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PubMed1997

[Arachnoid cyst of the middle cranial fossa with extraocular muscle paresis: case report].

Arachnoid cysts in the middle cranial fossa usually present with skull deformity, intracranial hypertension, epilepsy, focal symptoms and delayed mental development. Some cases, however, have neither symptoms nor signs. We have encountered a patient with an arachnoid cyst of the middle cranial fossa with extraocular muscle paresis and who was treated with cyst wall fenestration with good results. An 11-year-old boy presenting with double vision was diagnosed as having an arachnoid cyst in the middle cranial fossa with extraocular muscle paresis. He had no signs of increased intracranial pressure. This patient underwent a cyst membranectomy. Postoperatively this symptom rapidly subsided. Double vision disappeared two months postoperatively. To our knowledge, if those cases associated with increased intracranial pressure signs are excluded, this is the first case reported so far of a middle cranial fossa arachnoid cyst with extraocular muscle paresis. This report illustrates that extraocular muscle paresis can be caused by an arachnoid cyst in the middle cranial fossa and that knowledge of this could be helpful in its early diagnosis and treatment.

Arachnoid Cysts↗

PubMed2004

Phrenic paresis and respiratory insufficiency associated with cervical spondylotic myelopathy.

Cervical spondylotic myelopathy is a common disease caused by chronic segmental compression of the spinal cord. Despite the fact that the columns of the nuclei of the phrenic nerve are located between the 3rd and 5th cervical nerve segments, phrenic nerve paresis is not usually clinically significant. We present one case of cervical spondylotic myelopathy with bilateral phrenic paresis in whom magnetic resonance imaging and surgical findings confirmed intrinsic cord disease as being the cause of this syndrome. This case report suggests that one pathophysiology of clinical phrenic nerve paresis may be segmental damage to the anterior horns caused by cervical spondylosis.

Cervical Vertebrae↗

PubMed2005

Segmental zoster paresis of the upper extremity: a case report.

Segmental zoster paresis, a rare complication of herpes zoster, is characterized by focal, asymmetric motor weakness in the myotome that corresponds to the dermatome of the rash. The pathogenesis of segmental zoster paresis is inflammation caused by the spread of the herpes virus. Motor damage may affect the root, plexus, or peripheral nerve. A woman in her early seventies with right shoulder pain and shoulder girdle muscle weakness was diagnosed with involvement of the C5-7 motor roots and upper truncus of the brachial plexus as a complication of herpes zoster. Recognition of herpes zoster as a cause of acute motor weakness is important in avoiding unnecessary interventions as well as in determining the treatment and outcome of the patient. This case is presented to emphasize that herpes zoster infection may be complicated by segmental paresis, which should be considered in the differential diagnosis of acute painful motor weakness of the upper extremity.

Aged↗

PubMed2006

Decreased capillarization and a shift to fast myosin heavy chain IIx in the biceps brachii muscle from young adults with spastic paresis.

Muscle spasticity and paresis are conditions that occur secondary to upper motor neuron lesions. The co-existence of decreased motor unit recruitment and intermittent over-activity generates confusion concerning the effect on muscle fiber characteristics. In order to increase the knowledge about the effect of upper motor lesion on capillarization and muscle fiber composition, the biceps brachii muscle from seven young adults with long duration of spastic paresis and seven age-matched controls were analyzed using morphological and enzyme- and immuno-histochemical techniques. The spastic muscles had a 38% lower capillary density (p=0.002), 30% fewer capillaries around each muscle fiber (p=0.02), and 16% fewer capillaries when related to the fiber size (p=0.04). The frequency of fibers expressing myosin heavy chain (MyHC) IIx increased (30% vs. 4%, p=0.006), while the percentage of fibers expressing MyHC I and MyHC IIa, respectively, decreased (22% vs. 46% and 7% vs. 29%, p<0.01). The high proportion of muscle fibers with low oxidative capacity and low capillary supply indicates that biceps brachii muscle from patients with upper motor lesions fatigue more easily than normal controls. We also observed a significantly higher variability in fiber size for fibers expressing MyHC I (p<0.04), and, in three of the subjects, a small amount of small fibers expressing developmental MyHCs was found. These results suggest that, although intermittent stretch reflex contractions might have an impact on the muscle characteristics in spastic paresis, the muscle phenotypic properties are more adapted to decreased voluntary motor unit recruitment.

Adolescent↗

PubMed1989

Intracranial aneurysms with superior division paresis of the oculomotor nerve.

Five patients with intracranial aneurysms had unilateral ptosis, limitation of supraduction, and normal pupillary reactivity. The most common aneurysm location for superior division paresis of the oculomotor nerve was the superior cerebellar-posterior cerebral artery junction, where aneurysms (3) of the basilar artery compressed and flattened the interpeduncular oculomotor nerve from below. A superior cerebellar artery aneurysm and brain stem infarction affected the intra-axial course of the oculomotor nerve producing superior division paresis. Only an aneurysm of the intracavernous carotid artery resulted in superior division paresis at the expected anatomic site of bifurcation of the oculomotor nerve into its superior and inferior divisions. Because the superior division supplies innervation exclusively to the superior rectus muscle and levator palpebrae, an aneurysm involving this branch does not affect the pupillo-constrictor fibers. Consequently, cerebral angiography should be considered in the initial evaluation of this ocular motor deficit.

Adult↗

PubMed1988

Parturient paresis and hypocalcemia in ruminant livestock.

Parturient paresis (hypocalcemia) is most likely to affect dairy cattle around the time of parturition. It causes progressive neuromuscular dysfunction and flaccid paralysis. Older dairy cows, cows with a history of parturient paresis during a previous lactation, high-producing cows, and cows from the Jersey and Guernsey breeds are at highest risk for developing parturient paresis. Nonparturient hypocalcemia may also occur and is related to events other than parturition, such as severe stress, that temporarily overwhelm the mechanisms of calcium homeostasis. Beef cattle, sheep, and goats are affected less frequently by hypocalcemia than are dairy cows. Because these species are not as stressed for milk production as dairy cattle, nonparturient hypocalcemia makes up a higher proportion of cases in nondairy ruminants. Clinical signs of hypocalcemia in beef cattle, sheep, and goats tend toward hyperesthesia and tetany rather than the classic flaccid paralysis that occurs in dairy cattle with parturient hypocalcemia. Prompt and effective treatment of hypocalcemia helps to reduce the incidence of secondary complications, such as muscle damage or mastitis. The standard treatment regimen of 500 ml of 23 per cent calcium gluconate, administered intravenously, will elicit a favorable response in approximately 75 per cent of recumbent cows within 2 hours of treatment. Relapses following successful initial therapy are common and may be prevented in part by supplementation of intravenous treatment with an additional 500 ml of 23 per cent calcium gluconate administered subcutaneously. Proper nursing care following treatment speeds recovery and reduces the incidence of secondary complications owing to hypocalcemia.

Animals↗

PubMed2006

[Treatment of parturient paresis with high-dose calcium].

The goal of the present study was to evaluate a calcium dose that was higher than the conventional dose for treatment of parturient paresis in cows. Thirty cows with parturient paresis received 1000 ml of 40 per cent calcium borogluconate solution supplemented with 6 per cent magnesium hypophosphite. Cows in group A received 200 ml of the solution intravenously over a 10-minute period, and the remaining 800 ml via a slow intravenous drip over a six-hour period. Cows in group B received 500 ml of the solution intravenously over a 20-minute period, and the remaining 500 ml via a slow intravenous drip over a six-hour period. Afterwards, the cows were monitored continuously and examined every hour for eight hours. Samples of blood were collected from all the cows before treatment and at 10, 20, 40, 60, 90, 120, 180, 240, 300, 360, 420 and 480 minutes and 24, 48 and 72 hours after treatment. The concentrations of total calcium, ionised calcium, inorganic phosphorus and magnesium were determined. Cows that did not stand within 12 hours of treatment received one or more additional treatments. There was no significant difference in the recovery rate between the two groups. Of the 30 cows, 14 (47 per cent) rised after one treatment and 15 others (50 per cent) were cured after two or more treatments. One cow did not respond to repeated treatments and was euthanased four days after the start of treatment. The results of electrolyte analyses before treatment did not differ significantly between the two groups. In 27 (90 per cent) cows, the concentrations of calcium and inorganic phosphorus were lower than normal and in 3 (10 per cent) cows, only the concentration of inorganic phosphorus was lower than normal. The concentration of total calcium increased markedly ten minutes after the start of treatment in both groups, and at eight hours, the mean concentration of calcium was within the normal range. At 24 and 48 hours, the mean concentration of calcium was below normal, but at 72 hours it was again within the normal range. The concentration of inorganic phosphorus increased slowly in both groups, although it was not within the normal range at eight hours. In both groups, it achieved normal values at 24, 48 and 72 hours. The mean electrolyte concentrations did not differ significantly at any measuring point between cows that stood within eight hours of treatment and those that did not. Our results indicate that increasing the dose of calcium administered does not improve the recovery rate of cows with parturient paresis.

Animals↗

PubMed2002

Ankle-foot orthosis has limited effect on walking test parameters among patients with peripheral ankle dorsiflexor paresis.

The aim of this study was to determine the relationship between ankle dorsiflexor strength and performances on several walking tests and to determine the effect of ankle-foot orthosis (AFO) use on walking tests. The following tests were used: 10-metre walking test (with and without three stairs), a complex walking task (6-minute walk with cognitive loading) and a subjective evaluation (SIP68 mobility scale and questionnaire). Isometric strength of the ankle dorsiflexors was measured. All walking tests were performed with and without AFO in random order. When relating torque values to walking performances, the highest correlation was found with the "10 metre" and "10 metre with stairs" test (r = -0.51, i.e. an inverse relationship). No threshold in the degree of paresis was found below which walking disability suddenly increased. No significant improvement could be demonstrated from AFO use on the 10-metre tests. Improvement on the 6-minute test was nearly significant (p = 0.06), the questionnaire revealed a positive opinion on AFO use related to overall walking function and effort. Thus, we have to conclude that these walking tests do not aid the clinician in estimating the severity of (progression of) the paresis nor to detect differences in degree of paresis between subjects.

Adult↗

PubMed2002

A pilot study on the recovery from paresis after lumbar disc herniation.

BACKGROUND: Although the existence of a motor defect in discogenic sciatica is a sign of severity, the literature does not provide evidence for an immediate requirement for surgery. OBJECTIVE: To assess the course of sciatica with discogenic paresis and to determine possible prognostic factors for recovery or improvement. STUDY DESIGN: This open prospective multicenter study included patients with discogenic sciatica with paresis that had been developing for less than 1 month and was rated < or =3 on a 5-grade scale. Pain, the strength of 11 muscles, return to work, and analgesic intake were assessed at 1, 3, and 6 months. Recovery and improvement were defined by pain not exceeding 20 mm or < or =50% of the initial pain score and a score of either 5 (recovery) or 4 (improvement) for the weakest muscle at inclusion. RESULTS: Sixty-seven patients were enrolled; 39 (58%) patients were treated surgically and 28 (42%) medically. Surgically treated patients differed from medically treated patients by a higher rate of extruded herniation, a higher number of paretic muscles (6.3 vs. 5; P = 0.051), and a longer course of sciatica (31.4 vs. 17.3 days; P = 0.034). At 6 months, 7 (10.4%) patients were lost to follow-up; 32 (53.3%) had improved, including 18 (30%) recovered, 33 (85%) back to work and having a professional activity, and 22 (39%) still taking analgesics. The only significant difference between recovered and not recovered patients was mean age at inclusion (43 vs. 51 years, P = 0.034). There were no significant differences between improved and not improved patients. Moreover, the outcome was not different in the two treatment groups: there were 17 (53%) improvements in surgically treated patients, including 8 (25%) recoveries, and 14 (56%) improvements in medically treated patients, including 8 (40%) recoveries. CONCLUSION: This pilot study showed no difference between surgical or medical management for recovery or improvement in patients with discogenic paresis. These results need confirmation by a randomized study.

Adult↗

PubMed2001

Acoustic neuroma: predominance of Antoni type B cells in tumors of patients with vestibular paresis.

OBJECTIVE: This study aimed to investigate whether in patients with acoustic neuroma (AN), the presence or absence of vestibular symptoms is related to the histologic characteristics of the tumor. STUDY DESIGN: The study design was a retrospective clinical study. SETTING: The study was conducted at a tertiary referral center. PATIENTS: A group of eight patients with unilateral AN and normal vestibular function was compared with a group of AN patients, matched for tumor size, with vestibular paresis. METHODS: The methods were vestibular examination of the patients and morphometric analysis of the histologic specimens of their tumors. MAIN OUTCOME MEASURES: The outcomes were measured by vestibular function and by the relative quantity of Antoni type A or type B cell tissue. RESULTS: The tumors of patients with vestibular paresis appeared to contain significantly more Antoni B cells and fewer Antoni A cells than did the tumors of patients with normal vestibular function. CONCLUSIONS: Besides morphologic differences, type B cells may display a distinct behavior compared with type A cells. Presumably, in AN patients the development of a vestibular paresis appears to be related to the biologic activity of type B cells in the tumor.

Humans↗

PubMed1992

The site of brainstem lesions causing semicircular canal paresis: an MRI study.

Ten patients with canal paresis of central origin and ten patients with peripheral canal paresis were studied using MRI of the brainstem to identify lesions within the central vestibular pathways. In the central group, the magnitude of the canal paresis was generally lower than in the peripheral group and removal of fixation had little effect on the nystagmic response. In the peripheral group, removal of fixation enhanced the nystagmus and lessened the discrepancy between the two ears. Statistical processing of the MRI showed that in the central group significant spatially coincident lesions occurred within the medial vestibular nucleus, lateral vestibular nucleus and proximal portion of the vestibular fascicle.

Adult↗

PubMed1980

Observations of the use of 1 alpha hydroxycholecalciferol in the prevention of bovine parturient paresis.

Varying doses of 1 alpha-hydroxycholecalciferol (1 alpha-HCC) (50, 150, 250 and 350 micrograms) in propylene glycol were injected intramuscularly into 30 dry adult Israeli Friesian cows. Fourteen of these animals received a second dose; four were given 250 or 350 micrograms 48 hours after the first dose and 10 were given 350 micrograms 72 hours after the first dose. Plasma calcium rose after 24 hours at all dose levels except 50 micrograms. A dose-dependent peak in plasma calcium was reached after three to four days, followed by a return to baseline five days (150 micrograms) and eight days (250 and 350 micrograms) post injection respectively. Repeating the injection 48 or 72 hours later increased the time span by three and four days respectively. The effect of plasma inorganic phosphate was double that on plasma calcium. Plasma magnesium declined slightly three days post injection. High calcium feeding in conjunction with one or two injections of 350 micrograms 1 alpha-HCC did not modify the response of plasma calcium. An injection of 350 micrograms of 1 alpha-HCC was given once to 40 parturient paresis-prone cows of the same breed and twice at 72-hour intervals to 37 such cows. Six of the animals received 5 mg of flumethasone together with the second injection and 13 received it 48 hours later. This was to induce parturition, which occurred within 24 to 48 hours. None of the cows injected earlier than 24 hours prepartum developed parturient paresis in comparison with 22 out of 60 control animals which did. The results suggest that 1 alpha-HCC is useful in the prevention of bovine parturient paresis.

Animals↗

PubMed2000

Hypertension, hyperekplexia, and pyramidal paresis due to vascular compression of the medulla.

MRI showed impingement of the vertebral artery on the left lateral medulla in two patients with arterial hypertension, exaggerated startle reflexes (hyperekplexia), and progressive spastic paresis. One patient underwent microvascular decompression with normalization of arterial hypertension, disappearance of hyperekplexia, and improvement of spastic paresis. The combination of arterial hypertension, hyperekplexia, and progressive spastic paresis should arouse suspicion of neurovascular compression of the lateral medulla.

Electromyography↗

PubMed1992

Postauricular response in motor paresis with intracranial lesions.

The clinical usefulness of the postauricular response (PAR) in the evaluation of motor paresis was studied in 105 patients with intracranial lesions and 25 normal volunteers. Click stimuli at 90 dB hearing level were delivered in each ear, and PARs recorded from bilateral posterior auricular muscles with reference to the vertex (Cz). No volunteer demonstrated PAR in the relaxed posture, but in tensed postures increasing muscle tone PARs were elicited with a latency of 11.5 +/- 0.7 msec and an amplitude of 6.2 +/- 2.8 muV. Sixty-two patients (59%) had high-amplitude PARs in the relaxed posture. PARs were enhanced more frequently in paretic patients than in non-paretic patients (p less than 0.01). In subcortical lesions, the PAR latency had a significant correlation with the degree of motor paresis (p less than 0.005). In patients, the enhanced PAR amplitude suggested the presence of motor paresis associated with deep-seated mass lesions. The enhanced response is thought to be associated with dysfunction of the pyramidal and extrapyramidal tracts.

Brain Diseases↗

PubMed1977

Efficacy and safety of 1alpha-hydroxyvitamin D3 for prevention of parturient paresis.

Four trials involved intravenous or intramuscular injections of 1alpha-hydroxyvitavin D3 to test efficacy in preventing parturient paresis. Use of .1 mg intravenously afforded total protection compared with an incidence of 33% (2/6) in controls. Intramuscular injections of .1 mg in 2 ml propylene glycol and .3, .5, and 1.0 mg in 5 ml corn oil resulted in 0, 15.7, 20, and 0% incidence of parturient paresis compared with 33, 16.7, 37.5, and 37.5% incidence of parturient paresis in the controls. There was a rapid increase in serum calcium (12 to 24 h) in response to intravenous treatment, whereas the response to intramuscular injections was gradual but was maintained longer. To evaluate the safety of 1alpha-hydroxyvitamin D3, eight cows, two per treatment, were given intramuscular doses of .5, 1.0, 1.5, or 3.0 mg (three 1.0 mg injections) in 5 ml corn oil. No clinical or pathological evidence of hypervitaminosis C or soft tissue calcification was found. Tissue taken from the injection site 15 days after last injection contained 3 to 38 IU vitamin D activity per 100 g wet tissue compared with control of 8 to 15 IU per 100 g. Total vitamin D activity of milk taken the 11th milking postpartum from cows receiving .5 or 1.0 mg had a mean of 13.4 and 22.6 IU vitamin D activity per liter compared to 19 IU per liter for control milk. Milk from the 5th milking postpartum in the cows receiving .5 mg had a mean activity of 14.5 IU per liter. Milk from animals slaughtered for retention studies had a mean activity of 22 IU per liter.

Animals↗

PubMed1986

Effect of synthetic bovine parathyroid hormone in dairy cows: prevention of hypocalcemic parturient paresis.

Intravenous infusion of synthetic bovine parathyroid hormone for 96 h increased 1,25-dihydroxyvitamin D, Mg, Ca, and hydroxyproline in plasma of pregnant cows within 16, 24, 48, and 72 h, respectively. Plasma Ca concentration was maximal at the end of the 96-h infusion (15.1 mg/100 ml). Plasma concentration of 1,25-dihydroxyvitamin D at 96 h was twice that before parathyroid hormone infusion, indicating that parathyroid hormone stimulated 1,25-dihydroxyvitamin D production in the presence of hypercalcemia. The urinary excretion of hydroxyproline indicated that at least 48 h of parathyroid hormone stimulation was required to stimulate bone resorption in the pregnant cow. Eight periparturient cows were on a high Ca diet prepartum. Four cows were treated with intravenous parathyroid hormone prior to parturition. Four cows were untreated. All four untreated cows developed parturient paresis. None of the cows treated with parathyroid hormone developed parturient paresis. However, two cows that received parathyroid hormone for less than 24 h prior to parturition became hypocalcemic, but not recumbent. Plasma Ca concentrations remained within normal limits in the two other cows that received greater than 60 h parathyroid hormone infusion prior to parturition. We conclude that exogenous parathyroid hormone (1-34) can prevent parturient paresis if administered at least 60 h prior to parturition.

Animals↗

PubMed1988

Ammonium chloride and ammonium sulfate for prevention of parturient paresis in dairy cows.

Forty-eight Holstein cows with two or more previous lactations and no history of parturient paresis were randomly assigned to one of four prepartum diets in a 2 x 2 factorial design to determine the effect of dietary supplementation with ammonium salts and Ca intake on serum Ca concentrations at calving. Four diets provided either 53 g total dietary Ca/d or 105 g Ca/d and were either supplemented with ammonium salts [100 g/d each of NH4Cl and (NH4)2SO4] or unsupplemented. Anion-cation balance of the diets, calculated as milliequivalents (Na + K)--(Cl + S), was -75 meq/kg DM with ammonium salts and +189 meq/kg DM without ammonium salts. Experimental diets were fed from 21 d prior to expected parturition until calving. Calcium intake during the feeding period did not affect the incidence of parturient paresis or serum concentrations of ionized Ca at calving. The incidence of parturient paresis was 4% with and 17% without the ammonium salts. Cows fed diets containing ammonium salts had higher serum ionized and total Ca concentrations at parturition. Serum concentrations of Mg, P, Na, K, and Cl on the day of parturition were unaffected by dietary treatment.

Ammonium Chloride↗

PubMed1992

1 alpha-hydroxyvitamin D3 plus 25-hydroxyvitamin D3 reduces parturient paresis in dairy cows fed high dietary calcium.

The effectiveness of a combination of 1 alpha-hydroxyvitamin D3 and 25-hydroxyvitamin D3 for reducing incidence of parturient paresis in aged Holstein cows was tested. Intramuscular injection of .5 mg of 1 alpha-hydroxyvitamin D3 plus 4 mg of 25-hydroxyvitamin D3 increased plasma 1,25-dihydroxyvitamin D concentrations through parturition. Treatment with 1 alpha-hydroxyvitamin D3 plus 25-hydroxyvitamin D3 raised prepartum serum Ca approximately 2 mg/dl and prepartum serum P approximately 4 to 5 mg/dl higher than untreated controls. Both treated and control cows had approximately a 2-mg/dl decrease in serum Ca following parturition. The prepartum diet of alfalfa silage and hay was supplemented with a grain mixture supplying 100 g of Ca/d from ground limestone. Under these dietary conditions, incidence of parturient paresis was reduced from 33 to 8%. In a separate experiment, treatment with 1 alpha-hydroxyvitamin D3 plus 25-hydroxyvitamin D3 did not reduce incidence of parturient paresis when cows consumed mixed diets of different feed-stuff composition. Further experiments are required to determine specifically the factor or factors responsible for the difference in response to active vitamin D compound administration between the two experiments. Prepartum dietary Ca intake may be one such factor.

Animals↗