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Influence of canal paresis and compensation on gain and time constant of nystagmus slow-phase velocity to yaw-axis rotation.

In order to assess the influence of canal paresis and compensation on the yaw-axis rotatory chair test parameters gain and time constant, a study was conducted in 435 patients diagnosed with unilateral peripheral vestibulopathy. Patients were grouped according to the amount of canal paresis found in the caloric test and by the result of a bedside examination of the vestibulo-ocular reflex (VOR). The time constant of the VOR diminishes as canal paresis increases and, when using a high-velocity sinusoidal test, there is a similar reduction in gain. Mean time constant was reduced when rotations were to the side of the lesion (ipsilesional) and to the normal (contralesional) and differences between both rotations were found for 21-80%, canal paresis. Ipsilesional gain was significantly less than contralesional gain, which had a normal result independent of the amount of canal paresis; differences between them were significant when canal paresis was > 41%. Spontaneous nystagmus significantly influenced the appearance of asymmetries in gain and time constant in the tests performed while, with high-velocity sinusoidal rotation, gain was found to be significantly different for ipsilesional and contralesional rotations in non-acute symptomatic patients.

Adolescent↗

Propagation disturbance of motor unit action potentials during transient paresis in generalized myotonia: a high-density surface EMG study.

Patients with autosomal recessive generalized myotonia, or Becker's disease, often suffer from a peculiar transient paresis. As yet, the relationship between this transient paresis and the defect in the gene encoding for a voltage gated Cl- channel protein in the muscle membrane of these patients is unclear. In order to gain a better understanding of the electrophysiological properties of the muscle fibre membrane in these generalized myotonia patients, we have studied transient paresis with a novel high-density surface EMG (sEMG) technique. We conclude that the transient paresis is explained by a deteriorating muscle membrane function, ending in conduction block and paresis. Multi-channel sEMG during the period of force decline in transient paresis shows a decrease in peak-peak amplitude of the motor unit action potentials from endplate towards tendon. This disturbance increases with time and place, indicating a deteriorating membrane function, and ends in a complete blocking of propagation within seconds. Spatiotemporally, this leads to a V-shaped sEMG pattern. In a more general sense, this contribution shows how spatiotemporal information, available through non-invasive high-density sEMG, may provide novel insights into electrophysiological aspects of membrane dysfunction.

Action Potentials↗

The side and somatotopical location of single small infarcts in the corona radiata and pontine base in relation to contralateral limb paresis and dysarthria.

The aim of this study was to investigate whether the side and location of single small infarcts (< or = 3 cm) in the corona radiata (28 patients) and pontine base (36 patients) influence the incidence of contralateral upper or lower limb paresis and dysarthria. While the severity of contralateral limb paresis was not significantly different between right and left corona radiata lesions, infarcts presenting with contralateral limb paresis and/or dysarthria presented significantly more often in the left than in the right hemisphere, and left infarcts were significantly smaller than right infarcts. Lesions related to dysarthria and upper and lower limb paresis were arranged anterior-posteriorly in the paraventricular corona radiata region. Pontine base infarcts presenting with dysarthria also presented significantly more often in the left than in the right pons. Dysarthria showed a significant correlation with lesions presenting in the dorsomedial portion of the pontine base, upper limb paresis with those in the dorsomedial and dorsolateral portions, and lower limb paresis with lesions in the ventromedial portion. These results suggest greater influence of the left descending motor fibers on contralateral limb movement and articulation than of the right and face-arm-leg somatotopy of motor fibers in the paraventricular corona radiata region (anteroposterior) and in the pontine base (dorsoventral).

Adult↗

Postictal paresis in children with benign rolandic epilepsy.

Following a search for the presence of postictal paresis in a cohort of 70 patients with benign rolandic epilepsy of childhood, the symptomatology of the seizures and the presence of postictal paresis were reviewed. All children underwent a neurologic evaluation, including electroencephalography (EEG) and neuroimaging. Eight of the 70 patients (3 girls and 5 boys) were found to have postictal paresis. All patients had partial motor seizures involving predominantly the upper extremities and, to a lesser degree, the face and lower extremities. In all eight patients, the motor deficits resolved within 60 minutes. Follow-up neurologic examination was nonfocal in all patients. Seven of the eight patients experienced postictal paresis once, and one patient had two such episodes. Three of the eight patients experienced a brief speech arrest. The EEG in all patients demonstrated centrotemporal sharp waves. In seven patients, the sharp waves were bilateral and independent, and in one patient, the rolandic sharp waves were unilateral. A horizontal dipole with positivity at the central region was found in all patients using an average montage. In conclusion, we found an 11.5% association of postictal paresis in children with benign rolandic epilepsy of childhood, whereas 38% of children also had a brief speech arrest. The EEG was characteristic for benign rolandic epilepsy of childhood with bilateral asynchronous discharges in seven of eight patients (83%) and the presence of dipole in all patients. The presence of postictal paresis should not exclude the diagnosis of benign rolandic epilepsy of childhood.

Child↗

Recurring hypocalcemia of bovine parturient paresis is associated with failure to produce 1,25-dihydroxyvitamin D.

Parturient paresis (milk fever) is a hypocalcemic disorder caused by the onset of lactation in the dairy cow. In most cows a complete recovery follows a single iv calcium treatment to correct the acute hypocalcemia. However, about 20% of cows treated for parturient paresis experience recurring episodes of hypocalcemia (relapses) requiring further treatment. Analysis of plasma from 8 nonrelapsing parturient paretic and 11 relapsing parturient paretic cows revealed differences in plasma 1,25-dihydroxyvitamin D [1,25-(OH)2D] concentrations before and during the development of hypocalcemia. In nonrelapsing cows, plasma 1,25-(OH)2D increased to 4- to 5-fold as plasma calcium concentrations declined during the first stage of parturient paresis. In relapsing cows, decreases in plasma calcium concentrations during the first stage of parturient paresis were accompanied by just a 2- to 2.5-fold increase in plasma 1,25-(OH)2D. Plasma 1,25-(OH)2D eventually increased 4- to 5-fold in the relapsing cows, but this response was delayed 24-48 h compared with the response in the nonrelapsing cows. Plasma PTH concentration profiles were similar in relapsing and nonrelapsing cows, suggesting that renal 25-hydroxyvitamin D 1 alpha-hydroxylase was temporarily refractory to stimulation by PTH in the relapsing cows. In both groups of cows recovery from parturient paresis began about 12-24 h after plasma 1,25-(OH)2D concentrations had increased 4- to 5-fold. These data imply that lack of production of 1,25-(OH)2D is an important factor in predisposing the cow to relapses of parturient paresis and is critical for recovery from the hypocalcemia associated with the onset of lactation.

Animals↗

[Symptomatological and electrophysiological study on cold paresis in juvenile muscular atrophy of distal upper extremity (Hirayama's disease)].

Patients with juvenile muscular atrophy of distal upper extremity (Hirayama's disease) often show marked weakness of the fingers occurring with exposure to cold. We term this phenomenon cold paresis. We conducted an original test to induce cold paresis (Cold Paresis Inducement Test) in 11 patients of this disease and 10 normal controls. Cold paresis was induced in 9 of 11 patients, but was not induced in the 2 patients who had the disease longer than 20 years and in all normal controls. We examined the electromyogram of abductor digiti minimi during 5 Hz and 20 Hz rate of ulnar nerve stimulation at cooling. The patients in whom cold paresis was induced exhibited a waning of amplitude of compound muscle action potential (M wave) during 20 Hz stimulation. This waning was aggravated by intravenous administration of anticholinesterase (edrohponium). We found a remarkable conduction delay of M waveform at the waning by means of waveform analysis. These results suggest that cold paresis may be caused by a conduction block of the muscle fiber membrane in re-innervating muscles after active denervation.

Adolescent↗

[A case of cortical infarction showing unilateral facial and hypoglossal paresis].

We describe a case presenting with facial and hypoglossal nerve paresis due to cortical cerebral infarction. A 54-year-old man visited our hospital complaining of sudden episode of dysarthria and facial paresis. Neurological findings revealed tongue deviation to the left and left facial paresis with forehead wrinkling while neither limb paralysis nor sensory impairment was observed. Head CT performed on day 3 after onset revealed a cortical infarction in the right prefrontal gyrus. Symptoms gradually improved with medical management. This patient had isolated facial and hypoglossal nerve paresis without other neurological symptoms. Patients with mild paresis of cranial nerves should be diagnosed carefully, because their paresis could be supranuclear type.

Cerebral Infarction↗

Asymmetrical bilateral paresis of the superior oblique muscle.

BACKGROUND: To review the preoperative signs of bilateral superior oblique paresis and to analyze their presence. METHODS: The proposed preoperative signs of bilateral superior oblique (SO) muscle paresis were separated into "certain signs" and "suspicious signs." The signs were analyzed for accuracy using case examples and statistics. RESULTS: A strong preoperative sign of bilateral SO muscle paresis was reversal of the hypertropia in the ipsilateral (and/or ipsi-supralateral) position and/or in the contralateral head tilt position. In such cases, the addition of a light contralateral weakening procedure to the operation aimed at the elimination of the hypertropia caused by the more affected SO muscle prevented development of the clinical picture of a contralateral SO muscle paresis. A suggestive preoperative sign of bilateral SO muscle weakness was marked reduction of the hypertropia in the ipsilateral (and ipsi-supralateral) position, as well as in the contralateral head tilt position. In these cases, a contralateral inferior oblique muscle weakening was deferred until after motility could be reassessed postoperatively. An additional sign of possible bilateral SO muscle weakness was the presence of a large V pattern. CONCLUSIONS: When planning surgery for apparent unilateral SO muscle paresis, the surgeon should be aware of the often subtle preoperative signs of bilateral SO muscle paresis. Early diagnosis allows the surgeon to avoid the reversal of the clinical picture or to advise the patient of the possibility of a bilateral problem.

Eye Movements↗

Relationship among glottal area, static supraglottic compression, and laryngeal function studies in unilateral vocal fold paresis and paralysis.

In this study, we evaluated the relationship between laryngeal function measures and glottal gap ratio and normalized measures of supraglottic behaviors in patients with unilateral vocal fold paresis (UVFP). Thirty-one patients were found to have unilateral vocal fold paresis by videoendoscopy and laryngeal electromyography, and 13 controls participated in this study. Patients with UVFP demonstrated significantly larger glottal gap ratios (p = 0.016) than control subjects. The nonparalyzed or contralateral vocal fold was associated with significantly more static false vocal fold compression (p = 0.03) compared with the paralyzed vocal fold or with the controls. Patients with unilateral vocal fold paresis were divided into subgroups: those with normal or abnormal maximum phonation time, flow, or pressure measures. Smaller glottal gap ratios were identified in patients with normal maximum phonation times and flow measures. Greater false vocal fold activity was identified in unilateral vocal fold paresis patients with normal laryngeal function measures than in unilateral vocal fold paresis patients with abnormal measures. These findings suggest that some patients with documented unilateral paresis and glottal incompetence can compensate for vocal fold weakness such that their acoustic and aerodynamic measures are normal.

Adult↗

Emotional facial paresis in temporal lobe epilepsy: its prevalence and lateralizing value.

The selection of patients with medically refractory temporal lobe epilepsy (TLE) for surgery depends on the concordance of data from clinical, imaging and electroencephalographic evaluation. Though clinical examination is often normal, emotional facial paresis has been described in patients with TLE. Utilizing a well-characterized group of mesial TLE (MTLE) patients, who have achieved excellent seizure outcome following anterior temporal lobectomy with amygdalohippocampectomy (ATL), we investigated the prevalence, predictive value and associations of emotional facial paresis. When compared to 8 out of 50 control subjects (16%), 36 out of 50 MTLE patients (72%) exhibited unilateral emotional facial paresis; the difference was highly significant (P<0.0001). The presence of contralateral emotional facial paresis correctly predicted the side of ATL in 86.1% patients. The occurrence of emotional facial paresis was significantly associated with longer duration of epilepsy prior to ATL and left ATL. Our observations confirm that emotional facial parersis contralateral to the side of mesial temporal sclerosis (MTS) is a valuable localizing sign in correctly predicting the epileptogenic temporal lobe. We hypothesize that the presence of an intact right hemisphere and pathological changes more extensive than MTS may be required for emotional facial paresis to readily manifest.

Adolescent↗

Arm and leg paresis as outcome predictors in stroke rehabilitation.

I used leg and arm paresis to predict outcome measured as extremity function in a prospective study of 75 consecutive hemiplegic patients admitted to an inpatient stroke rehabilitation unit. In each patient, extremity paresis was quantified according to the five-point scoring system advised by the Medical Research Council, upper extremity function was quantified using the Barthel Index subscore for feeding and dressing the upper body, and lower extremity function was quantified according to a five-point scoring of the ability to walk. Improvement was recorded for upper extremity function in 52% of the patients and for lower extremity function in 89%. Best extremity function was reached a mean +/- SEM of 9 +/- 3 and 10 +/- 4 weeks after stroke for the upper and lower extremities, respectively. In patients experiencing complete recovery, this occurred a mean +/- SEM of 7 +/- 2 weeks (for both upper and lower extremities) after the stroke. Only 8-11% of the patients with paresis scores of less than or equal to 2 regained independent extremity function after rehabilitation. Half of the patients with paresis scores of greater than or equal to 3 regained independent extremity function after rehabilitation, while the other half were able to perform extremity function with only minimal assistance. As predictors of extremity function, the Barthel Index subscore was slightly better (r = 0.64) than paresis score (r = 0.58). However, because evaluation of extremity paresis is easy, it appears to be useful as a preliminary predictor of outcome following stroke.

Arm↗

Unilateral oculomotor nerve paresis associated with anterior communicating artery aneurysm rupture--two case reports.

Two cases of complete unilateral oculomotor nerve palsy occurred after subarachnoid hemorrhage (SAH) due to a ruptured anterior communicating artery aneurysm. A 61-year-old female suffered left oculomotor nerve paresis after mild SAH. This paresis was probably related to pre-existing oculomotor nerve stretching caused by abnormal positioning of the posterior cerebral and superior cerebellar arteries in the premesencephalic cistern. A 70-year-old female suffered right oculomotor nerve paresis after severe SAH. Elevated intracranial pressure might have caused this paresis, but the reason for the unilateral occurrence was undetermined. Both patients were treated by clipping of the aneurysm, and the signs of oculomotor nerve paresis gradually resolved. A pattern of pupil-sparing paresis was observed during the early recovery stage in both patients.

Aged↗

[The determination of the sum potential amplitude for the prognostication of facial paresis of viral etiology].

In 29 patients with facial pareses of viral etiology the sum potential amplitude of the M. orbicularis oris was determined in a comparison of the two sides for prognostication purposes. If the sum potential amplitude is reduced by less than 70 per cent a return of good functions can be expected within 6-8 weeks. If the reduction of the sum potential amplitude lies between 70 and 95 per cent, a reliable prognosis is not possible, whereas with values below 95 per cent the paresis does not improve at all or hardly improves within 6-8 weeks. An evaluation of the returned function, about 1 year after the beginning of the paresis, i.e. at a time when the regeneration is basically completed, shows that all cases with an originally poor function (judged 6-8 weeks after onset of paresis) had changed into cases with a moderate function, and all cases with an originally moderate function had turned into cases with a good function. In another study concerning patients with idiopathic facial paresis the same method yielded results comparable to those of the above-mentioned study, so that the conclusion can be drawn that in the prognostication of the peripheral facial paresis by means of determining the sum potential amplitude-regardless of whether the facial paresis is of viral or idiopathic etiology-the same yardsticks have to be applied.

Action Potentials↗

[The relationship between low pH in the umbilical cord artery in neonates and later development of cerebral paresis].

Routine determination of the pH in umbilical arterial blood immediately after delivery is a commonly employed variable for assessing the risk of subsequent cerebral paresis caused by hypoxia. Opinions differ regarding the lower limit for normal NS-pH (acidosis limit) and this is due mainly to variable conceptions of what a normal delivery is. Lower limits from 7.04 to 7.14 are thus observed if the limit -2 SD is chosen. Even if the limit of 7.04 is chosen, only very few of the infants who are acidotic on delivery subsequently develop cerebral paresis. The most important reason for this is that the prevalence of cerebral paresis developed as a result of hypoxia during delivery is very low and that a low NS-pH value most probably originates from a neonate who recovers without cerebral paresis. Another reason is that the relationship between the pH value and the degree of hypoxia is far from perfect and this holds also true for the relationship between the degree of hypoxia and cerebral paresis. It is therefore concluded that in connection with cerebral paresis, NS-pH does not fulfill the requirements of a diagnostic test. Determination of NS-pH may, on the other hand, be of significance for neonatal treatment as the combination of a low Apgar score and NS-pH is a reasonable predictor for the neonatal morbidity.

Cerebral Palsy↗

Voice range in superior laryngeal nerve paresis and paralysis.

Evaluation of Physiologic Frequency Range (PFR) and Musical Frequency Range (MRP) of Phonation was performed on 56 adults (singers and nonsingers) presenting with superior laryngeal nerve (SLN) paresis or paralysis confirmed by laryngeal electromyography. The most common etiology was neuritis (69.7%), followed by iatrogenic and unknown causes,each accounting for 10.2% of cases, and finally trauma (8.9%). Both female and male singers with SLN paresis or paralysis had significantly higher PFR and MPR than nonsingers. Female classical singers presented PFR and MPR of up to 10 semitones (ST) higher than nonclassical singers and nonsingers. The lowest PFR and musical ranges were found in patients with SLN paresis associated with recurrent laryngeal nerve paresis or paralysis. The authors suggest that voice range measurement is a useful parameter for analyzing the effects of SLN paresis or paralysis on voice and that it may also assist in measuring outcome following voice therapy.

Adult↗

Parkinson's disease of post-encephalitic type following general paresis--an autopsied case.

A clinico-pathological report is given of a case of Parkinson's disease following a general paresis. A 66-year-old male, with no previous history of febrile disease or viral encephalitides, developed a dementing illness. The general paresis was diagnosed from serological studies at the age of 45. He underwent a series of penicillin plus fever therapies as treatment for neurosyphilis. He also developed generalized rigidity and slow mobility 12 years after the diagnosis of general paresis. An anti-Parkinson drug was given. Finally he fell in a state of muteness and became bedridden. He had been hospitalized for 21 years and died from bronchopneumonia. The pathological findings were strikingly similar to post-encephalitic parkinsonism in addition to a healed state of general paresis. They consisted of a widespread nerve cells loss, gliosis and the presence of Alzheimer's neurofibrillary tangles in the substantia nigra. In the cerebral cortex, a diffuse loss of nerve cells and the presence of a weak positive iron reaction were observed. The coexistence of general paresis and post-encephalitic parkinsonism is unusual and the authors discussed the etiological relationship between the two different conditions.

Aged↗

Effects of long-term dietary supplementation with clinoptilolite on incidence of parturient paresis and serum concentrations of total calcium, phosphate, magnesium, potassium, and sodium in dairy cows.

OBJECTIVE: To determine whether dietary supplementation with clinoptilolite affects the incidence of parturient paresis and serum concentrations of total calcium (tCa), inorganic phosphorus (PO(4) (2)), magnesium (Mg2+), potassium (K+), and sodium (Na+) in dairy cattle. ANIMALS: 52 dairy cows. Procedure-Cows were placed into 3 groups. The first 2 groups (group A [n = 17] and group B [17]) were offered a concentrate supplemented with 1.25% and 2.5% clinoptilolite, respectively. The third (group C [n = 18]) served as a control and was offered the concentrate alone. The experiment started 1 month before parturition and lasted until the beginning of the next nonlactating period. Around the time of calving, all cows were monitored for the development of parturient paresis. Blood samples were taken at the commencement of the experiment, on the day of calving, and thereafter at monthly intervals to measure serum tCa, PO(4) (2), Mg2+, K+, and Na+ concentrations. Results-The incidence of parturient paresis in group B cows was significantly lower, compared with group C cows. However, serum concentrations of tCa, P(O4) (2), Mg2+, K+, and Na+ were not significantly affected by long-term supplementation with clinoptilolite. CONCLUSIONS AND CLINICAL RELEVANCE: In the context of this experiment, clinoptilolite supplementation at 2.5% appeared to have reduced the incidence of parturient paresis in dairy cows, suggesting that its effectiveness depends on the amount incorporated in the ration of cows. Addition of clinoptilolite in the concentrate of dairy cows during the nonlactating period could be used as a cost-effective preventive treatment for parturient paresis.

Analysis of Variance↗

Epidemiology of parturient paresis: predisposing factors with emphasis on dry cow feeding and management.

Dry cow feeding and management were examined for predisposing factors for parturient paresis in 1,983 Holstein cows from New York Dairy Herd Improvement Cooperative records, monthly technician visits to 31 farms, and questionnaires. Variables were estimated transmitting ability, season of calving, lactation number, parturient paresis, estimated potential hours per day of exercise, and estimated nutrient intakes (protein, calcium, phosphorus, and energy) during the preceding dry period. Nutrient intakes were estimated by farmers for the average dry cow (season dependent) in their herd for the early (greater than or equal to 3 wk prepartum) and late portions of the dry period. Intakes were percentages of National Research Council requirements for a 550 kg dry cow in the last 2 mo of gestation. Nutrient intakes were coded by ranking the herds by percentage of each requirement. Codes represented the approximate lower third, middle third, and top third of the herds. Individual cows were assigned their herd nutrition codes by their season of calving. For stepwise discriminant analysis, the group variable was parturient paresis (94 cases, 1,889 controls). As lactation number (most important) and estimated transmitting ability (second most important) increased, incidence of parturient paresis increased. Parturient paresis was reduced with high dietary protein fed during the early stage of the dry period, with low phosphorus and high energy (lead feeding) closer to calving, and with decreased opportunity for exercise. Most cows were overfed calcium, especially in the late stage of the dry period, but calcium intake was not important when phosphorus was low.

Animals↗