Gene/Protein Disease Symptom Drug Enzyme Compound
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Query: UNIPROT:P50583 (asymmetrical)
12,197 document(s) hit in 31,850,051 MEDLINE articles (0.00 seconds)

The clinical eye signs of 31 myasthenic patients are presented and those signs important for an early diagnosis are then discussed: lid symptoms caused by fatigue (Simpson-test), characteristic lid twitches as well as alternating asymmetrical eye muscle pareses. The importance of an investigation with the tangent scale in the course of which tensilon is injected is pointed out. False diagnosis and differential diagnostic signs are then considered (disseminated sclerosis, aneeurysm, encephalitis, pseudopulbarparalysis). - Our electronystagmographical investigations of saccadic eye movements showed hypometric, alternating saccades with occasional nystagmuslike jerks. After Tensilon injection hypermetric saccades (overshoots) were observed which depended on a disproportion of the supranuclear oculomotor centers and the eye muscles. The "muscleparetic" nystagmus is a pathologically increased endposition nystagmus. The hypometric nystagmuslike jerks during a saccadic eye movement are caused by insufficient phasic innervation.
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PMID:[Diagnosis of myasthenic eye signs. Clinical signs and electronystagmographical findings of saccadic eye movements (author's transl)]. 120 48

Seventeen patients with relapsing remitting multiple sclerosis (MS) and mild physical disability had neuropsychological testing, magnetic resonance imaging (MRI) and single photon emission computerised tomography (SPECT) using technetium 99m (99mTc) hexamethyl-propyleneamine oxime (HMPAO). Performance in verbal fluency, naming and memory testing appeared to be impaired in MS patients compared with 17 age-sex and education matched normal controls. Weighted periventricular and confluent lesion scores and the width of the third ventricle, proved to be the most sensitive MRI measures in differentiating more cognitively impaired patients from those who were relatively unimpaired. Ratios of regional to whole brain activity, measured by SPECT, showed significant reduction in the frontal lobes and in the left temporal lobe of MS patients. A relationship was found between left temporal abnormality in 99mTc-HMPAO uptake and deficit in verbal fluency and verbal memory. Finally, asymmetrical lobar activity indicated a predominant left rather than right temporo-parietal involvement.
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PMID:SPECT, MRI and cognitive functions in multiple sclerosis. 201 35

Magnetic resonance imaging (MRI) was performed on 36 children and two adults (with clinical presentation during childhood) with white-matter disease of the central nervous system. Abnormalities were readily demonstrated in patients with multiple sclerosis, acute disseminated encephalomyelitis, leucodystrophies and subacute sclerosing panencephalitis: MRI demonstrated the extent and distribution of abnormalities more clearly than computed tomography for all these disorders. The abnormalities tended to be asymmetrical and multifocal in multiple sclerosis and acute disseminated encephalomyelitis, and more confluent and symmetrical in the leucodystrophies. Children with clinically isolated optic neuritis had a significantly lower frequency of MRI brain-lesions than adults with the same disorder. MRI should be regarded as the radiological investigation of choice when white-matter disease is suspected in children.
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PMID:Magnetic resonance imaging of inflammatory and demyelinating white-matter diseases of childhood. 233 83

Nineteen patients with suspected multiple sclerosis (MS) and 28 control subjects were foveally stimulated by a small cross formed by rectangular red-light-emitting diodes. By means of crossed polarizers one eye was exposed only to the horizontal bar of the cross, the other to the vertical. Stimulus onset asynchrony ranged from 0 to +/- 300 ms (the horizontal bar preceding or following the vertical). The task was to indicate whether the horizontal or vertical bar had appeared first. Compared with normal subjects, MS patients exhibited much higher time thresholds (ranging from -150 to +130 ms) and had considerable interocular latency differences (up to 29 ms), indicating unilateral or asymmetrical impairment of the visual pathways. The psychophysical latency differences of the patients were compared to monocular latencies and interocular latency differences of the visually evoked cortical potential (VEP) obtained by foveal stimulation. Under the stimulus conditions chosen in this study, the diagnostic value of the psychophysical measurements was equal to or, for McAlpine's classes I and II of definite and probable MS patients, better than that based on VEP recordings.
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PMID:Foveal interocular time thresholds and latency differences in multiple sclerosis. 397 39

We report a 63-year-old female, case of multiple sclerosis associated with lateralization of bone change. In 1969, at age 38 she lost sight in her right eye. After that, she had several episodes of remission and exacerbation. In 1992, left hemiparesis, sensory disturbance and vesicorectal disturbance appeared, and she was admitted to our hospital. Immediately, steroid pulse-therapy was initiated then steroids were tapered. Her muscle strength recovered to some degree. The left upper limb showed low skin temperature, edema and decreased circulation. In January and September of 1993, bone examinations were conducted using multiple scanning X-ray photodensitometry. Osteopenia was observed, especially in the left hand. The bone density in the right hand changed slightly during the 8-month course of the illness, but osteopenia in the left hand became more marked. The asymmetrical bone change suggested that osteopenia results from a disorder of the central nervous system, especially through autonomic disorder.
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PMID:[A case of multiple sclerosis associated with lateralization of bone change]. 756 40

Clinical and MRI investigations were carried out on 27 patients with acquired pendular nystagmus in an attempt to delineate possible sites of lesions responsible for pendular nystagmus and mechanisms underlying the frequent ocular disconjugacy of this nystagmus. The aetiologies were multiple sclerosis (n = 21), brainstem stroke (n = 3) and other neurological conditions. In at least 59% of the patients, pendular nystagmus appeared > 1 year after the first symptom of the disease. Patients MRIs were characterized by multiple areas of abnormal signal and were analysed statistically to identify areas where lesions overlapped significantly between patients. Statistically significant overlap occurred in areas containing the red nucleus, the central tegmental tract, the medial vestibular nucleus and the inferior olive. Patients with horizontal pendular nystagmus showed predominantly pontine lesions whereas patients with torsional pendular nystagmus showed predominantly medullary involvement. The nystagmus was conjugate in 15 patients and disconjugate in amplitude or direction in 12. Internuclear ophthalmoplegia or asymmetrical visual acuity occurred in similar proportions in both groups. Patients with conjugate pendular nystagmus had a higher incidence of symmetrical, "mirror image' lesions on MRI than patients with disconjugate nystagmus. The abundance of abnormal MRI signals in our sample suggests that large or multiple structural lesions may be required to elicit pendular nystagmus, predominantly in the pons but also in the midbrain and medulla. The involvement of structures projecting to the inferior olive supports the hypothesis that oscillatory properties of olivary neurons causes the rhythm of pendular nystagmus. The delay observed between the onset of the underlying disease and the pendular nystagmus supports a mechanism operating via neural deafferentation. Disconjugancies in pendular nystagmus cannot be explained on the basis of the associated internuclear ophthalmoplegias nor on the basis of asymmetrical visual acuity. The association between symmetrical MRI lesions and conjugate nystagmus suggests that asymmetrical damage to brainstem structures concerned with binocular alignment may underlie disconjugate pendular nystagmus.
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PMID:Clinical and MRI correlates in 27 patients with acquired pendular nystagmus. 880 Sep 42

This report describes the observations of two patients with a several years' history of multiple sclerosis who presented sudden neurologic impairment. The symptomatology was suggestive of a non-convulsive partial status epilepsy. The clinical presentation was a paroxysmal dysphasic phenomenon in the first case without any consciousness impairment, associated with slight right hemiparesis. Electroencephalographic investigations revealed asymmetrical patterns, left-sided slow waves and periodic lateralized epileptiform discharges (PLEDs). Antiepileptic treatments were partially effective and intravenous steroids were needed for complete recovery. For the second patient, clinical presentation was acute psychiatric symptoms with disorientation, alternating manic symptomatology and mutism. Electroencephalography showed left fronto-central rhythmic continuous slow wave and spike wave activity. Intravenous antiepileptic treatment quickly improved the symptomatology. These observations draw attention to the fact that an epileptic cause should not be ruled out when a patient with multiple sclerosis presents sudden neurologic or psychiatric impairment. An early diagnosis allows immediate antiepileptic treatment. Intravenous steroids can be added to stop seizures.
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PMID:[Partial non-convulsive status epilepsy in multiple sclerosis]. 1067 21

MRI has facilitated diagnostic assessment of the corpus callosum. Diagnostic classification of solitary or multiple lesions of the corpus callosum has not attracted much attention, although signal abnormalities are not uncommon. Our aim was to identify characteristic imaging features of lesions frequently encountered in practice. We reviewed the case histories of 59 patients with lesions shown on MRI. The nature of the lesions was based on clinical features and/or long term follow-up (ischaemic 20, Virchow-Robin spaces 3, diffuse axonal injury 7, multiple sclerosis 11, hydrocephalus 5, acute disseminated encephalomyelitis 5, Marchiafava-Bignami disease 4, lymphoma 2, glioblastoma hamartoma each 1). The location in the sagittal plane, the relationship to the borders of the corpus callosum and midline and the size were documented. The 20 ischaemic lesions were asymmetrical but adjacent to the midline; the latter was involved in new or large lesions. Diffuse axonal injury commonly resulted in large lesions, which tended to be asymmetrical; the midline and borders of the corpus callosum were always involved. Lesions in MS were small, at the lower border of the corpus callosum next to the septum pellucidum, and crossed the midline asymmetrically. Acute disseminated encephalomyelitis and the other perivenous inflammatory diseases caused relatively large, asymmetrical lesions. Hydrocephalus resulted in lesions of the upper part of the corpus callosum, and mostly in its posterior two thirds; they were found in the midline. Lesions in Marchiafava-Bignami disease were large, often symmetrically in the midline in the splenium and did not reach the edge of the corpus callosum.
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PMID:Classification of acquired lesions of the corpus callosum with MRI. 1115 83

Autoimmune diseases are caused by self-reactive lymphocytes that have escaped deletion. Here we have determined the structure of the trimolecular complex for a T cell receptor (TCR) from a patient with multiple sclerosis that causes autoimmunity in transgenic mice. The structure showed a TCR topology notably different from that of antimicrobial TCRs. Rather than being centered on the peptide-major histocompatibility complex, this TCR contacted only the N-terminal peptide segment and made asymmetrical interactions with the major histocompatibility complex helices. The interaction was dominated by the hypervariable complementarity-determining region 3 loops, indicating that unconventional topologies are possible because of the unique complementarity-determining region 3 sequences created during rearrangement. This topology reduces the interaction surface with peptide and alters the geometry for CD4 association. We propose that unusual TCR-binding properties can permit autoreactive T cells to escape deletion.
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PMID:Unconventional topology of self peptide-major histocompatibility complex binding by a human autoimmune T cell receptor. 1584 98

Magnetic resonance imaging (MRI) is the most important paraclinical test in the diagnosis of multiple sclerosis (MS) and for delineating its natural history. We investigate MRIs from a longitudinal study of 24 relapsing-remitting MS patients who had monthly MRI examinations for one year, and were not receiving active MS therapy during this period. We hypothesized that lesions occur randomly throughout the brain, and that patients are homogeneous with regard to spatial patterns of lesion presentation. We recorded the numbers and locations of enhancing lesions and hypointense lesions (black holes) in all scans, and found asymmetrical patterns of lesions about the mid-transaxial, mid-coronal, and mid-sagittal planes. Furthermore, in distinct subsets of patients, enhancing lesions and black holes tend to occur in the same locations. Clustering in lesion locations may be of functional significance, with consequent therapeutic implications.
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PMID:Asymmetries in the spatial distributions of enhancing lesions and black holes in relapsing-remitting MS. 1624 86


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