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PubMed1983

Tick paralysis in Brazil.

From July to December 1977 and from June to November 1978 the toxic effects of Amblyomma cajennense were studied in cattle sheep and goats. Locomotor disturbances commencing as hind-limb paralysis ascended to the upper nervous centres causing paralysis. This was observed in natural infections and confirmed experimentally. Tick paralysis is reported for the first time in Brazil, manifesting itself in a different form to that usually attributed clinically to the disease. Also for the first time reference is made to tick paralysis induced by all developmental stages of A. cajennense.

Animals↗

PubMedDate not supplied

Zoxazolamine-induced paralysis in two rat substrains: differences in hepatic drug metabolism.

Aldehyde dehydrogenase (ALDH) is involved in the metabolism of endogenous and exogenous aldehydes originating from biogenic amines, lipids, food and drugs. Rat liver contains at least two cytosolic ALDHs that can be stimulated by inducers of drug metabolism. Phenobarbital- type inducers increase ALDH1 activity while polycyclic aromatic hydrocarbons (such as benzo[alpha]pyrene) and 2,3,7,8-tetrachlorodibenzo-p-dioxin (TCDD) increase ALDH3c isoenzyme activity. Two rat substrains were isolated according to a different induction of hepatic ALDH after treatment with phenobarbital (PB). Animals that responded to treatment (RR) and those that did not respond (rr) were inbred and divided into two homogenous groups. These animals constituted an ideal experimental model due to their common origin. Apart from the dramatic induction of cytosolic ALDH1 and ALDH3c, the effects of PB on pentoxy-, ethoxy- and methoxy-resorufin-O-dealkylase (P-, E-, and MROD) between the two substrains were also studied. 3-Methylcholanthrene (3MC) greatly increased ALDH3c levels in both substrains, although it was slightly more pronounced in the rr rats, in which it was assessed either as ALDH3c or as total cytosolic ALDH. A similar trend was also noted in EROD, PROD and MROD activities. Dealkylation of the methoxy group was found to be statistically different between the two substrains (rr > RR). The relevance of the biochemical findings with the in vivo hepatic capacity for drug metabolism was investigated by measuring the duration of zoxazolamine paralysis. Both animal substrains were tested with zoxazolamine either without pretreatment or after administration of PB or 3MC: the paralysis produced by zoxazolamine lasted for a longer period in rr than in RR rats. After pretreatment with PB, the duration of paralysis was greatly reduced, but the differences between the two substrains remained. Pretreatment with various doses of 3MC produced differences in the duration of paralysis in RR and rr rats, although the time period was much shorter than that observed in control animals.

Aldehyde Dehydrogenase↗

PubMed2005

[Hypokalemic thyrotoxic periodic paralysis (HTPP). Rare differential diagnosis in case of acute tetraparesis in Europe].

BACKGROUND: Differential diagnosis of acute tetraparesis includes paraplegia caused by trauma, ischemia, inflammation or tumor, Guillain-Barré syndrome, periodic paralysis, myasthenia gravis, and dissociative paralysis. CASE REPORT: The case of a 45-year-old man is reported who noticed weakness of both legs after heavy labor. In the evening he was unable to climb stairs, at night he noticed additional weakness in both arms and dyspnea. After transfer to the authors' department profound tetraparesis, tachycardia and slight dyspnea were found on examination. Cranial nerve examination was unremarkable. Deep tendon reflexes, however, were only slightly diminished. Laboratory work-up revealed hypokalemia (potassium 1.9 mmol/l) and hyperthyreosis. Elevated TRAK and TPO antibodies as well as sonography and scintigraphy of the thyroid gland gave evidence of Graves' disease. After intravenous administration of potassium tetraparesis resolved completely. CONCLUSION: Hypokalemic thyrotoxic periodic paralysis (HTPP), a subtype of hypokalemic paralysis, is unusual in Caucasians. In Asian men the disease is more common. The underlying mechanism is an extra-intracellular shift of potassium in the voluntary muscle cells. In contrast to hereditary autosomal dominant paralyses, a genetic defect is not known. Usually, symptoms of hyperthyreosis in HTPP are mild which can hamper the correct diagnosis.

Acute Disease↗

PubMed2006

Bilateral diaphragm paralysis following cardiac surgery in children: 10-years' experience.

OBJECTIVE: To review the incidence and complications of conservative management of bilateral diaphragm paralysis following pediatric cardiac surgery. DESIGN AND SETTING: Retrospective clinical review based on computerized database with daily follow-up in a pediatric cardiac intensive care unit in a tertiary care center. PATIENT AND PARTICIPANTS: Were reviewed the data on nine patients with bilateral diaphragm paralysis from the 3,214 consecutive children (0.28%) after operations performed between 1995 and 2004. MEASUREMENTS AND RESULTS: A fluoroscopy-confirmed diagnosis of bilateral diaphragm paralysis was made in all nine patients. Mechanical ventilation was required for 14-62 days; maximum time to recovery was 7 weeks. Three patients underwent unilateral plication. Patients with a complicated postoperative course required longer mechanical ventilation. All patients were managed with a nasotracheal tube. One patient had minor subglottic stenosis. All patients survived. CONCLUSIONS: Bilateral diaphragm paralysis can be managed conservatively with good prognosis and minor complications. The recovery time is relatively short, less than 7 weeks.

Cardiac Surgical Procedures↗

PubMed2004

Ticks and tick paralysis: imaging findings on cranial MR.

Tick paralysis is an acute, progressive, and potentially fatal muscle paralysis secondary to a toxin secreted by a pregnant tick during a bite. Although tick bites can occur anywhere on the body, ticks are frequently overlooked on the scalp because of overlying hair. Children with acute neurologic symptoms frequently undergo MR scanning that may incidentally reveal the offending tick. Timely identification and removal of the tick leads to rapid recovery from tick paralysis. We report the MRI findings at 1.5 T of tick paralysis with an attached tick.

Child, Preschool↗

PubMed2001

Diagnosis of psychogenic paralysis: the role of motor evoked potentials.

BACKGROUND: In the nineties, there has been evidence that motor evoked potential (MEP) studies might improve the diagnosis of psychogenic paralysis. OBJECTIVE: To review a series of patients (1986-1999) who finally had a diagnosis of psychogenic paralysis at our Institutions. To detect if, over that period, the time taken to make the diagnosis had changed, and, if so, this had any relationship to the diagnostic tests used or to other variables. METHODS: We selected a patient sample (n=21) seen by the same team of neurologists, whose diagnostic criteria were homogeneously based on the DSM IV, and who were studied with MEPs. We analysed their clinical features, the type and timing of the investigations done, and the time taken to make the diagnosis. These variables acted as the dependent factors in a Multivariate Analysis of Variance (MANOVA) model, in which the year of observation was the fixed factor. RESULTS: The diagnosis was 50% earlier in the period 1993 to 1999 (10 patients) than in the period 1986-1992 (11 patients) (F = 28.3, p < 0.0001). The only associated change was an earlier MEP study (F=18.4, p < 0.0001), which invariably showed normal findings. CONCLUSION: MEP studies contributed to speed up the diagnosis of psychogenic paralysis. Possibly, normal MEPs rendered the neurologist confident about the physiological integrity of motor fibers in the corticospinal tract, anterior roots and plexuses. Such integrity, if nerve trunks and muscles are intact, and in the appropriate diagnostic context, implies a psychogenic cause for paralysis.

Adolescent↗

PubMed2002

Complete paralysis of the quadriceps muscle caused by traumatic iliacus hematoma: a case report.

A15-year-old girl who developed traumatic iliacus hematoma and complete paralysis of the quadriceps muscle is reported. The current case and literature review revealed that incomplete quadriceps paralysis associated with traumatic iliacus hematoma is likely to progress to complete paralysis in days or weeks as a result of increased intracompartmental pressure. However, surgical decompression of the femoral nerve could produce good results even in patients who have complete quadriceps paralysis preoperatively.

Accidental Falls↗

PubMed1985

Ankle-foot orthoses: effect on gait abnormalities in tibial nerve paralysis.

To study the biomechanical effects of gastrocnemius-soleus dysfunction and its potential remediation, the gait patterns of six able-bodied young adults were analyzed before and after induced temporary tibial nerve paralysis. Ambulation with the tibial nerve block was performed with and without the assistance of an ankle-foot orthosis (AFO) with a rigid anterior stop adjusted to either 5 degrees plantarflexion or 5 degrees dorsiflexion. The gait abnormalities resulting from tibial nerve paralysis include delayed advancement of the center of pressure, delayed ipsilateral heeloff and early contralateral heelstrike, decreased steplength, decreased ankle dorsiflexion moment, and increased knee flexion moment. This study provides quantitative information on the degree to which these abnormalities were corrected by appropriately adjusted AFOs. When using an AFO with an anterior stop, subjects with tibial nerve paralysis had improved advancement of the center of pressure (p less than 0.01). The body's ground reactive force line moved forward more normally, pivoting over the metatarsal head area and raising the heel earlier than observed with uncorrected tibial nerve paralysis, thus approximating the normal ankle dorsiflexion moment, normal timing of gait events, normal advancement of the hip, and normal steplength. The AFO with the anterior stop set at 5 degrees plantarflexion was more effective in restoring the values to normal than the AFO with the anterior stop set at 5 degrees dorsiflexion, but still did not consistently achieve the normal values. Only by using the AFO with the anterior stop set at 5 degrees plantarflexion was the increased knee flexion moment observed during the block reduced to normal levels (p less than 0.01).(ABSTRACT TRUNCATED AT 250 WORDS)

Adult↗

PubMed1993

Phenytoin increases specific triacylglycerol fatty esters in skeletal muscle from horses with hyperkalemic periodic paralysis.

Previous studies have demonstrated that phenytoin decreases the levels of triacylglycerols in several tissues other than skeletal muscle. Since phenytoin is clinically effective in several skeletal muscle disorders, triacylglycerol metabolism in skeletal muscle from four normal Quarter horses and four Quarter horses with hyperkalemic periodic paralysis was examined. The horses with hyperkalemic periodic paralysis had low levels of 18:3 in the phospholipids, low levels of 16:0, 16:1 and 18:3 in the free fatty acids and low levels of 20:4 in triacylglycerols. Triacylglycerol levels were increased in skeletal muscle from seven (three controls, four hyperkalemic periodic paralysis) of the eight horses on treatment with oral phenytoin for one week. Instead of an increase in all fatty ester types only 16:0, 16:1, 18:1 and 18:2 were significantly increased. Total lipid phosphorus and the distribution of phospholipid fatty esters and free fatty acids were not significantly altered by phenytoin treatment in most cases. An alteration in triacylglycerol metabolism by phenytoin was also observed in primary cultures of normal equine skeletal muscle radiolabeled with 18:1, but not in those radiolabeled with 18:2. These findings suggest that phenytoin does not just increase the levels of triacylglycerol in skeletal muscle, but alters the utilization and incorporation of fatty esters. These findings suggest a potential involvement of triacylglycerol metabolism in the clinical efficacy of phenytoin in hyperkalemic periodic paralysis.

Animals↗

PubMed1980

Sensitivity of the mature lateral geniculate nucleus to components of monocular paralysis.

Immobilization of the globe by tenotomization of the extrinsic muscles of one eye reduces the encounter rate for X-latency cells in the contralateral dorsal lateral geniculate nucleus (LGN) of adult cats. The reduction in the relative encounter rate for X-latency cells after tenotomy was comparable to that previously observed in the adult cat following concurrent paralysis of the extrinsic and intrinsic muscles of one eye by transection of cranial nerves III, IV, and VI. Paralysis of the intrinsic muscles alone by atropinization, on the other hand, had no detectable effect upon this aspect of LGN physiology. It appears, therefore, that monocular paralysis by cranial nerve section has its effects on LGN X-latency cells through its paralysis of the extrinsic eye muscles. Furthermore, the reduction in the relative encounter rate for X-latency cells produced by tenotomy occurred in spite of early, incomplete return of mobility of the globe. Thus, unilaterally diminished mobility of the globe, in contrast to the complete, sustained immobility characteristic of monocular praralysis, appears sufficient to alter this aspect of LGN physiology in adult cats. The general observation that sensory modifications, in the adult cat, are capable of inducing shifts in the relative recording probabilities for X- and Y-latency cells in the LGN has been repeatedly made. Further, recent, independent observations have provided confirmation for the phenomenon of X/Y ratio shifts in the LGN following adult-onset stimulus modification.

Animals↗

PubMed1990

Competitive and non-competitive NMDA antagonists limit dynorphin A-induced rat hindlimb paralysis.

It has been proposed that the endogenous opioid dynorphin A (Dyn A) contributes to the pathogenesis of posttraumatic spinal cord injury (SCI). Dyn A-related peptides given intrathecally (i.t.) produce hindlimb paralysis. These include Dyn A(1-17), Dyn A(1-13), Dyn A(2-17), and Dyn A(3-13). Because Dyn A(2-17) and Dyn A(3-13) are inactive at opiate receptors, Dyn A-induced paralysis may include a non-opioid component. Recently, it has been reported that competitive N-methyl-D-aspartate (NMDA) antagonists block the loss of tail-flick reflex caused by i.t. administration of Dyn A(1-13). In the present studies we examined whether competitive [(4-[3-phosphonopropyl]-2-piperazine-carboxylic acid (CPP)] or non-competitive (dextrorphan) NMDA antagonists could attenuate paralysis induced by Dyn A(1-17) or Dyn A(2-17). CPP or dextrorphan each significantly attenuated the neurologic dysfunction and mortality associated with Dyn A(1-17) administration. In addition, CPP and dextrorphan significantly reduced the neurologic dysfunction caused by Dyn A(2-17)(all P less than 0.05). From these data we suggest that the non-opioid component of Dyn A-induced paralysis is mediated in part by the NMDA receptor.

Animals↗

PubMed1989

Testosterone-induced acceleration of recovery from facial paralysis following crush axotomy of the facial nerve in male hamsters.

In this study, the effects of testosterone propionate (TP) on recovery from facial paralysis following crush axotomy of the facial nerve in male hamsters were examined. In the first experiment, TP (5 mg/ml sesame oil; 0.1 ml) was injected subcutaneously and on alternate days in one-half of the animals subjected to crush axotomies of the facial nerve, with the second half receiving vehicle alone. An accelerative effect of TP on recovery from facial paralysis was observed near the end of the first and beginning of the second week after crush axotomy. When the dosage and frequency were doubled in the next experiment, a greater accelerative effect of TP on recovery from facial paralysis was observed. In the last experiment, castrated animals were used in order to eliminate the endogenous source of the hormone and two different modes of hormone administration, TP implants vs TP injections, were compared. The results of that experiment indicate that continuous exposure to the hormone, in the form of subcutaneous implants of 100% crystalline TP, had the most pronounced effect on acceleration of recovery from facial paralysis. In addition, no differences in the responses of the castrated, axotomized animals and the normal, axotomized animals were found. This suggests that the presence of endogenous hormone contributes little to the acceleration of functional recovery observed with TP. Finally, the time course of the accelerative effect of TP suggests that the hormone is acting primarily at the level of the facial neuron, which contains androgen receptors, and perhaps secondarily at the level of the facial muscles, which are also known to contain androgen receptors.

Animals↗

PubMed1977

Neuromuscular paralysis caused by tick envenomation.

The Australian scrub-tick Ixodes holocyclus causes a series of significant toxic effects in its victims. The most important feature of tick envenomation is neuromuscular paralysis. Children poisoned by ticks may manifest only local motoneural effects, usually facial paralysis. Progressive ascending flaccid paralysis occurs if the removal of an embedded tick is delayed. The specific neurological features of tick-bite are discussed in the light of a series of 6 children who all showed signs of tick paralysis. Tick venom is known to slow nerve conduction, and may have a botulinum-like effect at the neuromuscular junction. The literature on the neurological effects of tick-envenomation is reviewed.

Australia↗

PubMed1988

GABA involvement in naloxone induced reversal of respiratory paralysis produced by thiopental.

No agent is yet available to reverse respiratory paralysis produced by CNS depressants, such as general anesthetics. In this study naloxone reversed respiratory paralysis induced by thiopental in rats. 25 mg/kg, i.v. thiopental produced anesthesia without altering respiratory rate, increased GABA, decreased glutamate, and had no effect on aspartate or glycine levels compared to controls in rat cortex and brain stem. Pretreatment of rats with thiosemicarbazide for 30 minutes abolished the anesthetic action as well as the respiratory depressant action of thiopental. 50 mg/kg, i.v. thiopental produced respiratory arrest with further increase in GABA and decrease in glutamate again in cortex and brain stem without affecting any of the amino acids studied in four regions of rat brain. Naloxone (2.5 mg/kg, i.v.) reversed respiratory paralysis, glutamate and GABA levels to control values in brain stem and cortex with no changes in caudate or cerebellum. These data suggest naloxone reverses respiratory paralysis produced by thiopental and involves GABA in its action.

Animals↗

PubMed1995

The median paralysis unit: a more pharmacologically relevant unit of biologic activity for botulinum toxin.

Although the LD50 has been used to quantify the biologically active toxin in clinical preparations of botulinum A toxin (Botox and Dysport), a discrepancy exists between the clinical potency of equivalent international units of different formulations of botulinum A toxin for multiple clinical indications. Our laboratory previously reported that a regional chemodenervation assay in the mouse could be utilized to detect the difference in the potencies of the clinical preparations of toxin [Pearce et al. (1994) Toxic. appl. Pharmac. 128, 69-77]. The purpose of this study was to quantify the regional paralysis produced by botulinum toxin and define a new pharmacologic/biologic unit of activity that more accurately reflects the mechanism of action of botulinum toxin in the clinical setting. Quantal analysis of regional paralysis revealed that the ED50, defined as the median paralysis unit (MPU) for Botox and Dysport, was 0.41 +/- 0.01 and 1.00 +/- 0.02 LD50 units, respectively. Differences in the potencies found in retrospective clinical studies comparing Botox and Dysport were accurately reflected, for the first time, by the dose of toxin expressed in terms of the MPU (median paralysis unit). The data suggested that the MPU may be a more appropriate measure of the biologic activity in therapeutic formulations of botulinum toxin.

Animals↗

PubMed1988

Vocal cord paralysis following child abuse.

Otorhinologic manifestations of child abuse are infrequently reported in the literature. Three cases of vocal cord paralysis following child abuse are presented. The pathophysiology of vocal cord paralysis is reviewed as it relates to pediatric vocal cord paralysis. Recognition of the possibility of vocal cord paralysis in an abused child who suffers significant head trauma or a strangulation injury is necessary to insure a more rapid diagnosis and initiation of effective therapy more promptly.

Airway Obstruction↗

PubMed1982

Antagonism of the ruthenium red-induced paralysis in mice by 4-aminopyridine, guanidine and lanthanum.

4-Aminopyridine and guanidine were administered intraperitoneally to mice during the complete flaccid paralysis induced by treatment with ruthenium red (RuR). At 1-8 min after 4-aminopyridine or guanidine the animals had recovered completely from the paralysis, whereas the control mice injected only with RuR remained paralytic for at least 60 min. Intraperitoneal injections of LaCl3 had no apparent effects on animal motility and did not reverse the paralysis produced by RuR. However, when La3 + was administered 30 min prior to RuR the occurrence of flaccid paralysis was totally prevented. The results obtained are discussed in terms of the possible antagonist effects of the compounds used on acetylcholine release at neuromuscular junctions.

4-Aminopyridine↗

PubMed2005

Non-traumatic congenital facial nerve paralysis; electroneurophysiologic evaluation of four cases.

Non-traumatic congenital facial paralysis is frequently due to intrauterine hypoplasia of the facial nerve and usually appears as a component of a syndrome. The experience about this problem is limited due to its rare occurrence and sometimes differential diagnosis of congenital facial paralysis of developmental origin from an acquired one in children and infants needs much effort. Controversy remains regarding the site of the lesion. Total facial paralysis is uncommon and inherited transmission has been reported on some occasion. Four children with congenital facial paralysis, whose family history is noncontributory, are presented in this report and the related literature is reviewed.

Child↗