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Most patients with obstetrical paralysis have some useful functional return, and early recognition and treatment help prevent rapidly developing shoulder contractures. Initial physical therapy includes passive range of motion exercises. Fixed contractures must be released prior to reconstructive surgery designed to improve funtion. An approach to the diagnosis, evaluation, and treatment of obstetrical paralysis is given.
A 20-year-old man developed a complete facial nerve paralysis following surgical reconstruction of the posterior ear canal with ionomeric cement. The paralysis developed gradually during the second and third postoperative weeks. Six weeks following the complete removal of the cement, the facial nerve recovered completely. The literature contains reports of diffusion of aluminum ions, which can reach toxic levels in tissue fluid and adjacent bone as the cement hardens. This side effect has been reported to cause an inflammatory response in the dura and brain and has led to fatalities. To our knowledge, there has been no other report of an ionomeric cement having a direct toxic effect on peripheral nerve transmission. Because ionomeric cements are used routinely in otosurgery, especially in canal reconstructions where the proximity to the facial nerve is evident, it is important to use caution when introducing ionomeric cements into near-nerve anatomic locations.
Peripheral nerve lesions are one of the most frequent causes of chronic incapacity. Upper or lower limb palsies due to brachial or lumbar plexus injuries, facial paralysis and nerve lesions caused by systemic diseases are one of the major goals of plastic and reconstructive surgery. However, the poor results obtained in repaired peripheral nerves during the Second World War lead to a pessimist vision of peripheral nerve repair. Nevertheless, a well understanding of microsurgical principles in reconstruction and molecular biology of nerve regeneration have improved the clinical results. Thus, although the results obtained are quite far from perfect, these procedures give to patients a hope in the recuperation of their lesions and then on function. Technical aspects in nerve repair are well established; the next step is to manipulate the biology. In this article we will comment the biological processes which appear in peripheral nerve regeneration, we will establish the main concepts on peripheral nerve repair applied in facial paralysis cases and, finally, we will proportionate some ideas about how clinical practice could be affected by manipulation of the peripheral nerve biology.
Unilateral laryngeal paralysis (ULP) involves all three functions (defensive, phonating, and respiratory) of the larynx. It is necessary to make comprehensive clinical studies in patients with ULP of unknown etiology to elucidate the causes of the paralysis. The study involved X-ray tomography of the larynx, lung, and mediastinum, ultrasonography of the thyroid, X-ray study of the skull and the cervical part of the vertebral column, and barium X-ray study of the esophagus. A hundred and twenty patients with ULP underwent clinical and functional studies of the vocal apparatus, with microlaryngoscopy with palpation of the arytenocricoid joint, studies of external respiratory function and the acoustic parameters of their voice. The examination has ascertained that the clinicofunctional status of the larynx in unilateral laryngoparalysis depends on the degree of approach and the quality of closure of the vocal cords (VC) and it is determined by the position of the paralyzed VC in horizontal and vertical planes, by the degree of paralyzed VC atrophy, and by the position and mobility of the arytenoid cartilage.
Missense mutations of the human skeletal muscle voltage-gated Na channel (hSkM1) underlie a variety of diseases, including hyperkalemic periodic paralysis (HyperPP), paramyotonia congenita, and potassium-aggravated myotonia. Another disorder of sarcolemmal excitability, hypokalemic periodic paralysis (HypoPP), which is usually caused by missense mutations of the S4 voltage sensors of the L-type Ca channel, was associated recently in one family with a mutation in the outermost arginine of the IIS4 voltage sensor (R669H) of hSkM1 (Bulman et al., 1999). Intriguingly, an arginine-to-histidine mutation at the homologous position in the L-type Ca(2+) channel (R528H) is a common cause of HypoPP. We have studied the gating properties of the hSkM1-R669H mutant Na channel experimentally in human embryonic kidney cells and found that it has no significant effects on activation or fast inactivation but does cause an enhancement of slow inactivation. R669H channels exhibit an approximately 10 mV hyperpolarized shift in the voltage dependence of slow inactivation and a twofold to fivefold prolongation of recovery after prolonged depolarization. In contrast, slow inactivation is often disrupted in HyperPP-associated Na channel mutants. These results demonstrate that, in R669H-associated HypoPP, enhanced slow inactivation does not preclude, and may contribute to, prolonged attacks of weakness and add support to previous evidence implicating the IIS4 voltage sensor in slow-inactivation gating.
Forty-seven patients undergoing elective/emergency surgery were investigated for the recovery pattern by numerically scoring the state of consciousness, skeletomuscular tone, respiration and blood pressure after the neuromuscular transmission at the level of thenar muscles returned to normalcy. Anaesthesia in them consisted of thiopentone induction and passive ventilation with nitrous oxide and oxygen mixtures (4 1/2:2 1/2 1) with consequent changes in PaCO-2 (22.0 to 90 mm Hg) after using 0.43 to 0.68 mg/kg d-tubocurarine or 2.3 to 3.8 mg/kg gallamine. In this series twelve patients were selected at random and biological assay of cerebrospinal fluid in them for curare/gallamine after 15 min anaesthesia and in the recovery phase was carried out on frog rectus muscle. All the patients recovered satisfactorily and did not present clinical signs of depression of central nervous system, even though all of them showed the presence of curare (ranging from 0.05 to 0.33 mug/ml) and gallamine (from 0.1 to 0.75 mug/ml) in the cerebrospinal fluid. This study therefore indicates that thiopentone, nitrous oxide and relaxant type of anaesthesia does not cause clinical syndrome of post-operative paralysis even when mild to moderate degree of hypocapnia is present and even when such a technique of anaesthesia is administered in poor-risk patients with associated changes in acid-base balance, electrolytes etc. Significant quantities of skeleto-muscular relaxant drug (used during the technique) when found in cerebrospinal fluid after the technique of anaesthesia need not induce post-operative paralysis in man.
The authors report two cases of paralysis of the posterior branch of the radial nerve as a result of compression of the nerve by a benign tumour, in both instances a lipoma. Analysis of the sixteen cases appearing in the literature reveals that the symptoms and signs are constant, characterised by the progressive development of paralysis of the muscles supplied by the deep branch of the radial nerve with the appearance of a tumefaction around the lateral part of the elbow. X-rays of the elbow confirm the diagnosis in the presence of a radiotranslucent polylobulated image. Surgical excision is followed by regression and the disappearance of a-l neurological signs after an average period of 8 months. In addition to a lipoma, compression may be caused by repeated contusion of the nerve by the border of the superficial part of the short supinator muscle in association with "tennis elbow". Section of this part of the muscle border results in complete recovery.
Bilateral facial paralysis(facial diplesia) is often observed in Guillain-Barré syndrome(GBS) and Fisher's syndrome (FS). We tried to observe injured facial nerves using three-dimensional(3-D) MRI in facial diplesia due to GBS and its variants and examined function of blood nerve barrier and clinical use of 3-D MRI for detecting injured facial nerves. In the four patients with GBS and its variants(GBS three cases, FS one case), while routine brain MRI did not show any abnormal findings, contrast-enhanced 3-D MRI revealed Gd-enhancement of the facial nerves. On the other hand, only one case showed visualization using contrast-enhanced 3-D MRI in twelve cases of Bell's palsy. Therefore, it may be presumed that the reason why the significantly higher rate of visualization in facial paralysis in GBS and its variants than in Bell's palsy is attributable to a difference in the mechanism of injury or the extreme seriousness of the disease. In conclusion, the observation of facial nerve using 3-D MRI was very useful to know the condition of the facial diplesia in GBS and its variants.
An 83-year-old man with a lifelong history of intermittent otorrhea and hearing loss was referred for management of a facial paralysis of 3 weeks' duration. Computed tomography (CT) of the head detected a neoplasm of the nasopharynx along with chronic otomastoiditis. A followup CT suggested the development of a nasopharyngeal abscess, which was confirmed by needle aspiration. A later coronal-projection CT showed definite bone destruction in the anterior petrous apex, confirming suspicions that a petrous apicitis was responsible for the facial paralysis and abscess. This article describes the management of this patient and reviews the historical, medical, and surgical aspects of petrous apicitis.
Facial paralysis in association with a parotid mass is usually associated with a diagnosis of malignancy. Benign parotid neoplasms and inflammatory processes resulting in facial paralysis are extremely rare. This report describes such a case and highlights some of the difficulties surrounding the diagnosis and management of these cases.
The aim of this paper was to address some of the unanswered questions regarding management of facial nerve paralysis in temporal bone fractures (TBF), such as the outcomes after late facial nerve decompression surgery. The study design was a retrospective review of a consecutive clinical series. Thirteen patients who underwent late decompression surgery for facial nerve paralysis due to TBF involving the perigeniculate ganglion region were analyzed. Patients were operated on 27-90 days after trauma. A transmastoid extralabyrinthine approach was used in all cases. Facial nerve-sheath slitting was performed routinely. Normal or subnormal facial nerve function (HB 1 or HB 2) was achieved in 7/9 cases (78%) evaluated at > or = 1 year after surgery. Good functional results were also obtained in two patients operated on 3 months after trauma. Bases on the outcomes observed in the present series, in patients unable to be operated on early, presenting 1 to 3 months with >95% denervation on EnoG, facial nerve decompression may have a beneficial effect.
We reported a 13-year-old boy and his family with hypokalemic periodic paralysis. He showed marked hyperuricemia during his paralytic attack, although neither ischemic forearm exercise test nor bicycle-ergometer exercise test revealed myogenic hyperuricemia when he was free from paralysis. Genetic analysis was performed to the proband and his affected elder brother, mother, and, maternal grand mother. We found the Arg528His mutation of CACNL1A3 gene in all the patients examined. The severity of the attacks and the age of onset did not vary in the different generations, and male predominancy was not evident in this family.
The threefold purpose of this report is to describe the epidemiology of acute flaccid paralysis (AFP), to determine the impact of the National Immunization Days (NID), and evaluate the quality of active surveillance in the Central African Republic (CAR) and Chad. The data in this study was obtained from the Enterovirus Division of the Pastear Institute in Bangui (National WHO Inter-country Reference Laboratory for the CAR and Chad and Regional Poliovirus Reference Laboratory in Africa). An increase in the number of AFP cases was observed in the CAR between 1995 and 2000 and in Chad between 1997 and 2000, mainly as a result of enhancement of the surveillance system. The goals set by the WHO in terms of the proportion of AFP cases with 2 specimens collected within 14 days of onset of paralysis and the number of cases with 60-day follow-up have not been reached in either country. The presence of 2 strains of wild poliovirus (types 1 and 3) and several genotypes (West African 13 and West African 7 for type 1 and Central African and Nigeria-P3 for type 3) not only show that Central Africa is still a significant reservoir for poliovirus transmission but also raise serious doubts about the quality of the NID organized over the last 3 years. The priority of the next NID round must be to reach unimmunized children who have been missed by routine immunization coverage.
A 23-year-old Japanese man was admitted to our hospital because of acute generalized muscle weakness and frequent vomiting. He had been diagnosed as having hypokalemic periodic paralysis, since he had recurrent episodes of transient generalized muscle weakness with a hypokalemia. Laboratory studies have revealed a severe hypokalemic hyperchloremic metabolic acidosis, elevated serum levels of creatine phosphokinase and ammonia. The urinary level of the hippuric acid, a metabolic product of toluene, was found to be extremely high, suggesting that he had been exposed to toluene. With intravenous supplement of potasium, his muscle strength improved. Chronic exposure to toluene induces various neurological disorders, such as encephalopathy, cerebellar and pyramidal signs, peripheral neuropathy. In addition, it should be kept in mind that hypokalemic muscle weakness can be induced by the renal tubular acidosis resulting from chronic toluene exposure, and that it is by no means easy to distinguish hypokalemic periodic paralysis if it occurs recurrently.
BACKGROUND: Thyrotoxic periodic paralysis (TPP) is a complication of hyperthyroidism. MATERIALS AND METHODS: We describe two patients with TPP. RESULTS: A 26-year-old man from Vietnam had weight loss, tachycardia, palpitations and heat intolerance for five months. Episodic leg and arm weakness developed three months after debut of symptoms. The second patient, a 23-year old woman from the Philippines, had had episodic leg weakness in the evenings after dinner for three weeks. Her attacks resolved spontaneously overnight. Physical examination of both patients revealed tachycardia and symmetrical proximal weakness involving both arms and legs. ECG and electrolyte analysis indicated a severe hypokalaemia; thyroid function tests showed hyperthyroidism. Both patients were diagnosed as having Graves' thyrotoxicosis and TPP. They were initially treated with propranolol and subsequently with carbimazole. The first patient had recurrence of thyrotoxicosis and paralysis after 16 months, whereas the second patient has remained symptom-free. INTERPRETATION: TPP is most common in Asian males, very few cases are reported in females. In Western countries TPP is rare, but with increasing immigration, TPP is likely to occur more frequently.
We report a case of thyrotoxicosis in a 37 year old male, in whom hypokalemic periodic paralysis was the first manifestation of the disease. We comment about the differential diagnosis with other types of periodic paralysis, and the importance of a correct diagnosis to avoid permanent muscle damage.
Electroneurography at present constitutes an indispensable method for the investigation of peripheral facial paralysis. It should be carried out at an early stage, in the form of three successive examinations at 3 day intervals. If decompression is necessary, it should theoretically be carried out during the first 15 days, before destruction of nerves, which is a feature of sequelae, can take place. Electroneuronography appears to be, for this purpose, on a par with histology. The authors urge that patients suffering from from facial paralysis should be referred to O.-R.-L. departments right from the start and not when all other methods of treatment have been tried, often with reprehensible empiricism, and found unsuccessful.
The simplest method of dealing with a frigore facial paralysis surgically seems to be by a minima neurolysis using a speculum and tackling it through the ear-drum as in otiospongiosis. In this manner, the Eustachian tube is exposed between the deep surface of the incus and the tendon of the musculus stapedius. Results were consistently good in 26 cases. The quality of recovery depends more on the duration of the paralysis than on operative technique.