Thyrotoxic periodic paralysis presenting with quadriparesis and hyperreflexia.

Thyrotoxic periodic paralysis (TPP) is a rare complication of hyperthyroidism that manifests as painless flaccid paralysis. An East Asian man in his late 20s presented to the emergency department with an acute onset of quadriparesis associated with hypertonia and hyperreflexia. His initial symptoms and signs suggested involvement of the brain and spinal cord; however, MRI of the neuroaxis was normal. His serum potassium concentration was low, and thyroid test results were consistent with hyperthyroidism. The patient was diagnosed with TPP associated with Graves' disease and was treated with potassium supplementation, propranolol and methimazole. Motor strength improved to his baseline level of power; bulk was normal, and tone was increased. Although flaccid paralysis is a typical presentation of TPP, brisk reflexes and muscle spasticity cannot rule out this condition. This case highlights the importance of considering TPP as a possible diagnosis in patients presenting with acute quadriparesis.

Results of acute cerebral infarction treatment with hyperbaric oxygen therapy, 2020-2022.

BACKGROUND: Cerebral stroke is the third leading cause of death after cardiovascular disease, cancer and the leading cause of disability for patients. Hyperbaric oxygen is a non-drug treatment that has the potential to improve brain function for patients with ischaemic stroke. The objective of this study was to evaluate the results of treatment of acute cerebral infarction with hyperbaric oxygen therapy (HBOT). MATERIALS AND METHODS: This was a case-control study. One hundred ninety-five patients diagnosed with cerebral infarction, with signs of onset within 24 hours, were treated at the Centre for Underwater Medicine and Hyperbaric Oxygen of Vietnam National Institute of Maritime Medicine during the period from January 2020 to December 2022. Study group included 100 patients with acute cerebral infarction treated with a combination of HBOT and medication and reference group included 95 patients treated by medication only (antiplatelets drugs, statins, control of associated risks factors) RESULTS: After 7 days of treatment with hyperbaric oxygen (HBO), symptoms such as headache, dizziness, nausea, sensory disturbances, and Glasgow score of the study group improved better than that of the reference group (p < 0.01). Movement recovery in the study group was better than the reference group: the percentage of patients with mild and moderate paralysis in the study group increased higher than that of the reference group (86.0% and 68.4%), the degree of complete paralysis of the study group decreased more than that of the reference group (14.0% and 31.6%). The degree of independence in daily activities in the study group was better than the reference group. In the study group, the percentage of patients with complete independence in daily life increased from 27.0% to 84.0%. In the reference group, the rate of patients who were independent in their daily activities increased from 37.9% to 51.6%. The average number of treatment days of the study group was 10.32 ± 2.41 days and it the reference group 14.51 ± 3.24 days. CONCLUSIONS: Hyperbaric oxygen therapy is a non-drug treatment with many good effects in the treatment of cerebral infarction, especially acute cerebral infarction. HBOT reduces and improves functional symptoms, improves mobility, and reduces treatment time for patients.

Combined laryngeal framework surgery and cricopharyngeal muscle-origin transection: a novel effective surgery for dysphagia with pharyngolaryngeal palsy and cricopharyngeal dysfunction under local anesthesia.

BACKGROUND: Cricopharyngeal myotomy and laryngeal framework surgery can improve swallowing function in patients with severe dysphagia. We developed a novel surgical technique for severe dysphagia associated with pharyngolaryngeal paralysis and cricopharyngeal dysfunction, performed under local anesthesia, and investigated its effectiveness. METHODS: We included nine patients who underwent cricopharyngeal muscle-origin transection with laryngeal framework surgery through a horizontal skin incision under local anesthesia. CONCLUSIONS: All patients demonstrated significant improvement in the Food Intake LEVEL Scale without complications. Thus, this surgical technique may serve as a useful and less invasive treatment option for patients with severe dysphagia.

Immediate effects of electroacupuncture in oculomotor nerve palsy following brainstem infarction: A case report.

INTRODUCTION: Research has demonstrated that electroacupuncture (EA) stimulation of paralyzed muscles significantly improves nerve regeneration and functional recovery. DESCRIPTION: An 81-year-old man with no history of diabetes mellitus or hypertension presented with a history of brainstem infarction. Initially, the patient had medial rectus palsy in the left eye and diplopia to the right in both eyes, which almost returned to normal after six sessions of EA. METHODS: The CARE guidelines informed the case study report. The patient was diagnosed with oculomotor nerve palsy (ONP) and photographed to document ONP recovery after treatment. The selected acupuncture points and surgical methods are listed in the table. DISCUSSION: Pharmacological treatment of oculomotor palsy is not ideal, and its long-term use has side effects. Although acupuncture is a promising treatment for ONP, existing treatments involve many acupuncture points and long cycles, resulting in poor patient compliance. We chose an innovative modality, electrical stimulation of paralyzed muscles, which may be an effective and safe complementary alternative therapy for ONP.

Thyrotoxic periodic paralysis associated with lactic metabolic acidosis: Case report of an African man and review of literature.

BACKGROUND: Thyrotoxic periodic paralysis (TPP) is a rare and most often acquired subtype of hypokalemic periodic paralysis. The association of varying degrees of muscle weakness, hyperthyroidism and hypokalemia characterizes it. The treatment requires potassium supplementation, control of hyperthyroidism and prevention measures. It is a frequent disease in Asian men, but much rare in Caucasian or African populations. This is the first report of TPP associated with lactic metabolic acidosis in an African man. CASE PRESENTATION: A 23 year-old African man, native from Morocco, with recurrent episodes of tetraparesis for eleven months, and abdominal pain, was referred for evaluation. Biochemical investigations showed severe hypokalemia associated with hyperthyroidism and lactic metabolic acidosis. His EKG showed signs of hypokalemia such as sinus tachycardia and U waves. After potassium supplementation, neurological recuperation was quick and complete. Thyroid ultrasound identified a hypoechogenic and hypervascularized goiter, associated with high levels of thyroid antibodies, in favor of Grave's disease. With antithyroid drugs and life-style changes, the patient did not have any other attack. REVIEW OF LITERATURE: In addition to the case report, this article presents an extended review of literature, from the first large study reporting the diagnosis and incidence of TPP in 1957 to nowadays. Are reported here the latest information concerning epidemiology, clinical manifestations, complementary examinations, management and genetic finding. The lactic acidosis observed initially is exceptional, never described in TPP. TPP is a diagnostic and therapeutic emergency, requiring careful potassium supplementation, in order to avoid the risk of the onset of rebound hyperkalemia, to be maintained until the etiological treatment is effective. Paraclinical assessment with emergency EKG and electromyogram are essential to assess the impact. DISCUSSION: It is essential in the face of any hypokalaemic periodic paralysis, including in non-Asian subjects, to search hyperthyroidism. CONCLUSIONS: This report demonstrates the importance of thyroid testing in case of acute muscle weakness, even in non-Asian patients in order to diagnose TPP. This is a rare but possible etiology, to be distinguished from the familial form of hypokalemic periodic paralysis. It also questions on the impact of TPP on energetic metabolism, in particular on lactic metabolism.

[Effect of staged acupuncture on serum irisin level and neurological rehabilitation in patients with ischemic stroke].

OBJECTIVE: To observe the effect of staged acupuncture on serum irisin level, neurological deficit, balance ability and spasticity in patients with ischemic stroke. METHODS: Sixty patients with ischemic stroke were randomly divided into a staged acupuncture group and a routine acupuncture group, 30 cases in each group; another 30 healthy subjects were selected as a normal group. The patients with ischemic stroke were treated with aspirin (100 mg each time, once a day, changing to 50 mg for prophylactic dose after 4 weeks). The patients in the staged acupuncture group were treated with staged acupuncture (acupoints were selected according to the soft paralysis period, spasticity period and recovery period, sequelae period) and rehabilitation treatment, while the patients in the routine acupuncture group were treated with acupuncture of soft paralysis-period as the staged acupuncture group and rehabilitation treatment. All the treatment was given once a day, 5 times a week, 2 weeks as a course of treatment, and 4 consecutive courses of treatment were provided. Before treatment and at 2 weeks, 4 weeks, 6 weeks and 8 weeks into treatment, the serum irisin level was measured, and the scores of National Institutes of Health stroke scale (NIHSS), Fugl-Meyer assessment scale-balance (FM-B) and comprehensive spasticity scale (CSS) were compared, and the correlation between the serum irisin level and NIHSS and FM-B scores in the two groups was analyzed. RESULTS: Before treatment, the serum irisin levels in the two groups were lower than those in the normal group (P<0.01). Compared before treatment, the serum irisin levels and FM-B scores were increased (P<0.01), and the NIHSS scores were decreased at 2, 4, 6 and 8 weeks into treatment in the two groups (P<0.01). At 4, 6 and 8 weeks into treatment, in the staged acupuncture group, the serum irisin levels and FM-B scores were higher than those in the routine acupuncture group (P<0.01, P<0.05), and the NIHSS scores were lower than those in the routine acupuncture group (P<0.01). After treatment, the CSS scores in the two groups were increased first and then decreased. Compared before treatment, the CSS scores were increased at 2, 4, 6 and 8 weeks into treatment in the two groups (P<0.01). At 4, 6 and 8 weeks into treatment, the CSS scores in the staged acupuncture group were lower than those in the routine acupuncture group (P<0.01). The serum irisin level was negatively correlated with NIHSS score (r =-0.772, P =0.000), and positively correlated with FM-B score (r =0.675, P =0.000). CONCLUSION: The severity of neurological deficit and balance ability are related to serum irisin level in patients with ischemic stroke. The staged acupuncture could increase the serum irisin level, improve the neurological function, balance ability and spasticity in patients with ischemic stroke.

Distal renal tubular acidosis presenting with an acute hypokalemic paralysis in an older child with severe vesicoureteral reflux and syringomyelia: a case report.

BACKGROUND: Distal renal tubular acidosis (dRTA) is the most common type of renal tubular acidosis (RTA) in children. Pediatric dRTA is usually genetic and rarely occurs due to acquired issues such as obstructive uropathies, recurrent urinary tract infections (UTIs), and chronic kidney disease (CKD). Although persistent hypokalemia frequently occurs with dRTA, acute hypokalemic paralysis is not frequently reported, especially in older children. CASE PRESENTATION: An eight-year-old girl presented with an acute first episode of paralysis. A physical examination revealed normal vital signs, short stature consistent with her genetic potential, and decreased muscle strength of her upper and lower extremities. Preexisting conditions included stage 4 CKD due to recurrent UTIs, severe vesicoureteral reflux and bilateral hydronephrosis, neurogenic bladder, and multisegment thoracic syringomyelia. Her laboratory work-up revealed hypokalemic, hyperchloremic metabolic acidosis with a normal anion gap. She also had a urine osmolal gap of 1.9 mOsmol/kg with a high urine pH. Intravenous potassium replacement resulted in a complete resolution of her paralysis. She was diagnosed with dRTA and discharged with oral bicarbonate and slow-release potassium supplementation. CONCLUSIONS: This case report highlights the importance of considering dRTA in the differential diagnosis of hypokalemic acute paralysis in children. Additionally, in children with neurogenic lower urinary tract dysfunction and recurrent UTIs, early diagnosis of spinal cord etiology is crucial to treat promptly, slow the progression of CKD, and prevent long-term complications such as RTA.

Fascial manipulation as an adjunct to physiotherapy management in obstetric brachial plexus palsy: A case report.

The integrity of connective tissue sheaths surrounding the nerves influences both the severity and the potential for recovery of brachial plexus lesions. This study presents an innovative, early onset, multidisciplinary approach to obstetric brachial plexus palsy. This approach is aimed at functional recovery of the nerve lesion and includes mobilization of the fascia using the Fascial Manipulation® method. This case study discusses how, in addition to conventional treatment, interventions aimed at the fascial system can potentially affect tension around the neural sheaths, enhance proprioceptive input and facilitate movement to influence obstetric brachial plexus palsy outcomes.

A 17-year-old boy who presented with acute mononeuropathy was found to have Type 1 diabetes.

Diabetic neuropathy in children and adolescents with Type 1 diabetes mellitus is rare and is usually subclinical and a complication of the late diabetes period. A 17-year-old boy admitted with a right foot drop of sudden onset was diagnosed with peroneal nerve palsy. He had had osmotic polyuria, polydipsia and weight loss for the past 2 months; his blood glucose was 25 mmol/L (<7.8), HbA1c 15.2% (4.0-5.6) and vitamin B12 125 pg/ml (180-914). The peroneal nerve palsy resolved within 3 months with blood glucose regulation and B12 supplementation. Diabetes should be borne in mind in the differential diagnosis of unusual cases of mononeuropathy.Abbreviations: DCCTS: Diabetes Control and Complications Trial Study; DM: diabetes mellitus; DN: diabetic neuropathy; GAD: glutamic acid decarboxylase; PN: peripheral neuropathy; T1DM: Type 1 diabetes mellitus.

Low-dose oral propranolol for treatment of thyrotoxic periodic paralysis with hypokalaemia in the emergency department: A case report.

WHAT IS KNOWN AND OBJECTIVE: Thyrotoxic periodic paralysis (TPP) with hypokalaemia is a rare acute phenomenon. Reports of the use of high-dose non-selective ß-blockers describe symptom resolution, but often administration does not occur promptly enough in the treatment course and patients may experience overcorrection and hyperkalaemia. CASE DESCRIPTION: A 37-year-old Hispanic male developed TPP. Patient was successfully treated with low-dose oral propranolol and potassium supplementation with no overcorrection. WHAT IS NEW AND CONCLUSION: Delay in the administration of non-selective ß-blockers may lead to overcorrection of potassium with exogenous supplementation. Low-dose propranolol administered in the Emergency Department was successful in preventing overcorrection of potassium.

An atypical presentation of high potassium renal secretion rate in a patient with thyrotoxic periodic paralysis: a case report.

BACKGROUND: Hypokalemia is one of the most common clinical electrolyte imbalance problems, and thyrotoxic periodic paralysis (TPP) is a leading cause of presentation to the emergency department. Low renal potassium secretion rates, a normal acid-base balance in the blood, and hyperthyroidism are the hallmarks of suspected TPP. CASE PRESENTATION: Here we report the case of a 36-year-old man who presented to the emergency department with a sudden onset of acute muscle weakness at 5 h prior to admission. Biochemistry tests revealed hypokalemia with hyperthyroidism and renal potassium wasting. TPP was initially not favored due to the presence of renal potassium wasting. However, his serum potassium level rebounded rapidly within several hours after potassium supplementation, indicating that the intracellular shifting of potassium ions was the main etiology for his hypokalemia. The early stage of TPP development may have contributed to this paradox. CONCLUSION: Therefore, it is premature to rule out TPP based on the presentation of high renal potassium secretion rates alone. This finding may result in an incorrect impression being made in the early stage of TTP and may consequently lead to an inappropriate potassium supplementation policy.

The possible anti-apoptotic and antioxidant effects of acetyl l-carnitine as an add-on therapy on a relapsing-remitting model of experimental autoimmune encephalomyelitis in rats.

Multiple sclerosis (MS) is a progressive inflammatory autoimmune demyelinating disease of the brain and spinal cord. Glucocorticoids (GCs) are the standard treatment of MS, however they have several drawbacks like oxidative stress and apoptosis. This study was designed to evaluate some possible antioxidant, anti-apoptotic and immune modulatory effects of Acetyl-l-carnitine (ALCAR) when used either alone or as an add-on therapy with dexamethasone for treatment of a relapsing-remitting (RR) experimental autoimmune encephalomyelitis (EAE) as a model of MS. This experiment was performed on 50 female Sprague Dawley rats divided into; normal control group, untreated EAE group, EAE group treated by dexamethasone, EAE group treated by ALCAR, and EAE group treated by both dexamethasone and ALCAR. The clinical score of the motor deficit of EAE was recorded daily. At the end of experiment, rats were sacrificed and the brain and spinal cord were processed for assessment of reduced glutathione (GSH), malondialdehyde (MDA) and caspase-3 activity. Histopathological changes and immunohistochemical expression of Bcl-2 and CD4+ T cell were carried out. Combination of both dexamethasone and ALCAR provided marked antioxidant and anti-apoptotic effects represented by significant decrease in MDA, caspase-3 and significant increase in GSH, Bcl-2 expression, and it also exhibited marked immunosuppressive effect represented by significant decrease in CD4+ T cells expression with significant improvement in clinical outcome when compared to untreated EAE group or to dexamethasone treated group. These findings pave the way for using ALCAR as an adjuvant therapy during long-term use of dexamethasone in MS.

Botulismo en la UCI: proceso de cuidados / Botulism in the ICU: nursing care plan

Introducción y valoración del caso. El botulismo es una enfermedad poco frecuente en Europa, causada por la bacteria Clostridium botulinum, de declaración obligatoria, no transmisible de persona a persona y potencialmente mortal (entre un 5 y 10%) si no se trata rápidamente. Se obtuvo el dictamen favorable del Comité de Ética de Investigación Clínica. Se presenta el proceso de cuidados enfermero de un varón de 49 años con diagnóstico de intoxicación bacteriana por Clostridium botulinum, secundario a la ingesta de alubias en mal estado, que estuvo ingresado en la UCI un total de 35 días. Diagnósticos y planificación. Valoración enfermera de forma holística durante las primeras 24 h, con priorización de los sistemas que presentaron un deterioro más rápido: el neurológico y el respiratorio. Se priorizaron 9 diagnósticos según la taxonomía NANDA: riesgo de respuesta alérgica, patrón respiratorio ineficaz, deterioro de la mucosa oral, deterioro de la movilidad física, riesgo de síndrome de desuso, riesgo de motilidad gastrointestinal disfuncional, deterioro de la eliminación urinaria, riesgo de confusión aguda y riesgo de cansancio del rol del cuidador. Discusión. El proceso de cuidados enfermero, estandarizado y organizado con la taxonomía NANDA y priorizado con el método sistemático AREA, garantizó los mejores cuidados basados en la evidencia y prueba de ello fue la mejoría de las puntuaciones de los indicadores de resultado NOC. Resultó imposible comparar la actuación enfermera con la de otros casos documentados

Introduction and case evaluation. Botulism is a rare disease in Europe, caused by the bacterium Clostridium botulinum, notifiable, non-transmissible person-to-person and potentially fatal (between 5 and 10%) if not treated quickly. The favourable opinion of the Clinical Research Ethics Committee was obtained. We present the nursing care plan of a 49-year-old man with a diagnosis of bacterial intoxication caused by Clostridium botulinum, secondary to ingestion of beans in poor condition, who was admitted to the ICU for a total of 35 days. Diagnosis and planning. Holistic nursing evaluation during the first 24hours, with prioritisation of the systems that were deteriorating fastest: neurological and respiratory. Nine diagnoses were prioritised according to the NANDA taxonomy: Risk for allergy response, Ineffective breathing pattern, impaired oral mucous membrane, Impaired physical mobility, Risk for disuse syndrome, Risk for dysfunctional gastrointestinal motility, Impaired urinary elimination, Risk for acute confusion and Risk for caregiver role strain. Discussion. The nursing care plan, standardised and organised with the NANDA taxonomy and prioritised with the outcome-present state-test (OPT) model, guaranteed the best care based on evidence, as the NOC scores improvement demonstrated. It was impossible to compare the nursing intervention with other case reports

Strength training for partially paralysed muscles in people with recent spinal cord injury: a within-participant randomised controlled trial.

STUDY DESIGN: Within-participant randomised controlled trial. OBJECTIVES: To determine whether strength training combined with usual care increases strength in partially paralysed muscles of people with recent spinal cord injury (SCI) more than usual care alone. SETTINGS: SCI units in Australia and India. METHODS: Thirty people with recent SCI undergoing inpatient rehabilitation participated in this 12-week trial. One of the following muscle groups was selected as the target muscle group for each participant: the elbow flexors, elbow extensors, knee flexors or knee extensors. The target muscle on one side of the body was randomly allocated to the experimental group and the same muscle on the other side of the body was allocated to the control group. Strength training was administered to the experimental muscle but not to the control muscle. Participants were assessed at baseline and 12 weeks later. The primary outcome was maximal isometric muscle strength, and the secondary outcomes were spasticity, fatigue and participants' perception of function and strength. RESULTS: There were no dropouts, and participants received 98% of the training sessions. The mean (95% confidence interval (CI)) between-group difference for isometric strength was 4.3 Nm (1.9-6.8) with a clinically meaningful treatment effect of 2.7 Nm. The mean (95% CI) between-group difference for spasticity was 0.03/5 points (-0.25 to 0.32). CONCLUSION: Strength training increases strength in partially paralysed muscles of people with recent SCI, although it is not clear whether the size of the treatment effect is clinically meaningful. Strength training has no deleterious effects on spasticity.

A brain-spine interface alleviating gait deficits after spinal cord injury in primates.

Spinal cord injury disrupts the communication between the brain and the spinal circuits that orchestrate movement. To bypass the lesion, brain-computer interfaces have directly linked cortical activity to electrical stimulation of muscles, and have thus restored grasping abilities after hand paralysis. Theoretically, this strategy could also restore control over leg muscle activity for walking. However, replicating the complex sequence of individual muscle activation patterns underlying natural and adaptive locomotor movements poses formidable conceptual and technological challenges. Recently, it was shown in rats that epidural electrical stimulation of the lumbar spinal cord can reproduce the natural activation of synergistic muscle groups producing locomotion. Here we interface leg motor cortex activity with epidural electrical stimulation protocols to establish a brain-spine interface that alleviated gait deficits after a spinal cord injury in non-human primates. Rhesus monkeys (Macaca mulatta) were implanted with an intracortical microelectrode array in the leg area of the motor cortex and with a spinal cord stimulation system composed of a spatially selective epidural implant and a pulse generator with real-time triggering capabilities. We designed and implemented wireless control systems that linked online neural decoding of extension and flexion motor states with stimulation protocols promoting these movements. These systems allowed the monkeys to behave freely without any restrictions or constraining tethered electronics. After validation of the brain-spine interface in intact (uninjured) monkeys, we performed a unilateral corticospinal tract lesion at the thoracic level. As early as six days post-injury and without prior training of the monkeys, the brain-spine interface restored weight-bearing locomotion of the paralysed leg on a treadmill and overground. The implantable components integrated in the brain-spine interface have all been approved for investigational applications in similar human research, suggesting a practical translational pathway for proof-of-concept studies in people with spinal cord injury.

A minimal dose of electrically induced muscle activity regulates distinct gene signaling pathways in humans with spinal cord injury.

Paralysis after a spinal cord injury (SCI) induces physiological adaptations that compromise the musculoskeletal and metabolic systems. Unlike non-SCI individuals, people with spinal cord injury experience minimal muscle activity which compromises optimal glucose utilization and metabolic control. Acute or chronic muscle activity, induced through electrical stimulation, may regulate key genes that enhance oxidative metabolism in paralyzed muscle. We investigated the short and long term effects of electrically induced exercise on mRNA expression of human paralyzed muscle. We developed an exercise dose that activated the muscle for only 0.6% of the day. The short term effects were assessed 3 hours after a single dose of exercise, while the long term effects were assessed after training 5 days per week for at least one year (adherence 81%). We found a single dose of exercise regulated 117 biological pathways as compared to 35 pathways after one year of training. A single dose of electrical stimulation increased the mRNA expression of transcriptional, translational, and enzyme regulators of metabolism important to shift muscle toward an oxidative phenotype (PGC-1α, NR4A3, IFRD1, ABRA, PDK4). However, chronic training increased the mRNA expression of specific metabolic pathway genes (BRP44, BRP44L, SDHB, ACADVL), mitochondrial fission and fusion genes (MFF, MFN1, MFN2), and slow muscle fiber genes (MYH6, MYH7, MYL3, MYL2). These findings support that a dose of electrical stimulation (∼10 minutes/day) regulates metabolic gene signaling pathways in human paralyzed muscle. Regulating these pathways early after SCI may contribute to reducing diabetes in people with longstanding paralysis from SCI.

Parálisis periódica hipopotasémica tirotóxica: a propósito de un caso / Thyrotoxic hypokalemic periodic paralysis. A case report

La parálisis periódica hipopotasémica tirotóxica (PPT) es una rara complicación de la tirotoxicosis caracterizada por la aparición de episodios de debilidad muscular asociados a hipopotasemia en pacientes con hipertiroidismo, más frecuentemente con enfermedad de Graves-Basedow. El tratamiento con antitiroideos y suplementos de potasio revierte la sintomatología de debilidad muscular y evita la reaparición de estos síntomas (AU)

Thyrotoxic hypokalemic periodic paralysis is an uncommon complication of thyrotoxicosis, characterized by attacks of generalized muscular weakness associated with hypokalemia in patients with hyperthyroidism, most frequently with Graves-Basedow disease. Treatment with antithyroid drugs and potassium supplements reversed the symptoms and the episodes of acute muscular weakness did not reappear (AU)

Hypokalemic paralysis in a young obese female.

BACKGROUND: Profound hypokalemia with paralysis usually poses a diagnostic and therapeutic challenge. METHODS: We report on a 28-y-old obese Chinese female presenting with sudden onset of flaccid quadriparesis upon awaking in the morning. There is no family history of hyperthyroidism. She experienced body weight loss of 7 kg in 2 months. RESULTS: The most conspicuous blood biochemistry is marked hypokalemia (1.8 mmol/l) and hypophosphatemia (0.5 mmol/l) associated with low urine K(+) and phosphate excretion. Surreptitious laxatives and/or diuretics abuse-related hypokalemic paralysis were tentatively made. However, her relatively normal blood acid-base status and the absence of low urine Na(+) and/or Cl(-) excretion made these diagnoses unlikely. Furthermore, she developed rebound hyperkalemia (5.7 mmol/l) after only 80 mmol K(+) supplementation. Thyroid function test confirmed hyperthyroidism due to Graves' disease. Control of the hyperthyroidism completely abolished her periodic paralysis. CONCLUSIONS: Thyrotoxic periodic paralysis (TPP) should be kept in mind as a cause of paralysis in female, even with obesity, despite its predominance in adult males.

The effects of spinal cord injury and exercise on bone mass: a literature review.

INTRODUCTION: Bone loss is a common and often debilitating condition that accompanies spinal cord injury. Because bone loss after spinal cord injury is multifactorial, it can be difficult to assess and treat. This process becomes even more complex as secondary conditions associated with aging are introduced. PURPOSE: There are two purposes of this literature review. The first is to summarize information concerning the mechanisms of bone loss and osteoporosis after spinal cord injury. The second is to summarize existing data concerning the effects of exercise on bone loss after spinal cord injury. METHOD: Literature was reviewed concerning the bone loss process and the non-pharmacological treatment options for ameliorating bone loss after spinal cord injury. RESULTS: (Part One) Osteoporosis is universal in persons with chronic complete spinal cord injury, which increases the risk of bone fracture. Bone loss after spinal cord injury is both sublesional and regional with the greatest areas of bone demineralization being in the sublesional trabecular laden areas of the distal and proximal epiphyses of the femur and tibia. (Part Two) While passive weight bearing of paralyzed lower extremities appears to be ineffective, stressing the bones through muscular contractions initiated by electrical stimulation (FES) have yielded positive results in some cases. The intensity, frequency, and duration of stress to the bones appear to be important determinants of improved bone parameters. Although further quantification of these components is needed, some generalized guidelines can be deduced from completed research. Intensities showing positive results have been loads of one to one and a half times body weight for FES exercise or having participants FES cycle at their highest power output. Safety precautions must be used to decrease risk of bone fracture. Generally, the frequency is effective with three or more weekly exercise sessions. Studies of duration suggest that several months to one or more years of FES are necessary. DISCUSSION: In order to promote healthy and independent aging in patients with spinal cord injury, it is important to understand the processes, consequences and effective treatments involved with bone loss.

Altered mRNA expression after long-term soleus electrical stimulation training in humans with paralysis.

In humans, spinal cord injury (SCI) induces deleterious changes in skeletal muscle that may be prevented or reversed by electrical stimulation muscle training. The molecular mechanisms underlying muscle stimulation training remain unknown. We studied two unique SCI subjects whose right soleus received >6 years of training (30 minutes/day, 5 days/week). Training preserved torque, fatigue index, contractile speed, and cross-sectional area in the trained leg, but not the untrained leg. Training decreased 10 mRNAs required for fast-twitch contractions and mRNA that encodes for myostatin, an autocrine/paracrine hormone that inhibits muscle growth. Conversely, training increased 69 mRNAs that mediate the slow-twitch, oxidative phenotype, including PGC-1α, a transcriptional coactivator that inhibits muscle atrophy. When we discontinued right soleus training, training-induced effects diminished slowly, with some persisting for >6 months. Training of paralyzed muscle induces localized and long-lasting changes in skeletal muscle mRNA expression that improve muscle mass and function.