SP) at 1.5 times individual stimulus threshold level from the first dorsal interosseus muscle in 65 neurologic patients aged 11 to 80 years. When compared with 20 healthy volunteers and a subgroup of patients with peripheral neurologic conditions not affecting the tested pathways, the SP was significantly longer on the paretic side in cerebral ischemia (p < 0.001) and chronic inflammatory CNS diseases, such as multiple sclerosis or neurosarcoidosis (p < 0.01). There was a similar tendency in pyramidal tract lesions due to CNS tumors and spinal cord trauma. In lesser degrees of paresis, SP duration is more sensitive than central motor conduction time (CMCT), but its specificity awaits further evaluation. SP is dependent on the integration of motor excitatory and inhibitory pathways and, possibly, sensorimotor reflex systems. In contrast to SP duration, which proved to be an independent variable giving supplementary information over the usual CMCT measurement, SP onset latency correlates well with CMCT and peripheral nerve conduction slowing, as in polyradiculoneuritis.

Silent period measurement revives as a valuable diagnostic tool with transcranial magnetic stimulation.

Following magnetic transcranial stimulation (TCS) a post-excitatory pause can be observed in surface electromyographic (EMG) recordings from pre-innervated muscles. We studied the duration of this silent period (SP) in the abductor pollicis brevis muscle while varying the stimulus intensity (SI) and the amount of the voluntary tonic contraction in 23 normal adults aged 20-78 years. A multivariate linear regression analysis revealed a positive correlation of SP with SI and a slight negative correlation with age. In 11 hemiparetic patients a relative increase of the SP was found on the affected side despite normal central motor conduction time. A marked shortening of the SP in relation to controls was observed in 6 parkinsonian patients.

[Speech apraxia in dialysis-associated aluminum encephalopathy]. / Sprechapraxie bei dialyseassoziierter Aluminiumenzephalopathie.

A 57-year-old man on long-term renal dialysis presented with speech dyspraxia, a symptom characteristic of early aluminium encephalopathy. Once fully developed, this condition has a poor prognosis despite deferoxamine (DFO) treatment.

Orofacial and respiratory tardive dyskinesia: potential side effects of 2-dimethylaminoethanol (deanol)?

A case of essential tremor since early adultness is presented, which has been treated successfully with the acetylcholine precursor 2-dimethylaminoethanol (deanol) for 10 years. Development of a marked dyskinesia syndrome affecting predominantly orofacial and respiratory musculature has been noticed with this medication. Partial remission after discontinuation and a favorable response to anticholinergics are suggestive of an adverse drug effect.

Polyradiculoneuritis following botulinum toxin therapy.

The development of Guillain-Barré syndrome is reported in a patient, who had previously received botulinum toxin type A injections into both orbicularis oculi muscles to treat idiopathic blepharospasm. The possibility of a causal relationship is discussed with consideration of the literature on adverse effects of vaccinations and of Clostridium botulinum and its toxin.

Morvan's fibrillary chorea. A case with possible manganese poisoning.

The clinical picture of Morvan's fibrillary chorea includes a. spontaneous muscular activity resulting from repetitive motor unit action potentials of peripheral origin (multiplets), b. autonomic dysregulation with profuse hyperhidrosis, and c. central nervous system involvement as shown by severe insomnia and hallucinosis. A case featuring all these symptoms is presented. Whereas known causative factors range from gold or mercury poisoning to autoimmune disorders, the presented case is the first one in which chronic manganese intoxication (occupational exposure) seems to be implicated. Manganese has been found to inhibit acetylcholine esterase, and, as a consequence, may produce peripheral and central cholinergic hyperactivity.