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Testosterone-induced acceleration of recovery from facial paralysis in male hamsters: temporal requirements of hormone exposure.

In this study, the temporal requirements of testosterone propionate (TP) exposure necessary for acceleration of recovery from facial paralysis to occur following facial nerve crush were examined. For each of two series of experiments, adult castrated male hamsters were subjected to crush axotomies of the facial nerve at its exit from the stylomastoid foramen. In the first experimental paradigm, one-half of the animals with facial nerve crush axotomies received subcutaneous TP capsules beginning on postoperative (PO) day 6 and continuing throughout the regeneration period, with the remainder of the animals sham implanted. The results indicate that, without the early exposure to TP, the accelerative effects of the hormone on facial nerve regeneration were abolished. In the second experimental paradigm, one-half of the animals with facial nerve crush axotomies received subcutaneous TP implants immediately after the crush surgeries and until PO day 7, with the remainder of the animals sham implanted. The results indicate that an early, discontinuous dose of TP immediately after crush surgeries was sufficient to produce a partial accelerative effect on the return of facial nerve function. It is hypothesized from these findings that there is a priming effect of TP that is exerted at the level of the neuron, temporally precedes behavioral recovery by a week or more and is critical to subsequent acceleration of recovery from facial paralysis.

Animals↗

Respiratory mechanics of Pekin ducks under four conditions: pressure breathing, anesthesia, paralysis or breathing CO2-enriched gas.

Impedance magnitude (Z) of the lower respiratory system was studied in Pekin ducks, using forced oscillations of a small volume at the airways opening in the range 1.6-16 Hz. The experiments were performed on 5 awake ducks enclosed in a body plethysmograph and spontaneously breathing ambient air at a transrespiratory pressure (Prs, the pressure difference between the lung and the body surface) which was varied in steps from -10 cm H2O (compression) to +10 cm H2O (distension). In 3 anesthetized birds, the effects of CO2 breathing and muscular paralysis were also studied. Analysis of end-expiratory Z data yielded estimates of respiratory resistance (R), inertance (I) and compliance (C). During positive or negative pressure breathing in conscious ducks, minute volume (V) and end-tidal CO2 (PETCO2) remained unchanged from normal (Prs = zero) while tidal volume (VT) and ventilatory period (Ttot) decreased. The respiratory system in late expiration can be modelled well with a simple series R-I-C mechanical model at Prs values of zero, +10 and -10 cm H2O. The value of Z increased at all frequencies studied during compression of the respiratory system (Prs = -10 cm H2O) and did not change much from normal (Prs = zero) during distension (Prs = +10 cm H2O). Both resistance and inertance increased during compression. During distension contradictory changes in resistance and inertance suggest that complex changes in flow profile and/or in flow pathways occurred with positive pressure breathing. Anesthesia or paralysis did not noticeably change the oscillatory resistance or inertance, but increased oscillatory compliance. CO2-breathing did not affect the respiratory impedance in late expiration, but reduced its flow dependence along the ventilatory cycle.

Airway Resistance↗

Magnetic resonance images in a case of "divergence paralysis".

The clinical syndrome of divergence paralysis has been described since the mid 19th century. Speculation still surrounds the possible existence of an anatomical center for divergence function. Our report explores this possibility and describes the magnetic resonance images of a patient with a unilateral 6th nerve palsy who later developed the clinical picture of divergence paralysis.

Abducens Nerve↗

Preliminary characterization of toxins from the straw itch mite, Pyemotes tritici, which induce paralysis in the larvae of a moth.

Homogenates of whole mites (Pyemotes tritici) paralyze larvae of the greater wax moth Galleria mellonella. Injection of these homogenates into larvae produces symptoms identical to those obtained by bites from female mites. Since the paralytic activity is destroyed by heat and proteolytic enzymes and retained during dialysis, the toxic compounds appear to be proteins. Two protein fractions which differ both in molecular weight and toxicity were found following gel filtration of whole mite extracts. Larvae that are injected with proteins from the high molecular weight (c. 250,000) fraction (designated TxP-HMW) develop flaccid-muscle paralysis after 4-12 hr, while proteins in the low molecular weight fraction (c. 21,000) (designated TxP-LMW) induce a rapid, muscle-contracting paralysis.

Animals↗

Spinal paralysis and catalepsy induced by intrathecal injection of opioid agonists.

The intrathecal administration of high (1.05 mumol) doses of D-Ala2-Met5-enkephalinamide (DAMA), D-Ala2-Leu5-enkephalinamide (DADLE), Try-D-Thr-Gly-Phe-Leu-Thr, MR2034-TA, dextrorphan tartrate, U50,488H, levorphanol tartrate, methadone hydrochloride, and 1-methyl-4-phenyl-4-propionoxypiperidine induced spinal hypokinesia. The first 5 of these compounds caused spinal paralysis, whereas the other compounds and lower doses of the first 4 induced waxy catalepsy that was restricted to the hindquarters of rats. The paralysis induced by DAMA was not reversible by IT injections of 50 micrograms naltrexone, indicating, together with the paralytic effects of dextrorphan, that traditional opiate receptors are not involved in this behavioral effect. The spinal catalepsy induced by 0.26 mumol of DAMA was prevented by IT pretreatment with 10 micrograms of naltrexone. In view of this finding and the observation that spinal catalepsy can be induced by agonists of all opiate receptor classes, it seems likely that spinal catalepsy is produced by activation of specific opiate receptors, although the subtype remains to be established.

Animals↗

Hyperinsulinaemia in thyrotoxic hypokalaemic periodic paralysis.

To test the hypothesis that there is an abnormal serum insulin response to a carbohydrate load in thyrotoxic hypokalaemic periodic paralysis (THPP), 18 men with THPP and 15 with uncomplicated thyrotoxicosis were studied during an oral glucose tolerance test. The THPP group had significantly higher fasting insulin concentrations (27.6 [3.6] vs 13.4 [1.8] mU/l; p less than 0.005) and a higher overall insulin response to oral glucose (p less than 0.001 by ANOVA) than the thyrotoxicosis group. There were no significant differences in fasting or stimulated glucose. Hyperinsulinaemia may be an important factor in the precipitation of acute paralysis in THPP.

Acute Disease↗

Facial nerve paralysis in acute otomastoiditis as presenting symptom of FAB M2, T8;21 leukemic relapse. Case report and review of the literature.

Granulocytic sarcoma (chloroma) is a rare solid, extramedullary tumour composed of immature granulocytes, occurring during granulocytic leukemia. Leukemic involvement of the temporal bone is not uncommon and may present in a variety of ways. Symptomatic facial nerve paralysis is one of these. The authors report a case of facial nerve paralysis as the presenting symptom of leukemic relapse in a 16-year-old white male, affected by acute myelogenous leukemia FAB M2, karyotype 46xy, T8;21.

Acute Disease↗

Ion-channel defects and aberrant excitability in myotonia and periodic paralysis.

The myotonias and periodic paralyses are a diverse group of skeletal muscle disorders that share a common pathophysiological mechanism: all are caused by derangements in the electrical excitability of the sarcolemma. Mutations within coding regions of ion-channel genes have been identified recently as the underlying molecular defects in these heritable disorders. Chloride-channel mutations cause a reduction in the resting conductance, which enhances excitability and gives rise to myotonia. By contrast, missense mutations in the L-type Ca2+ channel reduce the electrical excitability of the fiber and cause a form of periodic paralysis. Mutations of the sodium channel impair inactivation of the channel, which, depending on the type and severity of the functional defect, results in either paralysis or myotonia.

Calcium Channels↗

Cat scratch disease in the parotid gland presenting with facial paralysis.

Facial paralysis due to cat scratch disease (CSD) has not been described previously. A case is reported where this self limiting benign condition presented in a child with a parotid lump and a lower motor neurone facial paralysis affecting the marginal mandibular branch of the facial nerve simulating a malignant tumour of the parotid gland. This case demonstrates a highly unusual presentation of CSD.

Cat-Scratch Disease↗

Posterior interosseous nerve paralysis related to focal radial nerve constriction secondary to vasculitis.

A case of posterior interosseous nerve paralysis is reported with discussion of some characteristics that appear to distinguish it from entrapment neuropathy and neuralgic amyotrophy. The surgical implications are also discussed. More than ten similar cases have been reported, but the pathogenesis of this condition is still controversial. The patient presented with posterior interosseous nerve paralysis related to focal radial nerve constriction secondary to vasculitis in the perineurium. The constriction site was resected and the radial nerve was sutured. The patient recovered completely after 8 months.

Adult↗

Hypokalaemic thyrotoxic periodic paralysis: case report and review of an Oriental syndrome.

Presentations of acute systemic weakness are rare and appear dramatic and frightening to both patients and physicians. Aetiologies are multifactorial and diverse. Morbidity and mortality are associated with the unrecognized disease. One of the underlying disorders is hypokalaemic thyrotoxic periodic paralysis (HTPP), an uncommon disorder. HTPP is characterized by periodic occurrences of muscle weakness during attacks of hyperthyroidism and appears predominantly in Orientals. This article describes a patient of Chinese origin with hyperthyroidism and attacks of paralysis and considers several problems: a lack of familiarity with the syndrome, increasing numbers of patients with this disease in European hospitals as a result of migration of populations, and the importance of patient compliance in therapeutic management. Finally, a review of the literature concerning presentation, differential diagnosis, pathophysiology, and therapeutic management is provided.

Adrenergic beta-Antagonists↗

Vocal cord paralysis in children studied by monopolar electromyography.

Twelve children with symptoms of vocal cord paralysis were studied by monopolar needle electromyography. Recordings were used to verify complete or partial paralysis as well as to evaluate the etiology of the problem, paralytic or mechanical. These results then were useful in patient management. The monopolar electromyographic technique is of value in evaluating and treating vocal cord problems.

Adolescent↗

PCR diagnosis of primary herpesvirus type I in poliomyelitis-like paralysis and respiratory tract disease.

Successful and rapid recovery of HSV-1 DNA from the cerebrospinal fluid after amplification by polymerase chain reaction was obtained in a 7-year-old boy with subtotal and permanent upper extremity paralysis with rapid onset and magnetic resonance imaging evidence of cervical cord involvement. Early administration of intravenous acyclovir probably limited neuronal loss. The clinical course and outcome of this disorder best conformed with what has been described as poliomyelitis-like paralysis associated with respiratory tract infection (Hopkins syndrome).

Antibodies, Viral↗

Renal tubular acidosis complicated with hypokalemic periodic paralysis.

Three Chinese girls with hypokalemic periodic paralysis secondary to different types of renal tubular acidosis are presented. One girl has primary distal renal tubular acidosis complicated with nephrocalcinosis. Another has primary Sjögren syndrome with distal renal tubular acidosis, which occurs rarely with hypokalemic periodic paralysis in children. The third has an isolated proximal renal tubular acidosis complicated with multiple organ abnormalities, unilateral carotid artery stenosis, respiratory failure, and consciousness disturbance. The diagnostic evaluation and emergent and prophylactic treatment for these three types of renal tubular acidosis are discussed.

Acidosis, Renal Tubular↗

Facial nerve paralysis of dental origin in children.

Dental causes of facial nerve paralysis are rare and have not been previously reported in children. Two children are described with facial nerve paralysis of dental origin. The underlying mechanism of action and pathogenesis are discussed.

Adolescent↗

Effects of potassium supplementation on the recovery of thyrotoxic periodic paralysis.

Potassium supplements have been recommended to hasten recovery and prevent cardiopulmonary complications in patients with thyrotoxic periodic paralysis (TPP). However, this recommendation has not yet been proven efficacious. Thirty-two patients with acute attacks of TPP over a 3-year-period were divided into 2 groups. Group A (n = 12) was a control group treated with normal saline infusion 125 mL/hr only. Group B (n = 20) received intravenous KCl administration at a rate of 10 mmol/hr in normal saline 125 mL/hr. During the attack and for 6 hours after muscle recovery, hemodynamics were continuously recorded and muscle strength and plasma K(+) concentration were measured hourly. The sex, age, muscle strength, thyroid function, biochemical values including plasma K(+) levels, as well as the time from attack to therapy (3.6 +/- 1.6 v 3.3 +/- 1.0 hr) were not significant between the 2 groups. However, recovery time was significantly shorter in the KCl group than the control (6.3 +/- 3.8 v 13.5 +/- 7.5 hr, P < .01). Rebound hyperkalemia greater than 5.5 mmol/L occurred in 40% patients receiving KCl. The dose of KCl administered and peak K(+) concentration were positively correlated (r = 0.85, P < .001). In conclusion, KCl therapy proves to help the recovery of paralysis in TPP associated with rebound hyperkalemia. KCl supplementation should be given as small as possible (<10 mmol/hr) to avoid rebound hyperkalemia unless there are cardiopulmonary complications.

Adult↗

Peripheral facial nerve paralysis after peritonsillar infiltration of bupivacaine: a case report.

Peritonsillar infiltration of a local anesthetic solution for reduction of posttonsillectomy pain is commonly used although the benefit and complications of this technique have not yet been well established. We report a case of a 4-year-old boy who developed peripheral facial nerve paralysis after perioperative infiltration of bupivacaine and uneventful tonsillectomy. The paralysis was noticed a few minutes after extubation and resolved completely after 8 hours. We assumed this to be caused by the direct action of the local anesthetic agent on the facial nerve.

Adenoidectomy↗

New-onset facial paralysis and undiagnosed recurrence of cutaneous malignancy: evaluation and management.

Perineural invasion of cranial nerves, including the facial nerve by squamous cell carcinoma of the skin, is a poor prognostic factor for recurrent disease and disease-specific mortality. We discuss 2 patients who presented to the Otolaryngology/Head and Neck Surgery service with complete facial nerve paralysis and a history of skin cancer. Based on our experience with these patients, we recommend that patients who present with facial nerve paralysis and a history of cutaneous malignancy undergo aggressive management including early intervention and complete exploration of the facial nerve from the geniculate ganglion out to the periphery. Such rigorous care achieves the best possible oncologic outcomes for a proven aggressive disease.

Aged↗