Biomedical subjects

R Müri

Publications and source records attributed to R Müri.

6 recordsLinked to original sources

PubMed1998

[Recurrent cerebrovascular insult--manifestation of POEMS syndrome?].

The POEMS syndrome is a multisystem disorder characterised by polyneuropathy, organomegaly endocrinopathy, plasma cell dyscrasia and skin changes. Along with many further manifestations this rare syndrome may also include macroangiopathy and acute vascular obliteration. In the literature such vascular problems have received only little attention and most case reports refer to involvement of the coronary and lower limb arteries. To our knowledge, the association with recurrent strokes has not been described. We report on a 59-year-old male with a complete form of POEMS syndrome associated with multicentric Castleman's disease. Despite absence of vascular risk factors, myocardial infarctions and ischemic necroses of toes occurred, and recurrent ischemic strokes appeared during oral anticoagulation. Recurrent strokes may therefore represent a further complication of the POEMS syndrome.

Castleman Disease↗

PubMed1997

Cerebral ocular motor signs.

Eye movement disturbances resulting from cerebral lesions are reviewed and the specific roles of the different ocular motor areas are summarized. Three cortical areas may trigger saccades: the frontal eye field (FEF), the supplementary eye field (SEF) and the parietal eye field (PEF). The FEF could be involved mainly in intentional visual exploration (intentional saccades), the PEF mainly in reflexive visual exploration (reflexive saccades) and the SEF in the preparation of motor programs (sequences of saccades). Only bilateral lesions affecting these areas result in visible saccade disturbances (at bedside examination), as manifested in Balint's syndrome after parietal lesions, and ocular motor apraxia after fronto-parietal lesions. Other cortical areas prepare saccades: the posterior parietal cortex (near the PEF) controls visuomotor integration; the prefrontal cortex (i.e. area 46 of Brodmann) is involved in inhibition of unwanted reflexive saccades, prediction (predictive saccades) and spatial memory. Smooth pursuit is controlled by the FEF and the medial superior temporal area, located in the posterior part of the cerebral hemisphere. Eye movement disorders resulting from basal ganglia lesions are also reviewed. Lastly, the contribution of eye movement recordings in early diagnosis of some cerebral degenerative diseases (such as progressive supranuclear palsy or corticobasal degeneration) is emphasized.

Brain Diseases↗

PubMed1995

Cortical control of saccades.

A scheme for the cortical control of saccadic eye movements is proposed based partly on defects revealed by specific test paradigms in humans with discrete lesions. Three different cortical areas are capable of triggering saccades. The frontal eye field disengages fixation, and triggers intentional saccades to visible targets, to remembered target locations, or to the location where it is predicted that the target will reappear (i.e., saccades concerned with intentional exploration of the visual environment). The parietal eye field triggers saccades made reflexively on the sudden appearance of visual targets (i.e., saccades concerned with reflexive exploration of the visual environment). The supplementary eye field is important for triggering sequences of saccades and in controlling saccades made during head or body movement (i.e., saccades concerned with complex motor programming). Three other areas contribute to the preparation of certain types of saccades. The prefrontal cortex (area 46 of Brodmann) plays a crucial role for planning saccades to remembered target locations. The inferior parietal lobule is involved in the visuospatial integration used for calculating saccade amplitude. The hippocampus appears to control the temporal working memory required for memorization of the chronological order of sequences of saccades.

Cerebral Cortex↗

PubMed1992

Nuclear and infranuclear disorders.

Lesions of the brain stem can either affect the nuclei or the fascicles of the third, fourth or sixth cranial nerves and thus produce ocular motor disorders. Lesions of the oculomotor nuclear complex differ from lesions of the third nerve, since the motoneurones in the nucleus are specifically grouped. Similarly, a lesion of the sixth nerve nucleus results in a conjugate gaze palsy and not in an abducens palsy, because of 'interneurones' being intermingled with the abducens motoneurons. Isolated lesions of a nerve fascicle, which is the part of the cranial nerve running through the brain stem, usually cannot be distinguished clinically from lesions of the nerve outside the brain stem unless other brain stem signs are present. In the case of an isolated ocular motor nerve palsy, modern imaging techniques, particularly magnetic resonance imaging, may help to localize the lesion to the brain stem. Most often, however, brain stem lesions also involve structures surrounding the ocular motor nuclei or fascicles, sometimes leading to characteristic eponymic syndromes. In congenital eye movement disorders the pathoanatomical situation is more complex. Since the lesion takes place during intrauterine or early postnatal development, corrective misdirection of neurones occurs in addition to aplasia or hypoplasia of parts of the cranial nerves. Correspondingly, abnormal movements accompanying an attempted eye movement can be observed in some characteristic syndromes.

Abducens Nerve↗

PubMed1990

[Isolated trochlear nerve paralysis following head trauma].

39 cases with isolated trochlear nerve palsies of traumatic origin have been analyzed retrospectively. 18 patients (46%) had had cerebral contusion, 15 (39%) cerebral concussion, and 6 patients (15%) a minor head trauma. 33 patients had unilateral trochlear nerve palsies and 6 (all of them with cerebral contusion) bilateral. The degree of the palsies did not correlate with the severity of the head trauma. Essential pathogenetic mechanisms were frontal or occipital blows. We emphasize a fact hitherto underestimated in the literature, that even a relatively mild head trauma (cerebral concussion or minor head trauma) can cause isolated trochlear nerve palsies. This was the case in 21 of our 39 patients (54%). Simple clinical examination techniques are described (Bielschowsky phenomenon, pencil test), which allow detection of trochlear nerve palsies in most cases.

Adolescent↗

PubMed1986

Clinical and oculographic examinations of saccadic eye movements in the diagnosis of multiple sclerosis.

Saccades were examined clinically and with an improved version of infrared reflection oculography in 79 patients with multiple sclerosis (31 definite, 17 probable, 31 possible cases). With regard to employing saccade recordings in the diagnosis of multiple sclerosis, suitability of saccadic parameters and examination technique for routine use was investigated. Accuracy and peak velocity of 30 degrees and 20 degrees saccades detected mild abnormalities most reliably. Latencies were not reliable enough for routine examinations. The yield of pathology with infrared reflection oculography was improved by using separate normal ranges for abduction, adduction, and interocular differences. Additional examination of vestibulo-ocular reflex suppression seemed to be a reliable supplement to saccade testing, while smooth-pursuit testing cannot be recommended for routine diagnosis. Clinical examination of saccades revealed about half of the dissociated and half of the conjugate hypermetric disorders.

Adolescent↗