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PubMed2006

[Synthetical treatment for facial paralysis using static and dynamic techniques].

OBJECTIVE: To investigate a synthetical technique combining static and dynamic states for treating facial paralysis. METHODS: From October 1993 to November 2005, 93 patients (26 males, 67 females; aged 9-69 years; illness course, 6 months to 24 years) with facial paralysis were admitted for treatment, of whom 48 were unknown in their pathological origins, 32 had a history of intracranial or ear operation, 13 had their facial paralysis related to trauma. We applied synthetical techniques for treating facial paralysis, including denerved muscle (extensor hallucis brevis and extensor digitorum brevis) free graft using an operating or chemical technique, temporal muscular flap suspending, treatment of eye closure by uplifting zygomo-malar tissues and temporal muscular flap suspending, brow lifting by the Buried Guiding Suture Appliance, Botox injection, and the nerve amputation of normal side for mandibular marginal ramus paralysis. RESULTS: After the treatment for 82 patients with the method of the denerved muscle free graft combining femoral muscular flap suspending, 3 patients with the method of uplifting zygomo-malar tissues combining temporal muscular flap suspending for eye closure, 15 patients with the method of the Buried Guiding Suture for eyebrow lifting, 4 patients with the Botox injection and nerve amputation of normal side for the mandibular marginal ramus paralysis, 93 patients had a good therapeutic result. The follow-up for 3 months to 10 years in all the patients revealed that 75 patients were satisfied with their treatment results and 13 patients were almost satisfied according to the criteria for the facial symmetrical checking and the House-Brackmann grading system. The technique had advantages of a complete survival of the related small muscles, a hidden incision, less trauma for the Botox injection, and the denerved muscles for surrounding nerve inserting. CONCLUSION: The synthetical technique combining static and dynamic states for treating facial paralysis is a good therapeutic method and the therapies for facial paralysis should vary with the different conditions of the paralysis. We advocate an individuation treatment for facial paralysis.

Adolescent↗
PubMed1984

Combined use of integrated electromyography and score rating method for evaluation and prognosis of facial paralysis.

Degrees of peripheral facial paralysis were assessed by the paralysis score table in a modification of May's method together with the integrated EMG method. Paralysis scores and integrated EMGs from the frontal, orbicularis oculi and orbicularis oris muscles were obtained from 68 patients with facial paralysis. A linear regression analysis was tried in the cases of complete recovery with the following equation: Y = B log X + A, where Y = percentage of paralysis score or integrated EMG, B = recovery rate, A = constant and X = days after onset. The correlation coefficient of paralysis score and the days expressed in logarithmic form was 0.979. The paralysis scores obtained showed good correlation (0.933-0.941) with the value of the integrated EMG. The paralysis score for facial paralysis was thus confirmed by the objective EMG method. Recovery process from facial paralysis can be analysed numerically by the application of linear regression analysis in both methods.

Electromyography↗
PubMed1997

Recurrent laryngeal nerve paralysis: a complication of thyroidectomy.

OBJECTIVE: To study factors related to recurrent laryngeal nerve (RLN) paralysis, a major complication of thyroidectomy. DESIGN: Retrospective study of outcome of patients' medical records. PATIENTS AND METHODS: Records of 361 patients who underwent thyroidectomy by otolaryngologists at Ramathibodi Hospital were reviewed for RLN paralysis. MAIN OUTCOME MEASURES: RLN injury was analyzed in relation to types of surgery, RLN identification, and histopathology. The analysis was based on the number of RLNs at risk. RESULTS: The incidence of permanent RLN paralysis was 2.38%. Both the permanent RLN paralysis and temporary RLN paralysis were significantly related to the histopathologic findings of malignancy (p < .005). The positive identification of RLN and the types of surgery were not found to be significant factors in either permanent RLN paralysis or temporary RLN paralysis. CONCLUSIONS: There was insufficient evidence to support that the identification of RLNs during surgery would be a significant factor in reducing the likelihood of RLN paralysis. However, RLNs should be identified to avoid iatrogenic injury and subsequent paralysis. Meticulous surgical technique should be applied in patients whose results of fine-needle aspiration biopsy suggested malignancy, as there is the possibility of difficult surgery and potential iatrogenic RLN paralysis in this group of thyroid patients.

Adolescent↗
PubMed1997

[Current status of clinical and molecular-biological research on familial periodic paralysis].

Types of periodic paralysis seen in Japan are numerous: the one most frequently seen is hypokalemic periodic paralysis. Among them, approximately 50% are secondary to thyrotoxicosis. Number of families of familial hyperkalemic periodic paralysis have also been reported so far. Several cases of hyperkalemic periodic paralysis secondary to thyrotoxicosis have also been reported exclusively from Japan. As the pathogenesis of hypokalemic periodic paralysis, depolarization block induced by membrane permeability change in the face of hypokalemia triggered by excess insulin was strongly suggested and supported experimentally in part. Recent linkage analysis on familial hypokalemic periodic paralysis revealed that the abnormality is linked to a mutation in voltage-gated Ca channel. The difficulty remains how to explain the cause of hypokalemia which is almost always preceding the attack of periodic paralysis of this type. The cause of hyperkalemic periodic paralysis was shown to be the mutation in voltage-gated Na channel. Failure of inactivation of the channel causes an increase in inward sodium current which results in depolarization and accumulation of potassium. The explanation of the pathogenesis of paralysis is straight-forward when compared to that of hypokalemic periodic paralysis.

Calcium Channels↗
PubMed2003

Clinical analysis of cervical radiculopathy causing deltoid paralysis.

In general, deltoid paralysis develops in patients with cervical disc herniation (CDH) or cervical spondylotic radiculopathy (CSR) at the level of C4/5, resulting in compression of the C5 nerve root. Therefore, little attention has been paid to CDH or CSR at other levels as the possible cause of deltoid paralysis. In addition, the surgical outcomes for deltoid paralysis have not been fully described. Fourteen patients with single-level CDH or CSR, who had undergone anterior cervical decompression and fusion for deltoid paralysis, were included in this study. The severity of deltoid paralysis was classified into five grades according to manual motor power test, and the severity of radiculopathy was recorded on a visual analog scale (zero to ten points). The degree of improvement in both the severity of deltoid paralysis and radiculopathy following surgery was evaluated. Of 14 patients, one had C3/4 CDH, four had C4/5 CDH, three had C4/5 CSR, one had C5/6 CDH, and five had C5/6 CSR. Both deltoid paralysis and radiculopathy improved significantly with surgery (2.57+/-0.51 grades vs 4.14+/-0.66, P=0.001, and 7.64+/-1.65 points vs 3.21+/-0.58, P=0.001, respectively). In conclusion, the current study demonstrates that deltoid paralysis can develop due to CDH or CSR not only C4/5, but also at the levels of C3/4 and C5/6, and that surgical decompression significantly improves the degree of deltoid paralysis due to cervical radiculopathy.

Adult↗
PubMed1991

A strychnine-sensitive site is involved in dynorphin-induced paralysis and loss of the tail-flick reflex.

Dynorphin A(1-13) administered intrathecally to rats induces a reversible hindlimb paralysis and permanent loss of the tail-flick reflex in a dose-dependent and all-or-none manner. The loss of the tail-flick reflex has been determined to result from neurotoxicity linked to the N-methyl-D-aspartate (NMDA) receptor. Recently, it has been reported that NMDA antagonists attenuate irreversible paralysis induced by dynorphin A(1-17) and dynorphin A(2-17). In the present studies, we examined whether repeated injections of dynorphin A(1-13) acetate salt could change the characteristics of the reversible paralysis. Injections repeated every 48 h resulted in hindlimb paralysis upon each injection which was not different in terms of magnitude or duration (P greater than 0.60). Injections repeated at 2 h intervals resulted in desensitization of the paralytic effects (P less than 0.05). We also examined if strychnine sulfate, a glycine antagonist would alter the paralytic response to dynorphin. Strychnine protected rats from paralysis (P less than 0.01) and loss of the tail-flick reflex with an ED50 of 7 nmol. We conclude that the reversible paralysis induced by dynorphin A(1-13) is repeatable which suggests that the paralysis results from nontoxic or subtoxic actions of dynorphin. Desensitization to the paralytic effects occurs with closely spaced injections by some unknown mechanism. In addition, we conclude that the spinal glycinergic inhibitory system may participate in the induction of the paralysis because strychnine antagonizes dynorphin-induced paralysis.(ABSTRACT TRUNCATED AT 250 WORDS)

Animals↗
PubMed1985

Aminoglycoside-induced biphasic hindlimb paralysis in the rat: a histological and electrophysiological assessment.

The intrathecal injection of gentamicin into a human patient with gram-negative bacterial meningitis as well as its intracisternal injection into rabbits caused spongy-like lesions in the gray matter and tetraplegia in rabbits. To characterize this neurotoxic effect, gentamicin was injected into the subarachnoid space of the lumbar spinal cord of the rat. A biphasic hindlimb paralysis ensued which consisted at first of a transient flaccid paralysis lasting 1 to 5 hr followed by a permanent flaccid paralysis which developed after 24 to 36 hr. The initial paralysis occurred simultaneously with the transient loss of reflex transmission through the cord but in the absence of lesions in the spinal cord or physiological alterations of neuromuscular transmission and muscle contraction. The onset of the second phase of paralysis occurred concomitant with changes in reflex transmission and appearance of lesions. Loss of neuromuscular transmission and appearance of signs of denervation (e.g., depolarization, alteration in action potential parameters, and chemosensitivity) appeared after the second phase of paralysis was established. Both the initial transient and late permanent paralysis originated in the spinal cord. The early transient paralysis appears to be due to a central block of transmission while the late paralysis apparently resulted from neuronal damage. The neurotoxic effects of aminoglycosides on neuronal elements in the spinal cord resulted in secondary effects (signs of denervation) in hindlimb muscles.

Action Potentials↗
PubMed1996

Vocal fold paralysis in infants twelve months of age and younger.

Seventeen cases of unilateral or bilateral vocal fold paralysis were diagnosed in infants younger than 12 months from 1991 to 1994 at the University of Iowa Hospitals and Clinics. Eight (47%) children with left vocal fold paralysis had a history of prior thoracic surgery--two to repair complex congenital anomalies and six to ligate a patent ductus arteriosus. During the study period, a total of 81 patent ductus arteriosus ligations were performed, yielding a 7.4% postoperative incidence of vocal fold paralysis. Seven (41%) children had idiopathic vocal fold paralysis (3 right, 1 left, 3 bilateral). Two (12%) children had VFP caused by central nervous system pathology (1 right, 1 bilateral). Tracheotomy was not required in any case. Prognosis for vocal fold paralysis varied with cause. With left vocal fold paralysis caused by thoracic surgery, no improvement was noted after an average follow-up of 6 months; with idiopathic vocal fold paralysis infants improved within an average of 6 weeks of diagnosis; with vocal fold paralysis caused by central nervous system pathology, treatment of the underlying condition was followed by return of vocal cord function. Irrespective of cause, the morbidity associated with vocal fold paralysis is minimal. Although tracheotomy is not required, careful airway observation is important. Differences and similarities of these results with other studies are discussed.

Ductus Arteriosus, Patent↗
PubMed2001

Phenotypic variation of a Thr704Met mutation in skeletal sodium channel gene in a family with paralysis periodica paramyotonica.

OBJECTIVES: Patients with paralysis periodica paramyotonica exhibit a clinical syndrome with characteristics of both hyperkalaemic periodic paralysis and paramyotonia congenita. In several types of periodic paralysis associated with hyperkalaemia, mutations in the skeletal muscle sodium channel (SCN4A) gene have been previously reported. Phenotypic variations of mutations in SCN4A, however, have not been described yet. The present study aimed to evaluate genetic variations in a family with clinical and electrophysiological characteristics of paralysis periodica paramyotonia. METHODS: Seven members of a family affected with symptoms of paralysis periodica paramyotonia were studied by electrophysiological and genetic analyses. There were increased serum potassium concentrations in four members during paralytic attacks induced by hyperkalaemic periodic paralysis provocation tests. Short exercise tests before and after cold immersion were carried out in four patients to distinguish electrophysiological characteristics of hyperkalaemic periodic paralysis and paramyotonia. Sequencing analyses of SCN4A were performed on one patient and a normal control to identify polymorphisms. Restriction fragment length polymorphism (RFLP) analysis was then performed at the identified polymorphic sites. RESULTS: Electrophysiological studies showed both exercise sensitivity and temperature sensitivity. Compound motor action potential (CMAP) amplitudes were decreased (7.3%-28.6%) after short exercise tests. The CMAP amplitudes were even more severely decreased (21.7%-56.5%) in short exercise tests after cold exposure. Three polymorphic sites, Gln371Glu, Thr704Met, and Aspl376Asn were identified in SCN4A. RFLP analyses showed that all affected patients carried the Thr704Met mutation, whereas unaffected family members and a normal control did not. CONCLUSION: Phenotypic variation of the Thr704Met mutation, which was previously reported in patients with hyperkalaemic periodic paralysis, is described in a family affected with paralysis periodica paramyotonia.

Adult↗
PubMed1992

Prognostic value of evoked and standard electromyography in acute facial paralysis.

Ninety-one patients with idiopathic (n = 62) and traumatic (n = 29) facial paralyses were available for evaluation at least 1 year after the onset of paralysis. In nine cases of idiopathic paralysis and in 12 cases of traumatic paralysis, total intratemporal nerve decompression was performed. The remaining patients were treated with steroids alone. All patients underwent evoked electromyography (EEMG) testing within 2 weeks of the onset of paralysis. Facial nerve recovery was graded using the House-Brackmann facial nerve recovery scale. Subjects were grouped according to maximal decline of compound muscle action potential (CAP), as determined by EEMG, and by level of recovery 1 year after onset of paralysis. Among patients who did not undergo surgical decompression of the facial nerve, incomplete clinical recovery (grade III or higher) was significantly associated with CAP decline of greater than 90% (p less than 0.05) for idiopathic paralysis. In contrast, there was no significant association between CAP decline of greater than 90% and clinical outcome in traumatic paralysis. These findings support previous reports of the prognostic value of EEMG in idiopathic facial paralysis, but suggest that this test may have less predictive value in the evaluation of facial paralysis as a result of trauma.

Action Potentials↗
PubMed2000

Laryngeal paralysis in cats: 16 cases (1990-1999).

OBJECTIVE: To determine clinical signs, physical examination findings, radiographic features, and concurrent diseases in cats with laryngeal paralysis, as well as evaluate the outcome of medical or surgical management. DESIGN: Retrospective study. ANIMALS: 16 cats. PROCEDURE: Medical records from January 1990 to April 1999 were examined for cats with laryngeal paralysis. Signalment, clinical signs, physical examination findings, cervical and thoracic radiographic findings, laryngeal examination results, and clinical outcome were reviewed. RESULTS: No breed or sex predilection was identified in 16 cats with laryngeal paralysis. The most common clinical signs included tachypnea or dyspnea, dysphagia, weight loss, change in vocalization, coughing, and lethargy. Clinical signs were evident for a median of 245 days. Airway obstruction was apparent on cervical and thoracic radiographic views in 9 cats. Examination of the larynx revealed bilateral laryngeal paralysis in 12 cats and unilateral laryngeal paralysis in 4 cats. The 4 cats with unilateral disease were managed with medical treatment, and 3 of these had acceptable long-term outcomes. Seven of 12 cats with bilateral paralysis underwent surgery; procedures performed included left arytenoid tie back, bilateral arytenoid tie back and ventriculo-cordectomy, and partial left arytenoidectomy. One cat was euthanatized as a result of complications from surgery. CONCLUSIONS AND CLINICAL RELEVANCE: Laryngeal paralysis is an uncommon cause of airway obstruction in cats. Cats with less severe clinical signs (often with unilateral paralysis) may be successfully managed with medical treatment, whereas cats with severe airway obstruction (often with bilateral paralysis) may benefit from surgical intervention.

Airway Obstruction↗
PubMed1997

Resolution of sleep paralysis by weak electromagnetic fields in a patient with multiple sclerosis.

Sleep paralysis refers to episodes of inability to move during the onset of sleep or more commonly upon awakening. Patients often describe the sensation of struggling to move and may experience simultaneous frightening vivid hallucinations and dreams. Sleep paralysis and other manifestations of dissociated states of wakefulness and sleep, which reflect deficient monoaminergic regulation of neural modulators of REM sleep, have been reported in patients with multiple sclerosis (MS). A 40 year old woman with remitting-progressive multiple sclerosis (MS) experienced episodes of sleep paralysis since the age of 16, four years prior to the onset of her neurological symptoms. Episodes of sleep paralysis, which manifested at a frequency of about once a week, occurred only upon awakening in the morning and were considered by the patient as a most terrifying experience. Periods of mental stress, sleep deprivation, physical fatigue and exacerbation of MS symptoms appeared to enhance the occurrence of sleep paralysis. In July of 1992 the patient began experimental treatment with AC pulsed applications of picotesla intensity electromagnetic fields (EMFs) of 5Hz frequency which were applied extracerebrally 1-2 times per week. During the course of treatment with EMFs the patient made a dramatic recovery of symptoms with improvement in vision, mobility, balance, bladder control, fatigue and short term memory. In addition, her baseline pattern reversal visual evoked potential studies, which showed abnormally prolonged latencies in both eyes, normalized 3 weeks after the initiation of magnetic therapy and remained normal more than 2.5 years later. Since the introduction of magnetic therapy episodes of sleep paralysis gradually diminished and abated completely over the past 3 years. This report suggests that MS may be associated with deficient REM sleep inhibitory neural mechanisms leading to sleep paralysis secondary to the intrusion of REM sleep atonia and dream imagery into the waking state. Pineal melatonin and monoaminergic neurons have been implicated in the induction and maintenance of REM sleep and the pathogenesis of sleep paralysis and it is suggested that resolution of sleep paralysis in this patient by AC pulsed applications of EMFs was related to enhancement of melatonin circadian rhythms and cerebral serotoninergic neurotransmission.

Adult↗
PubMed1998

Bilateral vocal cord paralysis following anterior cervical discectomy and fusion. Case report.

The authors report a rare case of bilateral vocal cord paralysis following anterior cervical discectomy and fusion (ACD/F) in a patient who had a preexisting, clinically silent, and unrecognized unilateral vocal cord paralysis from a remote cardiac surgical procedure. The patient, a 41-year-old woman who developed acute respiratory stridor and respiratory insufficiency at the time of extubation after undergoing a C6-7 ACD/F, required emergency reintubation and ventilation. Otolaryngological evaluation revealed bilateral vocal cord paralysis with one vocal cord showing evidence of acute paralysis and the other showing evidence of chronic paralysis. She eventually required a permanent tracheotomy. The patient had undergone previous cardiac surgical procedures to correct Fallot's tetralogy as a neonate and as a child. At those times, there were no recognized symptoms of transient or permanent vocal cord dysfunction. This case emphasizes the importance of identifying patients with preexisting unilateral vocal cord paralysis before performing neurosurgical procedures such as ACD/F, which can place the only functioning vocal cord at risk for paralysis. Guidelines for identifying patients with preexisting unilateral vocal cord paralysis and for modifying the surgical procedure for ACD/F to prevent the catastrophic complication of bilateral vocal cord paralysis are discussed.

Adult↗
PubMed1990

[A statistical study of clinical cases of malignant tumors first manifested by vocal cord paralysis].

One of the most important problems in dealing with vocal cord paralysis is to clarify the cause of paralysis. In those case where the definite cause is unknown, it is possible that an occult type of malignant tumors exists along the course of the vagus or recurrent laryngeal nerves. For the past 16 years, 62 out of 560 cases with vocal cord paralysis were diagnosed to have malignant tumors first manifested by paralysis of vocal cord. They consisted of 25 cases of thyroid carcinoma, 18 lung carcinoma, 13 esophageal carcinoma, 3 mediastinal tumors and 3 tumors of miscellaneous origin. Among these, 36 were male and 26 were female and the mean age was 63 years old. In 40 cases, paralysis was found on the left side, in 18 on the right and bilaterally in the remaining 4. There was a marked sexual difference in the origin of malignant tumors, i.e. the incidence of lung carcinoma was higher in male with paralysis on the left side, while that of thyroid carcinoma was higher in female. In some cases with thyroid carcinoma, vocal cord paralysis was noted more than a year before the detection of the tumor. Ultrasonography of the neck, chest x-ray, CT scan of the chest, fluoroscopy of the pharyngo-esophagus should be performed for the detection of malignant tumors in cases with left vocal cord paralysis, while ultrasonography of the neck and chest x-ray should be sufficient in right paralysis, although additional fluoroscopy of the pharyngo-esophagus seemed preferable in male.

Adult↗
PubMed2005

Sleep paralysis in adults reporting repressed, recovered, or continuous memories of childhood sexual abuse.

Sleep paralysis typically occurs as individuals awaken from rapid eye movement sleep before motor paralysis wanes. Many episodes are accompanied by tactile and visual hallucinations, often of threatening intruders in the bedroom. Pendergrast [Victims of Memory: Incest Accusations and Shattered Lives, HarperCollins, London, 1996] proposed that individuals who report repressed or recovered memories of childhood sexual abuse (CSA) may misinterpret episodes of sleep paralysis as reemerging fragments of dissociated ("repressed") memories of CSA. To investigate this issue, we administered a sleep paralysis questionnaire to people reporting either repressed (n = 18), recovered (n = 14), or continuous (n = 36) memories of CSA, or to a control group reporting no history of CSA (n = 16). The prevalence of sleep paralysis was: repressed memory group (44%), recovered memory group (43%), continuous memory group (47%), and control group (13%). Among the six individuals in the recovered memory group who had experienced sleep paralysis, one interpreted it as related to sexual abuse (i.e., a rate of 17%). All other participants who had reported sleep paralysis embraced other interpretations (e.g., saw a ghost). Dissociation and depressive symptoms were more common among those who had experienced sleep paralysis than among those who denied having experienced it.

Adult↗
PubMed2005

Delayed presentation of traumatic facial nerve (CN VII) paralysis.

Facial nerve paralysis (Cranial Nerve VII, CN VII) can be a disfiguring disorder with profound impact upon the patient. The etiology of facial nerve paralysis may be congenital, iatrogenic, or result from neoplasm, infection, trauma, or toxic exposure. In the emergency department, the most common cause of unilateral facial paralysis is Bell's palsy, also known as idiopathic facial paralysis (IFP). We report a case of delayed presentation of unilateral facial nerve paralysis 3 days after sustaining a traumatic head injury. Re-evaluation and imaging of this patient revealed a full facial paralysis and temporal bone fracture extending into the facial canal. Because cranial nerve injuries occur in approximately 5-10% of head-injured patients, a good history and physical examination is important to differentiate IFP from another etiology. Newer generation high-resolution computed tomography (CT) scans are commonly demonstrating these fractures. An understanding of this complication, appropriate patient follow-up, and early involvement of the Otolaryngologist is important in management of these patients. The mechanism as well as the timing of facial nerve paralysis will determine the proper evaluation, consultation, and management for the patient. Patients with total or immediate paralysis as well as those with poorly prognostic audiogram results are good candidates for surgical repair.

Accidents, Traffic↗
PubMed2006

Spontaneous recovery of diaphragmatic strength in unilateral diaphragmatic paralysis.

The aim of the present study was to evaluate diaphragmatic strength in patients with unilateral diaphragmatic paralysis and to determine whether patients with recent diaphragm paralysis develop lower inspiratory pressure than patients with longstanding diaphragmatic paralysis. Twenty patients (16 men and 4 women, 62+/-12 years) and six control subjects were included (4 men and 2 women, 53+/-15 years) in the study. Esophageal pressure during sharp sniff (Pes,sniff), bilateral cervical phrenic nerve magnetic stimulation (Pes,cms) and unilateral phrenic nerve stimulation (Pes,ums) (in nine patients) were measured. Sixteen patients presented right diaphragmatic paralysis and four, left diaphragmatic paralysis. Pes,sniff was higher in control subjects than in patients with diaphragmatic paralysis (respectively 110+/-22 cmH2O and 82+/-24 cmH2O, P<0.05). There was no difference in Pes,cms between patients with diaphragmatic paralysis and control subjects (14+/-7 cmH2O vs. 16+/-4 cmH2O; ns). Pes,ums after stimulation of the affected phrenic nerve was less than 4 cmH2O, was 8+/-2 cmH2O after stimulation of the intact phrenic nerve and was correlated to Pes,cms (R=0.87, P<0.01). There was a positive correlation between Pes,cms, Pes,ums of the intact hemidiaphragm, Pes,sniff and the time from the onset of symptoms and the diaphragmatic explorations (respectively R=0.86, P<0.0001; R=0.72, P<0.05; R=0.48, P<0.05). In conclusion, diaphragmatic strength after unilateral diaphragmatic paralysis seems to improve with time.

Adolescent↗
PubMed1998

In vivo evaluation of a closed loop monitoring strategy for induced paralysis.

OBJECTIVE: Reliable closed loop infusion systems for regulating paralysis level can be a great convenience to the anesthesiologists in automating their task. This paper describes the in vivo performance evaluation of a self-tuning controller that is designed to accommodate large variations in patient drug sensitivity, drug action delays and environmental interfering noise. METHODS: The infusion system was evaluated in six adult mongrel dogs. Following the manual induction of paralysis by an anesthesiologist, the controller regulated the infusion of vecuronium to maintain a desired level of paralysis. The integrated EMG response of the hypothenar muscle to a train-of-four stimulation of the ulnar nerve quantified the depth of paralysis. The controller's robustness was tested by contaminating the sensed twitch signal with electrocautery noise and electrode disconnection. RESULTS: The controller reached the initial level of paralysis of 100% in about 4.0 minutes and arrived at the desired level of 90% with an overshoot of 6.38% (+/-6.82). It maintained the desired level of paralysis with a 2.04% (+/-1.20) mean offset at 90% and 0.4% (+/-0.5) mean offset at 80% steady state level, respectively. The mean infusion rate to sustain 90% and 80% paralysis were 2.70 (+/-2.05) and 2.15 (+/-2.57) ((mg/kg)/min), respectively. CONCLUSIONS: The system adapted to a large variation in the sample subject drug sensitivity. It remained stable despite large amplitude disturbances and maintained the paralysis at the desired level following the removal of the disturbances.

Animals↗