Gene/Protein Disease Symptom Drug Enzyme Compound
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Query: UMLS:C0030552 (paresis)
 5,831 document(s) hit in 31,850,051 MEDLINE articles (0.00 seconds)

Two patients with findings ascribable to superior branch oculomotor nerve paresis and one patient with findings ascribable to an inferior branch paresis are described. In each patient the paresis was caused by an intra-axial midbrain lesion. These patients represent the first described cases of divisional oculomotor nerve paresis caused by intrinsic brainstem disease.
Ann Neurol 1989 Dec
PMID:Divisional oculomotor nerve paresis caused by intrinsic brainstem disease. 225 73

A case is described in which a presumed vascular accident resulted in long-standing visual difficulties in both reading and the analysis of vectors of moving objects. Clinical examination revealed minimal right optic atrophy with a relative superior altitudinal visual field defect associated with a positive Pulfrich effect. A partial head turn to the right in association with paresis of saccades and pursuit eye movements to the right was also evident. Spectacles for distance which incorporated a neutral density filter before the left eye were prescribed. These practically eliminated the Pulfrich effect and alleviated the problems of vector analysis. A near correction was provided which incorporated prisms with bases to the right. This eliminated the reading difficulties. The visual problems experienced by patients suffering from a positive Pulfrich effect are described and discussed.
Br J Ophthalmol 1989 Dec
PMID:The Pulfrich phenomenon and its alleviation with a neutral density filter. 261 Nov 82

From 1969-1985, 106 people contracted tetanus in Finland. The outcome of the disease was good in 78 cases (returned to work), poor in 27 (12 died, 5 institutionalized and 10 retired) and unknown in 1. Poor outcome was the result of a disease requiring respirator treatment. Other clinical factors significantly correlated with poor outcome were blood pressure lability, hyperglycemia, hyperthermia, tachycardia and anticoagulation therapy. Forty people who were representative of the whole series with regard to sex, age and severity of disease attended a follow-up study on average 7 years and 4 months later. Forty age- and sex-matched controls had the same examinations, and compared with them, the 40 patients still had significantly more muscle fatigue and cramps, nervousness, decreased mental capacity and difficulties in balance, speech and memory. They also had more clinical findings, such as peripheral paresis, muscular atrophy, decreased or absent tendon reflexes and decreased mental capacity than the controls.
Acta Neurol Scand 1989 Dec
PMID:Outcome and neurological sequelae of patients after tetanus. 261 76

Moebius syndrome is usually sporadic. The few familial cases reported in the literature have autosomal dominant inheritance, with absence of the associated congenital malformations often described in the sporadic form. Here we report two families with more than one member affected by congenital, unilateral paresis of cranial nerves, transmitted with autosomal dominant inheritance.
Acta Neurol (Napoli) 1989 Dec
PMID:Congenital oculo-facial paralysis (Moebius syndrome): evidence of dominant inheritance in two families. 261 29

Four hundred twenty-nine patients with bacterial meningitis were assigned on a nonselective alternating basis into one of two therapeutic regimens. Patients in Group I received dexamethasone in addition to standard antibacterial chemotherapy of ampicillin and chloramphenicol whereas those in Group II received antibacterial chemotherapy alone. Dexamethasone was given intramuscularly (8 mg to children younger than 12 years and 12 mg to adults every 12 hours for 3 days). Both treatment groups were comparable with regard to age, sex, duration of symptoms and state of consciousness at the time of hospitalization. A significant reduction in the case fatality rate (P less than 0.01) was observed in patients with pneumococcal meningitis receiving dexamethasone; only 7 of 52 patients died compared with 22 of 54 patients not receiving dexamethasone. A reduction in the overall neurologic sequelae (hearing impairment and paresis) was observed in patients receiving dexamethasone. This reduction was significant only in patients with Streptococcus pneumoniae meningitis; none of the 45 surviving patients receiving steroids had hearing loss whereas 4 of 32 patients not receiving dexamethasone had severe hearing loss (P less than 0.05). No significant difference was observed between the two groups with regard to time for patients to become afebrile or to regain consciousness or in the mean admission and 24- to 36-hour cerebrospinal fluid leukocyte count, glucose or protein content.
Pediatr Infect Dis J 1989 Dec
PMID:Dexamethasone treatment for bacterial meningitis in children and adults. 262 85

In 1986 in the CSR 978 cases of acute meningoencephalitis were notified, incl. 184 in the capital. In a group of 129 patients aged 1 to 63 years hospitalized at the First Clinic for Infectious Diseases in Prague-Bulovka (Paediatric Faculty Charles University) in 1986 the authors investigated the clinical course of acute meningoencephalitis in relation to the causal agent of the disease. The aetiological agent was assessed by isolation from cerebrospinal fluid or by isolation from faeces with the corresponding antibody response, or by serological examination only. In children under 15 years of age the etiological agent was assessed in 36%, in adults in 65%. In the investigated group, contrary to previous years (3), tick-borne encephalitis was involved which accounted for the majority of severe cases of the disease. The severe clinical course, manifested at first by symptoms of cerebral oedema with impaired consciousness, is more frequent with advancing age. In adults tick-borne encephalitis had a severe course in one third of the patients. In the other age groups the development was favourable, in particular in the group of children aged 4-10 years. As compared with previous years, there was no fatal case, no permanent paresis as a complication of the disease (2).
Cas Lek Cesk 1989 Dec 08
PMID:[The clinical picture and etiology of meningoencephalitis in hospitalized patients in 1986]. 263 95

Any attempt to classify and to understand the basic mechanism underlying the neurological symptoms as pyramidal and/or sensitive, should start from the fundamental laws of nervous system functioning: 1) the law of reciprocal innervation of Sherrington; 2) the law of hierarchy of levels of Jackson and 3) the law of supersensitivity of deafferented structures of Cannon. Paresis on one side, Jacksonian jerks on the other side represent two opposite conditions known respectively as negative and positive symptoms of corticomotor involvement. Unluckly involuntary movements cannot be explained with these three laws. They are the clinical expression of the disorganization and disintegration of functions: a true disregulation unrespectful of laws and general principles. They must be considered as the result of conflicts of antagonist functions controlling each other, i.e. tremor, chorea, myoclonus, torsion spasm etc. The author emphasizes the clinical-descriptive aspect of the problem.
Recenti Prog Med 1989 Dec
PMID:[Involuntary movements]. 269

Is characterized by several various signs. One of these, spasticity, involves a velocity dependent increase in muscle stiffness during stretch and by hyperactive tendon jerks. When intense, spasticity impedes residual strength in antagonistic muscles and interferes with attempts to move, especially if complicated by clonus and/or spasms. Assessment of spasticity is multifactorial and implies clinical as well as instrumental methods. The pathophysiological mechanisms responsive for the hyperexcitability of the myotatic reflex can be studied by methods of clinical neurophysiology. It appears that there are various factors involved at the spinal level, involving reduction in both pre- and post-synaptic inhibitions. Although spasticity is not responsible for the major part of the disability imposed by upper motor neurone syndrome, it should be reduced. The therapeutic methods are medical, surgical or from physical medicine. In many cases, the results have been validated by blind studies. As paresis is the most disabling effect, it would be worthwhile to develop drugs able to reduce spasticity and increase muscle strength at the same time. Recent trials suggest than TRH-T may be effective in this regard.
Recenti Prog Med 1989 Dec
PMID:[Pyramidal syndrome: its physiopathology and treatment]. 269 2

A 91-year-old man presented with the sudden onset of coma, vertical gaze paresis, and transient disturbance of horizontal gaze, with fixed but unequal pupils. Both cranial computed tomography and postmortem study documented infarction of the paramedian thalamus bilaterally and of the ventral mesencephalon, accounted for by presumably embolic occlusion of a single artery. This artery arose as an unpaired perforating artery originating from the proximal segment of one posterior cerebral artery and thus conformed to the variant anatomic configuration associated with such infarcts as described by Percheron.
J Clin Neuroophthalmol 1985 Dec
PMID:Neuro-ophthalmological findings with neuropathological correlation in bilateral thalamic-mesencephalic infarction. 293 25

The case of a 42-year-old man is reported, who on four occasions developed a hypokalaemic periodic paralysis after an intramuscular injection of "Ambene". The detailed examination of this patient shows, that it is the primary, autosomal dominant inherited form of hypokalaemic periodic paralysis, and not the secondary form, which is caused by a renal or gastrointestinal loss of potassium. Clinical and electrophysiological, as well as histopathological and electron microscopic findings are presented, showing the typical vacuolar myopathy with submicroscopic tubular structures. In the literature there is evidence for an increased sensitivity of the muscle membrane to insulin with an increased potassium-shift inside the cell in hypokalaemic periodic paralysis. "Ambene" is a combination, which contains amongst other substances dexamethasone and the local anaesthetic drug lidocain. In the present case the paresis was possibly caused by a combined effect of dexamethasone with a consequent hyperglycaemia and lidocain with a change in the excitability of the muscle membrane. The pathophysiological mechanism of hypokalaemic periodic paralysis is discussed in terms of the release by the combination of these two drugs. It has not previously been reported that "Ambene" can provoke a hypokalaemic periodic paralysis. This is a severe side effect because of the resulting cardiac and respiratory problems.
Nervenarzt 1985 Dec
PMID:[Hypokalemic periodic paralysis provoked by "Ambene"]. 293 67


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