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At least 37 records · Page 2Linked to original sources
PubMed1998

Masked bilateral superior oblique muscle paresis. A simple overcorrection phenomenon?

OBJECTIVE: This study aimed to determine a mechanism by which the masked bilateral superior oblique muscle paresis phenomenon may be explained. DESIGN: A retrospective study of the authors' patients with the preoperative diagnosis of a unilateral superior oblique muscle paresis was performed. Patients in whom an apparent contralateral superior oblique muscle paresis developed after surgery (masked bilateral superior oblique muscle paresis) were compared with those patients in whom this condition did not develop. PARTICIPANTS: One hundred eight patients participated. RESULTS: Of the 108 patients studied, 30 (27.7%) patients had signs of an apparent superior oblique muscle paresis develop in the contralateral eye after surgery. In comparing those patients in whom an apparent contralateral superior oblique muscle paresis did develop after surgery with those patients in whom this finding did not develop, no significant differences were found in the age at surgery; etiology (traumatic vs. nontraumatic); average hyperdeviations in primary gaze, ipsilateral and contralateral gazes, and ipsilateral and contralateral head tilts; average V pattern; inferior and superior oblique muscle function; extorsion on double Maddox rod testing; and objective fundus extorsion. CONCLUSION: Analysis of the authors' data showed that a surgical overcorrection of a unilateral superior oblique muscle paresis can masquerade as an apparent contralateral superior oblique muscle paresis. This is caused by a persistence of the head tilt and side gaze misalignment pattern from the original superior oblique muscle paresis.

Adult↗
PubMedDate not supplied

Pharyngeal swallowing in patients with paresis of the recurrent nerve.

Pharyngolaryngeal function during swallowing was investigated cineradiographically in 22 patients with paresis of the recurrent nerve. Nineteen of these patients (86%) had defective closure of the laryngeal vestibule: 10 patients had defective apposition of the corniculate cartilages, (paresis of the oblique cricoarytenoid muscle), 9 patients had defective apposition of the arytenoid cartilages, (paresis of the interarytenoid muscle), 13 patients had defective movement of the epiglottis (paresis of, i.a. the thyrohyoid muscle), 1 patient had defective closure of the subepiglottic portion of the vestibule (paresis of the thyroepiglottic muscle), 2 patients had defective closure of the supraglottic portion of the vestibule (paresis of the superior ventricular segment of the thyroarytenoid muscle). Five patients with immobility of the epiglottis also had paresis of the pharyngeal constrictor musculature indicating paresis of the superior laryngeal nerve. Our investigation has shown that patients with paresis of the recurrent nerve who present with dysphagia with or without aspiration should be examined cineradiographically for pharyngolaryngeal function during swallowing.

Adult↗
PubMed2004

Abductor sign: a reliable new sign to detect unilateral non-organic paresis of the lower limb.

OBJECTIVES: To test a new neurological sign, the "abductor sign," which can distinguish between organic and non-organic leg paresis using synergic movements of the bilateral hip abductors. METHODS: The subjects were 33 patients presenting with paresis of one leg, 17 of organic origin and 16 of non-organic origin (hysteria). To test the abductor sign, the examiner told the patient to abduct each leg, and opposed this movement with his hands placed on the lateral surfaces of the patient's legs. The leg contralateral to the abducted one showed opposite actions for organic paresis and non-organic paresis: for example, when the paretic leg was abducted, the sound leg stayed fixed in organic paresis, but moved in the hyperadducting direction in non-organic paresis. Hoover's sign was used for comparison in the same patients. RESULTS: The abductor sign gave the correct classification for all 33 cases. Hoover's sign was reliable if the results were carefully interpreted, but it was non-diagnostic for 16 patients because of strong hip extensors and in two because of strong hip flexors. Two patients with non-organic paresis succeeded in tricking the examiner by pretending full effort to lift the paretic leg. CONCLUSIONS: The abductor sign is a useful test to detect non-organic paresis, because (1) it is difficult for a hysterical patient to deceive the examiner, (2) the hip abductor is one of the most commonly involved muscles in pyramidal weakness, and (3) the results are easily visible as movement or non-movement of the unabducted leg.

Adult↗
PubMed1989

Motor paresis improved by sympathetic block. A motor form of reflex sympathetic dystrophy?

Four patients had a characteristic motor paresis that was dramatically improved by sympathetic block. The cause of this paresis could not be determined by the usual neurological examinations. It was similar to reflex sympathetic dystrophy in that the patients experienced severe pain, swelling, coldness, and muscle atrophy in the affected limbs or other parts of the body in the course of their illness. However, the motor paresis could precede the pain or develop after the pain had disappeared. Even in the absence of pain, the motor paresis was exacerbated by sympathetic stimulation using epinephrine, norepinephrine (nor-adrenalin), or isoproterenol hydrochloride (Proternol) loading and was improved by regional intravenous infusion of reserpine or by sympathetic ganglion block. Loading with pilocarpine, atropine sulfate (Bosmin), and edrophonium chloride (Antirex) did not influence the paresis. This motor paresis is thought to be due to abnormally increased sympathetic tone and may be considered a motor form of reflex sympathetic dystrophy. However, motor paresis closely related to sympathetic dysfunction is quite a new condition that we call "sympathetic motor paresis." This is important clinically because a long-standing effect can be expected from permanent sympathetic ganglion block with dehydrated ethanol.

Adult↗
PubMed2006

Mime therapy improves facial symmetry in people with long-term facial nerve paresis: a randomised controlled trial.

QUESTION: What is the effect of mime therapy on facial symmetry and severity of paresis in people with facial nerve paresis? DESIGN: Randomised controlled trial. PARTICIPANTS: 50 people recruited from the Outpatient department of two metropolitan hospitals with facial nerve paresis for more than nine months. INTERVENTION: The experimental group received three months of mime therapy consisting of massage, relaxation, inhibition of synkinesis, and co-ordination and emotional expression exercises. The control group was placed on a waiting list. OUTCOME MEASURES: Assessments were made on admission to the trial and three months later by a measurer blinded to group allocation. Facial symmetry was measured using the Sunnybrook Facial Grading System. Severity of paresis was measured using the House-Brackmann Facial Grading System. RESULTS: After three months of mime therapy, the experimental group had improved their facial symmetry by 20.4 points (95% CI 10.4 to 30.4) on the Sunnybrook Facial Grading System compared with the control group. In addition, the experimental group had reduced the severity of their paresis by 0.6 grade (95% CI 0.1 to 1.1) on the House-Brackmann Facial Grading System compared with the control group. These effects were independent of age, sex, and duration of paresis. CONCLUSION: Mime therapy improves facial symmetry and reduces the severity of paresis in people with facial nerve paresis.

Adult↗
PubMed2004

Delayed facial nerve paresis following acoustic neuroma resection and postoperative vasoactive treatment.

OBJECT: Delayed facial nerve paresis is a well known clinical phenomenon following acoustic neuroma surgery, typically occurring early during the postoperative course. The clinical course of the delayed facial nerve paresis and intraoperative electromyographic (EMG) signals were evaluated in a subgroup of patients who underwent vasoactive treatment for preservation of hearing and developed secondary deterioration after termination of treatment. METHODS: Between 1990 and 2001 seven patients were identified who received vasoactive treatment for preservation of hearing and developed a delayed facial nerve paresis after termination of medication. Intraoperative facial nerve EMG activity was analyzed in six patients. RESULTS: All patients developed a delayed facial nerve paresis between 2-5 days following termination of a 10 day treatment consisting of HES and nimodipine. Medication was re-initiated and the facial nerve paresis improved in all patients. In two patients intraoperative EMG signals revealed "A-trains" waveform patterns, which are highly suggestive for an immediate postoperative facial nerve paresis, whereas in four patients no pathognomonic EMG patterns could be recorded. CONCLUSIONS: The delayed onset of a facial paresis following termination of vasoactive treatment points to a disturbed microcirculation of the nerve as the main pathophysiological feature. Two groups could be identified on the basis of intraoperative EMG activity. In one group with presence of "A-trains" medication apparently masked the onset of an immediate postoperative facial nerve deficit. Four patients without "A-trains" did not develop a typical delayed facial nerve paresis during vasoactive treatment, but thereafter. The time lag between termination of treatment and onset of a delayed palsy points to a protective effect due to improved microcirculation.

Adult↗
PubMed2002

Motor mechanisms of vertical fusion in individuals with superior oblique paresis.

PURPOSE: We wanted to determine the mechanisms of motor vertical fusion in patients with superior oblique paresis and to correlate these mechanisms with surgical outcomes. METHODS: Ten patients with superior oblique paresis underwent 3-axis, bilateral, scleral search coil eye movement recordings. Eye movements associated with fusion were analyzed. RESULTS: Six patients had decompensated congenital superior oblique paresis and 4 had acquired superior oblique paresis. All patients with acquired superior oblique paresis relied predominantly on the vertical rectus muscles for motor fusion. Patients with congenital superior oblique paresis were less uniform in their mechanisms for motor fusion: 2 patients used predominantly the oblique muscles, 2 patients used predominantly the vertical recti, and 2 patients used predominantly the superior oblique in the hyperdeviated eye and the superior rectus in the hypodeviated eye. The last 2 patients developed the largest changes in torsional eye alignment relative to changes in vertical eye alignment and were the only patients to develop symptomatic surgical overcorrections. CONCLUSION: There are 3 different mechanisms for vertical fusion in individuals with superior oblique paresis, with the predominant mechanism being the vertical recti. A subset of patients with superior oblique paresis uses predominantly the superior oblique muscle in the hyperdeviated paretic eye and the superior rectus muscle in the fellow eye for fusion. This results in intorsion of both eyes, causing a large change in torsional alignment. The consequent cyclodisparity, in addition to the existing vertical deviation, may make fusion difficult. The differing patterns of vertical fusional vergence may have implications for surgical treatment.

Adolescent↗
PubMed1999

Divergence paresis: a nonlocalizing cause of diplopia.

OBJECTIVES: To determine the causes, clinical characteristics, and localizing value of divergence paresis, which is characterized by acquired and uncrossed diplopia when viewing distant targets, fusion when viewing near targets, and no limitation of ocular ductions. Controversy persists regarding the diseases underlying divergence paresis and the existence of a divergence "center." MATERIALS AND METHODS: The charts of 15 patients with divergence paresis examined between 1983 and 1998 were reviewed. All patients underwent neuroimaging and detailed ocular motility testing, with measurement of esotropia in prism diopters in 14 patients. RESULTS: Divergence paresis in 15 patients was idiopathic in three patients, was associated with central nervous system microangiopathy or infarct in seven patients, and clivus lymphoma, chronic lymphocytic leukemia with sinusitis, Wernicke ophthalmoplegia, Parkinson disease, myasthenia gravis, cryptic cerebellar vascular malformation, and childhood esotropia in one patient each (two patients had two diagnoses). The mean maximum esotropia was 10.4 prism diopters, and there was no significant correlation (Fisher exact test) between the magnitude of esotropia and vasculopathic etiology or posterior fossa lesion site. Although six patients had posterior fossa disease, neuroimaging showed no common circumscribed lesion site or evidence of increased intracranial pressure. CONCLUSIONS: Divergence paresis is an uncommon cause of acquired diplopia. Divergence paresis is associated with diverse central nervous system diseases and can be mimicked by myasthenia. The absence of a single consistent lesion in our study, which is the largest reported series, suggests that divergence paresis is a nonlocalizing cause of horizontal diplopia and that multiple or diffusely distributed neural structures may govern divergence. Alternatively, elusive divergence "centers" may not exist, and divergence paresis may arise from impaired inhibition or from defective passive antagonism of orbital structures to convergence.

Adolescent↗
PubMed2001

Abduction paresis with rostral pontine and/or mesencephalic lesions: Pseudoabducens palsy and its relation to the so-called posterior internuclear ophthalmoplegia of Lutz.

BACKGROUND: The existence of a prenuclear abduction paresis is still debated. METHODS: In a retrospective design, we identified 22 patients with isolated unilateral (n = 20) or bilateral (n = 2) abduction paresis and electrophysiologic abnormalities indicating rostral pontine and/or mesencephalic lesions. Another 11 patients had unilateral abduction paresis with additional ocular motor abnormalities indicating midbrain dysfunction. Eight of these 11 patients also had electrophysiological abnormalities supporting this location. Electrophysiological examinations in all patients included masseter and blink reflexes (MassR, BlinkR), brainstem auditory evoked potentials (BAEP), and direct current elctro-oculography (EOG). RESULTS: Unilateral MassR abnormalities in patients with unilateral abduction paresis were seen in 17 patients and were almost always (in 16 of 17 patients) on the side of the abduction paresis. Another 11 patients had bilateral MassR abnormalities. BlinkR was always normal. EOG disclosed slowed abduction saccades in the non-paretic eye in 6 patients and slowed saccades to the side opposite to the abduction paresis in another 5 patients. Re-examinations were done in 27 patients showing normalization or improvement of masseter reflex abnormalities in 18 of 20 patients and in all patients with EOG abnormalities. This was always associated with clinical improvement. CONCLUSIONS: Electrophysiologically documented or clinically evident rostral pontine and/or mesencephalic lesions in our patients exclude an infranuclear intrapontine 6th nerve lesion and indicate the existence of an abduction paresis of prenuclear origin. An increased tone of the antagonistic medial rectus muscle during lateral gaze either by abnormal convergence or impaired medial rectus inhibition seems most likely.

Abducens Nerve Diseases↗
PubMed1988

Use of 24-F-1,25-dihydroxyvitamin D3 to prevent parturient paresis in dairy cows.

Forty-one aged Jersey cows were fed a high Ca diet prior to parturition to predispose them to parturient paresis. Twenty-one of the cows were treated with 24-F-1,25-dihydroxyvitamin D3, a synthetic analogue of 1,25-dihydroxyvitamin D3, 7 d before the expected parturition. Treated cows received either 100 micrograms (n = 7) or 150 micrograms (n = 14) of 24-F-1,25-dihydroxyvitamin D3, intramuscularly at 7-d intervals until the cow calved. Incidence of parturient paresis among untreated animals was 85% (17/20). Injections of 100 micrograms of 24-F-1,25-dihydroxyvitamin D3 reduced the incidence of parturient paresis to 43% (3/7), whereas 150 micrograms injections of 24-F-1,25-dihydroxyvitamin D3 reduced the incidence of parturient paresis to 29% (4/14). Plasma concentrations of hydroxyproline were not elevated prior to parturition in 24-F-1,25-dihydroxyvitamin D3-treated cows, indicating that treatment did not stimulate bone resorption and that the ability of 24-F-1,25-dihydroxyvitamin D3 to prevent parturient paresis likely resides in its ability to stimulate intestinal Ca absorption prior to parturition. Further, cows treated with 24-F-1,25-dihydroxyvitamin D3 that developed parturient paresis had lower than normal plasma concentrations of 1,25-dihydroxyvitamin D, indicating that 24-F-1,25-dihydroxyvitamin D3 treatment impairs the metabolism of 25-hydroxyvitamin D in response to hypocalcemia. These data suggest that injection of 24-F-1,25-dihydroxyvitamin D3, delivered at 7-d intervals prior to parturition, can effectively reduce incidence of parturient paresis in dairy cows.

Animals↗
PubMed1978

The prophylactic use of vitamin D3 in parturient paresis in the cow in a practice district in eastern Norway. A retrospective investigation.

The prophylactic effect in parturient paresis of an intramuscular injection of 10 million i.u. vitamin D3 one week prior to the expected calving date, was investigated in 84 cows which had previously suffered from parturient paresis. Clinical observations in connection with the development of parturient paresis after injection of vitamin D3 were compared with corresponding observations made on cows within the same population at the previous calving when no vitamin D3 was administered. The incidence of clinical parturient paresis in cows given vitamin D3 was 44.3 per cent. There were no significant differences in the incidence of parturient paresis in cows injected with vitamin D3 during the periods less than 2, 2--4, 5--8 and greater than 8 days before parturition. Average plasma calcium levels (mg/100 ml) before first calcium treatment, results of treatment, and the incidence of retained placenta in vitamin D3 injected cows did not differ significantly from corresponding data for cows with clinical parturient paresis which had not been given vitamin D3 before calving. It is concluded that vitamin D3 does not have any prophylactic effect in parturient paresis in cows in Eastern Norway.

Animals↗
PubMed1994

[Atypical sciatica. Decreasing pain and increasing paresis--a serious sign].

During the last seven years 14 patients with lumbar disc hernias were admitted who presented with a short period of sciatica before experiencing relief of pain accompanied by paresis. Ten patients had marked paresis and were operated on, most of them during the first week after the start of paresis. Three patients had minor paresis in regression, and one patient suffered complete paralysis for five months. These four patients were not operated on. Motor function improved significantly in nine out of ten operated patients. Four of them had no paresis at all. The three patients with mild paresis in regression still showed some motor impairment 9-24 months later, and the condition of the patient with paralysis remained unchanged. In conclusion, patients who develop painless sciatica and marked paresis deteriorate seriously, and early surgery is necessary in order to avoid permanent disturbance of motor function.

Adult↗
PubMed1994

Prognostic criteria of discogenic paresis.

This discourse is aimed at elucidating prognostic criteria for the assessment of the course of a paresis in the case of lumbar disc herniation. Fourhundred and fifty patients were examined who had been operated on for lumbar disc herniation at the Orthopaedic University Clinic Mainz between 1986 and 1991. Of these, 240 showed radicular paralytic symptoms. They were examined prior to the operation, immediately afterwards and 1 year after the operation. The influence of the degree of intensity of the paresis, the time elapsed since the occurrence and other factors like nerve root affected, intraoperative findings, age, sex and weight of the patient were registered. It is obvious that the degree of intensity of a paresis is a good prognostic criterion for the assessment of the postoperative course. A paresis classified as grade III or IV receded in more than 70% of the cases within 6 months. For a paresis of grade II, the recovery rate was 40%. In the case of a total paresis, no complete neurological recovery was registered. The period of time which had elapsed since the occurrence of the paresis, the weight of the patient, the nerve root affected and other factors did not show any significant influence. As a criterion for an emergency or postponed operation on a herniated disc, the duration of paralytic symptoms should therefore be attributed less importance than the progression.

Adult↗
PubMed2005

Objective voice measures in nonsinging patients with unilateral superior laryngeal nerve paresis.

The clinical value of objective voice measures in nonsinging patients with superior laryngeal nerve dysfunction is unknown. In this study, patients with symptomatic unilateral superior nerve paresis were evaluated for maximum phonation time, frequency range of phonation, and mean flow rate. Patients with coexisting pathology, bilateral superior nerve paresis, and those with recurrent laryngeal nerve paresis were excluded from this analysis. A total of 35 nonsinging patients, 14 men and 21 women, with unilateral superior laryngeal nerve paresis were examined between 1999 and 2002. The severity of superior laryngeal nerve paresis ranged from 25% to 85% of normal recruitment with a mean of 70% superior laryngeal nerve recruitment in men and 65% in women by electromyography. In both men and women with superior laryngeal nerve paresis, the maximum phonation time and frequency range of phonation were decreased and the mean air flow rate was increased when compared with normal population values. The jitter percent, shimmer percent, and noise-to-harmonic ratio were also increased in patients when compared with normative data. Selected objective voice measures are abnormal in voice patients with superior laryngeal nerve paresis, which suggests that the measures may be useful as outcomes measures after therapy. More research is encouraged.

Adult↗
PubMed2000

Prevalence of laryngeal paresis in dogs undergoing general anaesthesia.

OBJECTIVE: To estimate the prevalence of laryngeal paresis within a selected population of dogs and identify some of the distinguishing characteristics of affected dogs. DESIGN: A prospective study involving laryngoscopic examination of 250 dogs. PROCEDURE: The laryngeal movements of 250 dogs undergoing general anaesthesia were observed. The severity of laryngeal paresis in these dogs was graded (0 = normal laryngeal movements, 4 = bilateral laryngeal paralysis). The following information was also recorded for each dog: age, sex, weight, breed, condition score, anaesthetic protocol, clinical suspicion of disease and observer. RESULTS: Twenty five percent of the dogs examined had some degree of laryngeal paresis. Affected dogs were significantly older than unaffected dogs (P < 0.001). There was a trend for the severity of laryngeal paresis to increase with age. There was no difference between the sexes. Dogs with laryngeal paresis were significantly heavier than normal animals (P < 0.02). Overweight animals had a significantly higher laryngeal grade than those with a normal condition score (P < 0.05). Labrador Retrievers and Rottweilers had a significantly higher risk of having laryngeal paresis (P < 0.05). Clinical suspicion was found to have high diagnostic value. An intra-class correlation coefficient for inter-rater reliability between the two observers was 0.95. CONCLUSIONS: Laryngeal paresis had a high prevalence in the animals surveyed and was strongly associated with age and breed. The results of this study are consistent with the concept of a progressive degenerative disease with a breed susceptibility. Clinical suspicion for the presence of the disease was a reliable indicator. The grading system used had a high degree of inter-observer agreement.

Anesthesia, General↗
PubMed2005

[Analysis of vocal fold paresis in the patient material of the Department of Otolaryngology in Wrocław from 1993 to 2002].

The aim of this paper was analysis of vocal fold paresis in the patients referred to ENT Department in Wrocław in the years 1993-2002. The study was performed on the base of 304 patients--209 women and 131 men. The average patient's age was 56 years. In all patients phoniatric examination and videostroboscopy were carried out. There were 38% cases of iatrogenic paresis mainly caused by thyroid surgery and cardiosurgery. In 30% causes we found the diseases which caused paresis (mainly infections, cancers, lesions of the central nervous system and injury of head, neck and chest). In about 30% causes we have not found the cause of paresis. Both vocal fold paresis in 98% was caused by thyroid surgery. Left vocal fold paresis was more often then paresis of the right side of vocal fold.

Adolescent↗
PubMed1990

[Herpes zoster paresis. A review of the literature and case reports].

The incidence of paresis due to herpes zoster (HZ) infections are reported very differently in the literature with rates varying from 0.5 to 31%. Many of the paresis are presumed to be undiagnosed on account of topographic dissociation, variable periods from the cutaneous affection to the muscular involvement, masking of the paresis by pain, paresis of the intercostal and abdominal muscles which are not obvious and difficulties in correlating the visceral symptoms with a herpes zoster eruption. Paresis of the cranial nerves are easily diagnosed and 50% of all HZ paresis are diagnosed from this region. Early acyclovir treatment has improved the prognosis. Four cases of hypotonic herpes zoster paresis in immunocompetent persons are described and the diagnostic difficulties are discussed.

Acyclovir↗
PubMed2005

Pathophysiology of spastic paresis. II: Emergence of muscle overactivity.

In the subacute and chronic stages of spastic paresis, stretch-sensitive (spastic) muscle overactivity emerges as a third fundamental mechanism of motor impairment, along with paresis and soft tissue contracture. Part II of this review primarily addresses the pathophysiology of the various forms of spastic overactivity. It is argued that muscle contracture is one of the factors that cause excessive responsiveness to stretch, which in turn aggravates contracture. Excessive responsiveness to stretch also impedes voluntary motor neuron recruitment, a concept termed stretch-sensitive paresis. None of the three mechanisms of impairment (paresis, contracture, and spastic overactivity) is symmetrically distributed between agonists and antagonists, which generates torque imbalance around joints and limb deformities. Thus, each may be best treated focally on an individual muscle-by-muscle basis. Intensive motor training of the less overactive muscles should disrupt the cycle of paresis-disuse-paresis, and concomitant use of aggressive stretch and focal weakening agents in their more overactive and shortened antagonists should break the cycle of overactivity-contracture-overactivity.

Contracture↗