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Query: UMLS:C0030552 (paresis)
 5,831 document(s) hit in 31,850,051 MEDLINE articles (0.00 seconds)

The anterior tarsal tunnel syndrome, first described in 1968 by Marinacci, is characterized by a compression of the deep peroneal nerve under the inferior extensor retinaculum. The patients complaint of pains on the dorsum of the foot, especially at night. Clinically result sensory deficits in the involved area between the first and second toes as well as paresis and atrophy of the extensor digitorum brevis. The distal latency of the deep peroneal nerve is increased, the EMG shows active and chronic denervation of the extensor digitorum brevis. In cases with partial anterior tarsal tunnel syndrome only the motoric branch to the extensor digitorum brevis or only the sensory branch of the deep peroneal nerve after the division under the inferior extensor retinaculum is compressed. Two cases with complete and one with partial anterior tarsal tunnel syndrome are presented, etiology, symptomatology, differential diagnosis and therapeutic possibilities are discussed.
J Neurol 1977 Dec 01
PMID:The anterior tarsal tunnel syndrome. 7 54

Beta-2-microglobulin was measured in specimens of cerebrospinal fluid (CSF) collected from 167 patients classified in 14 diagnostic categories at an outpatient Department of Neurology. In the control group of 29 subjects without any obvious disease of the nervous system, the concentration of beta-2-microglobulin was 1.15 +/- 0.37 mg/1 (M +/- s.d.). The concentration was almost significantly elevated in the groups with fresh brain infarct, central nervous system infection, and polyneuropathy. The serum concentrations of beta-2-microglobulin did not differ significantly among these diagnostic categories. The mean ratio between CSF and serum beta-2-microglobulin was 0.79 +/- 0.32 in the control group and more than 1.0 in the patients with brain infarcts, CNS infections and spinal paresis, but the differences were not statistically significant.
Acta Neurol Scand 1978 Dec
PMID:Cerebrospinal fluid beta 2-microglobulin in neurological disorders. 8 13

Centronuclear myopathy, which is unusual because of clinical myotonia, is described in two sisters. The diagnosis was established in adult life, but the first symptoms were noticed in infancy. The outstanding points of the clinical picture were mild amyotrophy, paresis, and clinical myotonia.
J Neurol Neurosurg Psychiatry 1978 Dec
PMID:Myotonia in centronuclear myopathy. 15 83

Report on peripheral nerve lesions due to total replacement of the hip-joint based on the literature and the authors' own experience. In 15 patients our diagnosis was made on clinical and electromyographic evidence. 16 endoprostheses had been inserted. The femoral nerve was involved on 12 occasions, the sciatic in 5, the glutei in 5, the obturator in 2, the lateral cutaneous femoris in 2 and the posterior cutaneous in 1 instances. One has to count on about 1% of such lesions. This type of paresis has to be distingushed from pseudopareses for which electromyography was proved very effective. Damage due to overstretching is probably the main cause. Treatment with thorough physiotherapy and faradic stimulation is needed. When this is done the prognosis is generally favourable. In some cases, however, these complications may limit the success of the operation and postoperative disability may be worse than before.
Z Orthop Ihre Grenzgeb 1975 Dec
PMID:[Peripheral nerve injury due to total replacement of the hip-joint (author's transl)]. 17 2

The risk of facial nerve paresis after parotidectomy is thought to be within acceptable limits, although it is difficult to find published data regarding the specific magnitude of this risk. This study reviews the subject and reports postoperative facial function in 100 consecutive patients who had parotidectomies at the Henry Ford Hospital during a 9-year period. Permanent weakness of a major branch was identified in 2 of 77 patients having lateral lobectomy for parotid disease. Both patients demonstrated marginal mandibular paresis after surgery for adenolymphoma. No weakness was noted in 16 patients undergoing total parotidectomy. No unanticipated nerve disability was noted in 4 patients having partial nerve sacrifice in extended procedures; 3 patients had complete sacrifice of the nerve.
Laryngoscope 1979 Dec
PMID:Facial nerve function in 100 consecutive parotidectomies. 22 63

A synthetic biologically active derivative of vitamin D (350 microgram of 1alpha-hydroxycholecalciferol [1alpha(OH)CC]) was injected into 2 nonlactating 7-year-old Israeli-Friesian cows. Plasma calcium values increased after 24 hours, peaked at 48 hours, and returned to base-line values 120 hours after injection. An injection of 350 microgram of 1alpha(OH)CC was given to 23 parturient-paresis-prone Israeli-Friesian cows from 7 days to 6 hours prepartum; 13 cows were injected once, 6 were injected twice, and 4 were injected 3 times, all at 48-hour intervals. Parturient-paresis-prone cows (n = 23) of the same breed were used as controls. Within 0 to 36 hours postpartum, plasma calcium concentrations were found to be higher in cows injected with 1alpha(OH)CC than in the control cows. The increase was highly significant (P less than 0.01) in cows injected at least twice. None of the cows injected with 1alpha(OH)CC, within 72 to 24 hours prior to calving developed parturient paresis; but 9 of 23 control cows developed parturient paresis. Prior to calving, none of the injected cows developed hypercalcemia and there was no local or systemic clinically detectable signs of toxiosis. When given at the right time prepartum, 1alpha(OH)CC is considered to be an improvement over previous methods of preventing bovine parturient paresis.
Am J Vet Res 1977 Dec
PMID:Use of 1alpha-hydroxycholecalciferol in the prevention of bovine parturient paresis. 24 72

Errors of visual egocentric localization are well-known in patients with paresis of ocular muscles or paresis of conjugate gaze. In the present paper a series of patients with unilateral vestibular disorder disclosed a constant lateralization of the visual agocentre in the absence of any ocular paresis. The perceptual illusion is associated with an altered resting position of the eyes caused by the vestibular imbalance. The disturbance of visual, egocentric localization was revealed only after elimination of the visual frame of reference and the extent of lateralization of the visual egocentre was proportional to the degree of resting deviation of the eyes. Although the findings are of limited clinical importance they have a considerable theoretical interest. From the clinical point of view they may provide a basis for further understnading of the complex-perceptual illusions which may accompany disorders affecting central vestibulo-ocular connections. The results indicate that the perceptual effects are related to an altered central evaluation of the oculomotor programme and thus depend upon the operation of an 'efference copy'. This hypothesis is discussed with reference to earlier and current theories of visual localization.
Brain 1979 Dec
PMID:Constant error of visual egocentric orientation in patients with acute vestibular disorder. 31 10

Diseases of the central nervous system (CNS) occurring during treatment of acute lymphoblastic leukemia (ALL) may be of leukemic or nonleukemic origin. Well known examples for CNS disease of nonleukemic origin are somnolence following prophylactic CNS irradiation, methotrexate-induced encephalopathy and acute infections caused by bacteria, viruses and toxoplasma gondii. Less known is the fact that also subacute CNS infections may occur in patients undergoing cytostatic therapy. Progressive multifocal leukoencephalopathy and subacute sclerosing panencephalitis (SSPE) are examples of this category of disease. Up to now 11 well documented cases of SSPE were reported occurring during treatment of ALL. Main clinical features were disorders of behaviour, consciousness and speach, seizures, paresis and inappropriate secretion of ADH. Several authors were able to demonstrate a deficiency of cellular immunity in patients with SSPE. In some cases this deficiency was consistent with reduced reactivity of T-lymphocytes against measles antigen only. The presence of inhibiting factors may be responsible for this phenomenon. Other authors found a normal or increased function of cellular immunity in SSPE; In hamsters occurrence of SSPE is induced by the simultaneous injection of hamster-adapted SSPE virus and antihamster lymphocyte serum. We, therefore, conclude that also in humans SSPE appearing during treatment of ALL is due to immunosuppression.
Monatsschr Kinderheilkd 1978 Dec
PMID:[Non-leukemic disease of the central nervous system in children with acute lymphoblastic leukemia. III. Subacute sclerosing panencephalitis (author's transl)]. 36 90

For the fiftieth anniversary of Berger's first EEG publication, some of his early recordings obtained between 1924 and 1931 are discussed and illustrated. Examples of his protocols from the Freiburg Berger Archives are reproduced. Three types of Berger's early investigations are described: (1) String-galvanometer recordings obtained between 1924 and 1926, mainly from trephined patients with cerebral diseases, which usually showed brain waves slowed to 6--8 per second; (2) Direct recordings from the cortex and white matter proving the cortical origin of the EEG in 1930; (3) Typical unpublished EEG recordings of epileptics and of petit-mal attacks obtained in 1930 and 1931. Berger's first six papers published between 1929 and 1933 described nearly all the main EEG findings of cerebral diseases and the EEG alterations of normals during attention, sleep, and narcosis, but they did not report on convulsive potentials in the EEGs of epileptics. Berger had, however, obtained excellent records of epileptic EEG features, here depicted in Figs. 4 through 7. These remained unpublished until 1933 and 1938, because Berger suspected that they contained artifacts caused by blinks and facial movements which he had recorded in his controls (Fig. 4). Only in 1933, after other authors had described large amplitudes of convulsive potentials in the cortex of animals, did Berger publish parts of the EEGs of a petit-mal attack and of focal attacks in progressive paresis. In 1938, Berger presented the EEG of the beginning of a petit-mal attack with large 3/s spikes and waves recorded in 1931 which were similar to those described by Gibbs and coworkers in 1935. In 1933 and 1938, Berger interpreted the abnormal brain potentials of epileptics as signs of a preconvulsive state of the forebrain and suggested that the periods of 3/s waves were cortical correlates of an epileptic absence.
Arch Psychiatr Nervenkr (1970) 1979 Dec
PMID:[Fiftieth anniversary of Hans Berger's publication of the electroencephalogram. His first records in 1924--1931 (author's transl)]. 39 91

The occurrence of unilateral phrenic nerve injury with the resultant hemidiaphragm paralysis or paresis can cause significant respiratory distress or respiratory failure in infants and children. An early bedside diagnosis of this problem will allow appropriate therapy and prevent needless diagnostic procedures. With the patient in the lateral decubitus position and the paralyzed side up, accentuated paradoxical inspiratory inward epigastric motion ipsilateral to the paralyzed hemidiaphragm can be seen. With the paralyzed hemidiaphragm down, abdominal motion appears to be normal as if the paralyzed hemidiaphragm were plicated. Thus, ventilation may be improved by changing body position as well as instituting ventilatory support while the potential for phrenic nerve recovery is evaluated.
Crit Care Med 1979 Dec
PMID:A physiological approach to hemidiaphragm paralysis. 50 71


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