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[Paralysis after long-term administration of neuromuscular blocking agents].

Paralysis after long-term administration of neuromuscular blocking agents especially pancuronium and vecuronium has been reported since 1970's. In this article, these papers were reviewed, and the etiology and the clinical features were analyzed. Most of the cases of muscle paralysis after prolonged use of pancuronium bromide were associated with concomitant use of large doses of steroids. In these cases, steroid myopathy and disuse atrophy have been implicated with causes of the paralysis. In patients with impaired hepatic and/or renal functions, metabolites of neuromuscular blocking agents might accumulate. In some patients with paralysis after neuromuscular blocking agents, underlying neuromuscular complications such as critical illness polyneuropathy have been implicated with the cause of the muscle paralysis. In order to avoid paralysis after long-term administration of neuromuscular blocking agents, following recommendations are made. 1) Monitor neuromuscular blockade. 2) Examine patient's neuromuscular status before starting to give relaxants. 3) Be careful in giving relaxants in patients with poor renal and/or hepatic functions. 4) Use smallest possible amount of relaxant. 5) Be careful about the drugs administered simultaneously especially steroids and antibiotics. 6) During the use of a neuromuscular blocking agent, perform physical therapy of extremities to avoid disuse atrophy especially when its administration is temporally terminated.

Humans↗

Thyrotoxic periodic paralysis: a report of 3 Malaysian cases and a review of its pathology.

UNLABELLED: Thyrotoxic periodic paralysis (TPP) is a medical emergency characterised by sudden onset of muscle weakness with hypokalemia that resolves with the treatment of hyperthyroidism. We report three cases of thyrotoxic periodic paralysis seen at the Accident and Emergency Care Department, University of Malaya Medical Centre in a period of four months. We also review the clinical presentation, pathophysiology, biochemical features and management of TPP. All three patients were young Asian males, presenting with muscle weakness of sudden onset. The first patient presented with lower limb weakness and had symptoms of thyrotoxicosis and goitre. He had a previous similar episode which resolved spontaneously. The second patient presented with quadriplegia, respiratory acidosis and had no signs and symptoms of thyrotoxicosis. The electrocardiogram of this patient showed normal sinus rhythm with U wave in V3 and a flat T wave, which are characteristic of hypokalaemia. The third patient, who was a known case of thyrotoxicosis, was admitted thrice for hypokalemic paralysis during the study period. All cases had low serum potassium, suppressed TSH and elevated T4 confirming thyrotoxic periodic paralysis. Potassium therapy was useful during the crisis; however prophylactic potassium has not been shown to prevent attacks as seen in one of our cases. CONCLUSION: Thyrotoxic periodic paralysis should be considered in the differential diagnosis of sudden onset paralysis in young male patients. Determination of the plasma potassium levels and thyroid hormones help in the diagnosis. The definitive treatment for TPP is the achievement of euthyroid state.

Administration, Oral↗

Detecting polio through surveillance for acute flaccid paralysis (AFP).

Accurate surveillance for polio is essential for eradication. Surveillance systems for polio has been developed under the guidance of the global polio eradication initiative. Surveillance of cases of acute flaccid paralysis among children less than 15 years of age is a key component for a well functioning polio surveillance system. The surveillance system works through a network of surveillance medical officers, the responsibility of them lies in assisting the health services departments of all states and maintaining a network of acute flaccid paralysis reporting sites and rapidly investigating the cases. Surveillance activities begin when a child comes in contact with a healthcare provider who in turn informs the officer in charge of acute flaccid paralysis surveillance. The goal of the polio network laboratories is to provide accurate and timely results of wild poliovirus detection in stool samples of cases of acute flaccid paralysis. Strong linkages have been established between the acute flaccid paralysis surveillance system and the laboratory network. Laboratories complete poliovirus isolation and if poliovirus is isolated, these are submitted for intratypic differentiations. Acute flaccid paralysis surveillance in India has demonstrated that the eradication activities implemented in India led to dramatic reduction and restriction in the number of cases and geographic spread of poliovirus transmission.

Acute Disease↗

Cluster of tick paralysis cases--Colorado, 2006.

Tick paralysis is a rare disease characterized by acute, ascending, flaccid paralysis that is often confused with other acute neurologic disorders or diseases (e.g., Guillain-Barré syndrome or botulism). Tick paralysis is thought to be caused by a toxin in tick saliva; the paralysis usually resolves within 24 hours after tick removal. During May 26-31, 2006, the Colorado Department of Public Health and Environment received reports of four recent cases of tick paralysis. The four patients lived (or had visited someone) within 20 miles of each other in the mountains of north central Colorado. This report summarizes the four cases and emphasizes the need to increase awareness of tick paralysis among health-care providers and persons in tick-infested areas.

Aged↗

Aetiological, clinical and metabolic profile of hypokalaemic periodic paralysis in adults: a single-centre experience.

BACKGROUND: Hypokalaemic periodic paralysis constitutes a heterogeneous group of disorders that present with acute muscular weakness. In this analysis, we discuss the aetiological factors that appear to be more common in the Indian population. METHODS: From 1995 to 2001, 31 patients presented with periodic paralysis (mean age 34.5 years, range 11-68 years). Of the 31 patients, 19 were men. The clinical and laboratory data of these patients were analysed. Patients were investigated for possible secondary causes of hypokalaemla. RESULTS: There were 13 patients (42%) with renal tubular acidosis, 13 with primary hyperaldosteronism (42%), 2 each with thyrotoxic periodic paralysis and sporadic periodic paralysis, and I with Gitelman syndrome. Of the 13 patients with renal tubular acidosis, 10 had proximal and 3 distal renal tubular acidosis. Three of these patients with renal tubular acidosis had Sjogren syndrome. The patients diagnosed to have renal tubular acidosis had significantly lower serum bicarbonate (18.7 [14.6] v. 29.6 [5.0] mEq/L; p < 0.05) and higher levels of chloride (107.5 [6.0] v. 99.5 [3.4] mEq/L; p < 0.05) compared with those who had primary hyperaldosteronism, although the potassium values were similar (2.4 [0.65] v. 2.26 [0.48] mEq/L; p = 0.43). All patients with primary hyperaldosteronism had hypertension at presentation and were proven to have adrenal adenomas. CONCLUSION: A significant number of patients in this study had secondary and potentially reversible causes of hypokalaemic periodic paralysis. The common causes were renal tubular acidosis and primary hyperaldosteronism. A detailed work-up for secondary causes should be undertaken in Indian patients with hypokalaemic periodic paralysis.

Acidosis, Renal Tubular↗

Stridor: intracranial pathology causing postextubation vocal cord paralysis.

During an 18-month period in a pediatric intensive care unit, nine patients with vocal cord paralysis were identified using flexible bronchoscopy. When tracheally extubated, each child was found to have stridor. The children ranged in age from 17 days to 5 1/2 years. Two patients had unilateral paralysis, but neither required tracheostomy. Seven patients displayed bilateral abductor vocal cord paralysis. Of these, six patients required tracheostomy. Surgical injury to the recurrent laryngeal nerve was the probable cause in two patients. The other seven patients had neurologic disorders with documented or suspected increases of intracranial pressure. Four of the seven patients with bilateral abductor vocal cord paralysis regained cord mobility within 4 months. Both children with unilateral cord paralysis have no stridor and vocalize well 1 year later. Cord paralysis in the setting of intracranial hypertension probably results from compression or ischemia of the vagus nerve before it exits the skull. Early visualization of the larynx should be done in patients who become stridulous when extubated, especially those with prior thoracic procedures or with neurologic disorders associated with intracranial hypertension.

Bronchoscopy↗

[Clinical study of cross-reinnervation in obstetrical paralysis].

It is known that cross-reinnervation occurs when regenerating nerve fibers recombine in brachial plexus injury, especially in obstetrical paralysis. This cross-reinnervation causes abnormal contraction in many muscles simultaneously during voluntary movement. To date, however, little has been reported on its pathophysiology, severity and prognosis. In order to clarify these problems, 362 cases of obstetrical paralysis were studied clinically and electromyographically, and abnormal muscle contractions during voluntary movement were analyzed. The results are as follows; Cross-reinnervation is seen in most cases which have suffered from transection or severe injury near the transection of the nerve fibers (including that in the neural tube), and which have got recovery better than manual muscle testing grade (2) "poor". Cross-reinnervation is caused by cross-reinnervation of nerve fibers which regenerate in the wrong muscles. Muscle contraction occurring in many muscles simultaneously is different from co-ordinate movement. Other paradoxical muscle action is found besides that of contraction. Cross-reinnervation can be classified into the following types by the muscle groups showing the contraction. Deltoid m., biceps brachii m. type, Deltoid m., biceps brachii m., triceps brachii m. type, Biceps brachii m., triceps brachii m. type, Deltoid m., biceps brachii m., triceps brachii m., forearm mm. type, Deltoid m., biceps brachii m., forearm mm. type, Biceps brachii m., triceps brachii m., forearm mm. type, Triceps brachii m., forearm mm. type. Abnormal muscle activity caused by cross-reinnervation is found from 4-6 months after nerve recovery from Wallerian degeneration, and it does not improve, but physical therapy or operative treatment can bring improvement in daily activities. Clinical severity of cross-reinnervation is correlated to the severity of paralysis and in proportion to the ratio of normally recovered nerve fibers and cross-reinnervated nerve fibers. It suggests that cross-reinnervation is caused by the discordant recovery from injury of nerve fibers in the brachial plexus. The site of cross-reinnervation depends on the severity of paralysis. Usually it spreads from the 5th and 6th cervical nerve roots to the upper trunk, medial trunk, posterior cord and lastly to the lower trunk and medial cord, determined by the severity of paralysis. This agrees with the way of spreading of obstetrical paralysis.

Activities of Daily Living↗

[Paralysis of the inner thumb muscles. Treatment by tendon transfer].

The management of paralysis of the intrinsic muscles of the thumb by tendon transfers cannot be realized by indiscriminate application of standard operations. For each of the three types of paralysis i. e.: -- paralysis of the external muscles of the thumb -- paralysis of the internal muscles of the thumb and -- combined paralysis of the external and internal muscles of the thumb, exists a different indication and for each one of the three elements of the procedure, namely: -- choice of the motor-muscle, -- location of the pulley and -- fixation of the transfer, the operative modalities must be adapted to each type of paralysis.

Humans↗

[Cause, diagnosis and course in 215 patients with vocal cord paralysis].

OBJECTIVE: To assess the different causes, the diagnostic process and natural course of vocal cord paralysis. DESIGN: A retrospective study. SETTING: Department of ENT, University Hospital Nijmegen, the Netherlands. METHOD: Between 1982 and 1990, 215 patients with the symptoms of vocal cord paralysis were routinely examined. In 40 patients additional examination was needed to determine the diagnosis. RESULTS: A substantial part of all cases (43%) were caused by previous medical intervention, for instance thyroid or thoracic surgery. Neoplasms of the head and neck region or thoracic cavity were a cause in 25%. In spite of extensive examination the cause of a vocal cord paralysis remained unclear in 18%. Physical examination combined with chest X-ray were the main diagnostic methods. Spontaneous recovery of a vocal cord paralysis was seen in 18% of all patients, but in the subgroup with paralysis after prolonged intubation or a viral infection it occurred in 46% and 62%, respectively. CONCLUSION: A vocal cord paralysis can have many causes. Physical examination and chest X-ray are important tools for diagnosis.

Adolescent↗

Equine hyperkalemic periodic paralysis: review and implications.

The purpose of this review is to present an up-to-date summary of the signs, diagnosis, treatment, and implications of equine hyperkalemic periodic paralysis. The review encompasses all original articles published between 1986 and early 1993. Hyperkalemic periodic paralysis is the result of a genetic mutation in the skeletal muscle sodium channel gene. It is inherited as an autosomal dominant trait; most affected horses are heterozygotes. The classical signs are muscle fasciculation, spasm, and weakness associated with hyperkalemia. However, these signs are only rarely observed in affected horses. Potential sequelae to attacks are abrasions and involuntary recumbency; these problems are not specific for hyperkalemic periodic paralysis, but they occur more frequently in hyperkalemic periodic paralysis-affected horses. It is also likely that hyperkalemic periodic paralysis results in greater muscle mass. There are suggestions that homozygotes may be more severely affected and show signs of upper respiratory obstruction as foals. The practitioner needs to be aware of the tests for hyperkalemic periodic paralysis, and their limitations, so that he can properly diagnose this condition. The industry has the difficult problem of deciding whether or not testing should be mandatory and the fate of positive horses.

Animals↗

Distribution of viral RNA in the spinal cord of DBA/2 mice developing biphasic paralysis following infection with the D variant of encephalomyocarditis virus (EMC-D).

DBA/2 mice infected with the D variant of encephalomyocarditis virus (EMC-D) (10(1) PFU/head) developed biphasic hind limb paralysis. As a first step in clarifying its pathogenesis, we examined the distribution of viral RNA in the spinal cord using in situ hybridization. At 3 days post inoculation (DPI), in the spinal cord of mice showing slight paralysis, viral RNA was observed in capillary endothelial cells and a few adjacent glia cells in the funiculus lateralis from thoracic to lumbar enlargement. At 7 DPI, in the spinal cord of mice showing apparent paralysis, viral RNA was observed in a larger number of glia cells in the demyelinated lesion associated with infiltration of macrophages in the funiculus lateralis and in a small number of degenerated neurons in the cornu ventrale. In the funiculus lateralis, viral RNA could not be observed after 28 DPI. On the other hand, viral RNA was observed in degenerated neurons in the cornu ventrale of mice showing the second phase paralysis at 42 DPI. Many CD4+T cells infiltrated around these degenerated neurons. These results suggest that: (1) the viral entry zone was the capillary endothelial cells in the funiculus lateralis; (2) first phase paralysis was due to demyelination caused by EMC-D and associated with macrophage infiltration; (3) second phase paralysis was due to degeneration of motor neurons bearing viral RNA associated with infiltration by CD4+T cells.

Animals↗

Delayed facial paralysis after acoustic neuroma surgery: factors influencing recovery.

Patients with satisfactory facial nerve function [House-Brackmann (HB) grade I or II] immediately after acoustic neuroma surgery are at risk for delayed facial paralysis. To study this problem, 255 consecutive patients who underwent acoustic neuroma excision with facial nerve preservation were identified. Delayed facial paralysis occurred in 62 (24.3%) patients; 90% ultimately recovered to their initial postoperative HB grade, and 98.3% recovered to within one grade of their initial HB level. Paralysis occurred at an average of 3.65 postoperative days (range, 1-16 days). The average time to maximal recovery for those with changes of 1, 2, 3, and 4 HB grades was 5.6, 21.5, 39.8, and 50.5 weeks, respectively. The early onset of paralysis (< 48 h after surgery) resulted in shorter average recovery times. Of patients who demonstrated nerve deterioration to grades IV-VI, 20 of 38 required tarsorrhaphy or gold-weight placement. We conclude that the over-whelming majority of patients with delayed facial paralysis after acoustic neuroma surgery do eventually recover to their postoperative HB grade. The magnitude and timecourse of delayed facial paralysis are predictive factors for subsequent recovery.

Adult↗

Physiology of REM sleep, cataplexy, and sleep paralysis.

The main neural structures generating muscle atonia and other phenomena characteristic of REM sleep are present in dorsolateral portions of the pons in the brainstem. Occurrence of REM sleep and the NREM-REM sleep cycle are probably determined by a balance or interaction between the cholinergic and cholinoceptive REM sleep-on neuronal populations and the monoaminergic REM sleep-off neuronal population. Neural activities producing generalized muscle atonia in REM sleep originate mainly in dorsolateral portions of the pontine reticular formation, descend through the medulla and spinal cord, and inhibit the motoneurons in the brainstem and spinal cord, bringing about postural atonia. Cataplexy and sleep paralysis are pathological, dissociated manifestations of the generalized muscle atonia characteristic REM sleep. Cataplexy is triggered by emotional stimuli, probably through activation of the neural structure generating the muscle atonia of REM sleep. During long-lasting cataplectic attacks, narcoleptic humans often experience sleep paralysis and vivid hypnagogic hallucinations in the latter sleep state. Sleep paralysis is caused by the marked dissociation between level of alertness and muscle atonia that often occurs in SOREM sleep episodes. Frequent SOREM sleep episodes in narcoleptic humans and dogs may occur when some of the neural mechanisms producing wakefulness and/or NREM sleep that normally inhibit the occurrence of REM sleep are abnormally weak, or when neural mechanisms facilitating the occurrence of REM sleep are hypersensitive or hyperactive, or both. Both abnormalities may contribute to the occurrence of SOREM sleep episodes and sleep paralysis, and also to the emotional triggering of cataplexy. Frequent occurrence of SOREM sleep episodes seems to be prerequisite but not sufficient for the occurrence of cataplexy. Some additional neural activities induced by emotion also contribute by inhibiting and/or activating the disturbed neural mechanisms related to SOREM sleep episodes. These abnormalities in neural mechanisms probably involve hypersensitivity or hyperactivity of muscarinic cholinergic and/or cholinoceptive neuronal populations in the pontine and suprapontine structures, and/or abnormally decreased activity of noradrenergic or serotonergic neuronal populations in the pons and/or other brainstem structures. This last monoaminergic neuronal population probably has a gating or inhibiting effect upon the cholinergic and cholinoceptive neuronal populations related to the generation of generalized muscle atonia and REM sleep. In spite of many studies and published reports on REM sleep, as well as on cataplexy and sleep paralysis, we are still far from a complete understanding of the physiological mechanisms producing muscle atonia in REM sleep and of the pathophysiological mechanisms of cataplexy and sleep paralysis--though it is apparent that these mechanisms are closely related.

Animals↗

[Submandibular secretion of immunoglobulins IgA and IgG in peripheral paralysis of the facial nerve].

INTRODUCTION: In all lesions of the facial nerve suprachoroidally localized, and due to disturbance of parasympathetic and sympathetic component, there comes to qualitative and quantitative disorders of the secretion of submandibular salivary gland. Glandular immunoglobulins IgA and IgG are the secretion of the specific plasma cells in the interstice of this gland. The mechanism of the secretion of immunoglobulins is not sufficiently clear, but it is certainly under the direct neurogenic control, since the disorders of the secretion emerge after the denervation of the submandibular salivary gland. The aim of the study was to prove the direct relation between the degree of submandibular immunoglobulin secretion IgA and IgG, and the degree of the lesion of the facial nerve U which is vitally important in the clinical estimation of the peripheral paralysis of this nerve. MATERIAL AND METHODS: In 35 patients with peripheral idiopathic facial nerve paralysis, the quantity of the secreted immunoglobulins IgA and IgG was examined by laser nephelometar BLN, Module 3. The quantity of the secreted immunoglobulins IgA and IgG (mg lit) in the saliva of the paralysed side was indirectly compared to the secreted immunoglobulins of the healthy, i.e. control side. The examination was performed three times: a) after the appearance of the disease, in the first 30 days; b) two to three months later; c) after six to twelve months. RESULTS: The quantity of the secreted immunoglobulins is significantly higher in the saliva samples taken from the paralysed side (9.50U204.77 mg lit), in comparison with the samples taken from the healthy side (9.50U70.36 mg lit). In the group of patients with favourable results and significantly higher secretion (p 0.01) normalization occurred in the final period of observation. In patients with unfavourable results the difference in secretion was continuously present (p 0.05) (table 1). DISCUSSION: In the lesions of the facial nerve suprachoroidally localized, there comes to disorder concerning the secretion of immunoglobulins IgA and IgG by submandibular salivary gland, which can be applied in the estimation of the degree of paralysis and the prognosis of the final result. CONCLUSION: The results of the research show that in the peripheral idiopathic facial nerve paralysis, there comes to increased secretion of immunoglobulins IgA and IgG in submandibular gland, at the paralysed side. In the patients who, during the paralysis, show quicker fall and normalization of the previously increased quantities of immunoglobulins, the recovery of the motor function of the facial nerve comes more successfully and more certainly. The degree of the secretion of immunoglobulins IgA and IgG can be used for the estimation of the severely of the pathological process in the suprachoroidal part of the nerve, and it can be used as a reliable parameter for the prognosis of the paralysis outcome.

Facial Paralysis↗

Progressive myopathy in hyperkalemic periodic paralysis.

A progressive degenerative myopathy has been well described in hypokalemic periodic paralysis but is not as widely recognized in hyperkalemic periodic paralysis. We studied four families with the latter disease in which some members developed a progressive myopathy. Episodes of paralysis were prolonged, lasting for months in some cases, and in one case paralysis was sufficiently severe to require ventilatory support. The progressive myopathy tended to develop at a time when attacks of paralysis were decreasing in frequency. Muscle biopsy specimens showed variability in fiber size, internal nuclei, and fibers with vacuoles. Electron microscopy showed myofibrillary degeneration and tubular aggregates. An abnormal biopsy specimen was more common in older patients. Our experience suggests that a progressive myopathy is as common in hyperkalemic periodic paralysis as it is in the hypokalemic disorder.

Adolescent↗

Self-veto mechanism of CD8+ cytotoxic effector T cells. Peptide-induced paralysis affects the peptide-MHC-recognizing cytotoxic T lymphocytes and is independent of Fas/Fas ligand interactions.

The lytic activity of CD8+ cytotoxic T lymphocyte (CTL) cell lines or clones can be inhibited by addition of the peptide recognized by these cells. The mechanisms underlying this phenomenon are not fully understood. Here we have analyzed peptide-induced CTL paralysis using in vivo generated ovalbumin (OVA)-specific CTL. Lytic activity of OVA-specific CTL was inhibited by addition of the immunodominant OVA-peptide SIINFEKL in a dose-dependent manner. Paralysis was induced rapidly and binding of the peptide to MHC class I molecules was required. Using mixing experiments with CTL populations of different peptide specificities restricted to the same MHC class I molecule we identified a veto-like mechanism: the cytotoxic activity of the peptide-recognizing CTL was inhibited while the lytic activity of the peptide-presenting CTL was unaltered. Only CD8+ CTL but not CD4+ T cells or B+ cells induced paralysis. After removal of the peptide-presenting CTL by magnetic cell sorting, paralysis was maintained and paralyzed CTL showed no signs of apoptosis. Loss of cytotoxicity could be induced in CTL populations from Fas-deficient (lpr+/lpr+) or Fas ligand-deficient (gld+/gld+) mice and mixtures thereof, implying that Fas/Fas ligand interactions are not involved during induction of paralysis. Hence, peptide-induced paralysis of CTL is due to a self-veto mechanism rather than to mutual killing of CTL. These findings may have implications for in vivo immunization with peptides, viral escape and peripheral tolerance mechanisms.

Animals↗

Paralysis has no effect on chest wall and respiratory system mechanics of mechanically ventilated, sedated patients.

OBJECTIVE: To evaluate the separate effects of sedation and paralysis on chest wall and respiratory system mechanics of mechanically ventilated, critically ill patients. SETTING: ICU of the University "La Sapienza" Hospital, Rome. PATIENTS AND PARTICIPANTS: 13 critically ill patients were enrolled in this study. All were affected by disease involving both lungs and chest wall mechanics (ARDS in 4 patients, closed chest trauma without flail chest in 4 patients, cardiogenic pulmonary oedema with fluidic overload in 5 patients). MEASUREMENTS AND RESULTS: Respiratory system and chest wall mechanics were evaluated during constant flow controlled mechanical ventilation in basal conditions (i.e. with the patients under apnoic sedation) and after paralysis with pancuronium bromide. In details, we simultaneously recorded airflow, tracheal pressure, esophageal pressure and tidal volume; with the end-inspiratory and end-expiratory airway occlusion technique we could evaluate respiratory system and chest wall elastance and resistances. Lung mechanics was evaluated by subtracting chest wall from respiratory system data. All data obtained in basal conditions (with the patients sedated with thiopental or propofol) and after muscle paralysis were compared using the Student's t test for paired data. The administration of pancuronium bromide to sedated patients induced a complete muscle paralysis without producing significant modification both to the viscoelastic and to the resistive parameters of chest wall and respiratory system. CONCLUSIONS: This study demonstrates the lack of additive effects of muscle paralysis in mechanically ventilated, sedated patients. Also in view of the possible side effects of muscle paralysis, our results question the usefulness of generalized administration of neuromuscular blocking drugs in mechanically ventilated patients.

Adult↗

Anaesthetic management of a patient with familial normokalaemic periodic paralysis.

PURPOSE: We describe the anaesthetic management of a patient with the autosomal dominant inherited disease, normokalaemic periodic paralysis. The disease results in intermittent bouts of limb and respiratory muscular weakness in association with hypothermia, stress, prolonged fasting or exercise. Unlike hypokalaemic and hyperkalaemic periodic paralysis, the more common variants of the disease, normokalaemic periodic paralysis is not accompanied by alterations in the plasma potassium concentration. CLINICAL FEATURES: A five-year-old boy presented for emergency scrotal exploration. He had a family history of periodic paralysis and had experienced previous episodes of weakness, two of which had required hospitalization for respiratory distress. On admission there was no evidence of weakness and serum potassium concentration was 4.2 mMol.L-1. A spinal anaesthetic was performed and the procedure was uncomplicated by muscle paralysis above the level of the spinal block. CONCLUSION: Avoidance of known precipitating factors and judicious use of neuromuscular blocking drugs has been advocated in patients with this disorder presenting for surgery. In appropriate circumstances, spinal anaesthesia represents a useful option in patients with normokalaemic periodic paralysis.

Anesthesia↗