Subdural Spread of Local Anesthetic Mimicking Cerebrovascular Accident: A Case Report of Horner's Syndrome, Upper Limb Paresthesia, and Motor Weakness After Thoracic Epidural Analgesia.

A 53-year-old woman underwent a thoracic epidural placement for a scheduled laparotomy. Postoperatively the patient had no appreciable epidural level after multiple epidural boluses and was noted to be severely hypotensive with right upper extremity weakness and numbness. She subsequently developed right-sided Horner's syndrome with worsening right upper extremity weakness and decreased sensation from C6 to T1. She regained full motor and sensory function in her right upper extremity with epidural removal. This unusual case raises awareness of the variability in the presentation of subdural spread and provides an example of an epidural complication that can mimic a cerebrovascular accident (CVA).

Abdominal wall muscle weakness outcomes after split abdominal flap repair of large congenital diaphragmatic hernias in newborn.

PURPOSE: Split abdominal wall muscle flap (SAWMF) is a technique to repair large defects in congenital diaphragmatic hernia (CDH). A possible objection to this intervention could be any associated abdominal muscle weakness. Our aim is to analyze the evolution of this abdominal muscle wall weakness. METHODS: Retrospective review of CDH repair by SAWMF (internal oblique muscle and transverse) from 2004 to 2023 focusing on the evolution of muscle wall weakness. RESULTS: Eighteen neonates of 148 CDH patients (12,1%) were repaired using SAWMF. Mean gestational age and birth weight were 35.7 ± 3.5 weeks and 2587 ± 816 g. Mean lung-to-head ratio was 1.49 ± 0.28 and 78% liver-up. Seven patients (38%) were prenatally treated by tracheal occlusion. Ninety-four percent of the flaps were used for primary repair and one to repair a recurrence. One patient (5.6%) experienced recurrence. Abdominal muscle wall weakness was present in the form of a bulge. Resolution of weakness at 1, 2 and 3 years was 67%, 89% and 94%, respectively. No patient required treatment for weakness or died. CONCLUSIONS: Abdominal muscular weakness after a split abdominal wall muscle flap repair is not a limitation for its realization since it is asymptomatic and presents a prompt spontaneous resolution. LEVEL OF EVIDENCE: IV.

Shoulder muscle weakness and proprioceptive impairments in type 2 diabetes mellitus: exploring correlations for improved clinical management.

Background: Type 2 diabetes mellitus (T2DM) is a prevalent metabolic disorder with systemic implications, potentially affecting musculoskeletal health. This study aimed to assess shoulder muscle strength and joint repositioning accuracy in individuals with T2DM, exploring potential correlations and shedding light on the musculoskeletal consequences of the condition. The objectives were two-fold: (1) to assess and compare shoulder strength and joint repositioning accuracy between individuals with T2DM and asymptomatic counterparts, and (2) to examine the correlation between shoulder strength and joint repositioning accuracy in individuals with T2DM. Methods: A cross-sectional study enrolled 172 participants using the convenience sampling method, including 86 individuals with T2DM and an age-matched asymptomatic group (n = 86). Shoulder strength was assessed using a handheld dynamometer, while joint repositioning accuracy was evaluated with an electronic digital inclinometer. Results: Individuals with T2DM exhibited reduced shoulder muscle strength compared to asymptomatic individuals (p < 0.001). Additionally, joint repositioning accuracy was significantly lower in the T2DM group (p < 0.001). Negative correlations were observed between shoulder strength and joint repositioning accuracy in various directions (ranging from -0.29 to -0.46, p < 0.001), indicating that higher muscle strength was associated with improved joint repositioning accuracy in individuals with T2DM. Conclusion: This study highlights the significant impact of T2DM on shoulder muscle strength and joint repositioning accuracy. Reduced strength and impaired accuracy are evident in individuals with T2DM, emphasizing the importance of addressing musculoskeletal aspects in diabetes management. The negative correlations suggest that enhancing shoulder muscle strength may lead to improved joint repositioning accuracy, potentially contributing to enhanced physical functioning in this population.

Incomplete Kawasaki disease with muscular weakness and bladder retention: a case report.

BACKGROUND: Kawasaki disease (KD) is an acute systemic immune vasculitis affecting multiple organs and systems in children, and is prevalent in children under 5 years of age. Muscular weakness is a rare manifestation of KD, and only 11 pediatric patients with KD combined with muscular weakness have been reported, of which evidence of myositis was found in 2/3 of the patients, and 1/3 could not be explained by myositis, the mechanism of which is still unclear. Cases of KD combined with bladder retention are even more rare, and there has been only 1 case report of KD combined with bladder retention in a child with no previous underlying disease. CASE PRESENTATION: We report a 22-month-old Asian child with incomplete Kawasaki disease (IKD) who initially presented with fever and progressive muscular weakness in the lower extremities, followed by the bladder and bowel retention abnormalities and rapid onset of heart failure, respiratory failure and shock. The child developed coronary artery ectasia (CAA) without the main clinical features of KD such as rash, conjunctival congestion, desquamation of the extremity endings, orofacial changes and enlarged lymph nodes in the neck. Creatine kinase and electromyography were normal. Temperature gradually normalized and muscle strength recovered slightly after intravenous immunoglobulin. The child could be helped to walk after 1 week of aspirin combined with steroid therapy. CONCLUSIONS: We present the case of a 22-month-old child with IKD. The child began with progressive muscular weakness in the extremities, followed by the bladder and bowel retention abnormalities, and rapidly developed heart failure, respiratory failure, and shock. Despite early failure to detect the disease, the child recovered rapidly and had a favorable prognosis. KD comorbidities with muscular weakness as the main manifestation are uncommon. This is the first case report of IKD combined with both muscular weakness and bladder and bowel retention, which may provide clinicians with diagnostic and therapeutic ideas, as well as a basis for future exploration of the mechanisms of KD combined with muscular weakness or bladder and bowel retention abnormalities.

Dry needling effects on motor impairments in a patient with traumatic brain injury: A case study.

BACKGROUND: Motor impairments are common consequences of traumatic brain injury (TBI). It affects the individuals' participation in activities of daily living (ADLs). Dry needling treatment (DNT) uses a specialized needle to alter cortical activity. This case study aims to examine the effects of DNT on spasticity, balance, gait, and self-independence in a single patient with TBI. CASE DESCRIPTION: A twenty-six-year-old male with a history of TBI, resulting in muscle weakness on the right side of the body, spasticity, distributed balance, and difficulties with independent gait participated in this study. The Berg balance scale (BBS), 6-min walk test (6MWT), Modified Ashworth Scale (MAS), and Functional Independence Measure (FIM) were used to evaluate balance, gait, spasticity, and functional performance, respectively. OUTCOME: After 36 DNT sessions extended over 12 weeks, the patient demonstrated improvements in spasticity, balance, gait, and functional capacity both immediately after the intervention and at the 4-week follow-up. CONCLUSION: This case study demonstrates that DNT is considered a novel intervention for treating spasticity and improving balance, gait, and functional capacity post-TBI. Further research is recommended to verify these findings.

Clinical Reasoning: A 55-Year-Old Woman With Painless Hand Weakness and Atrophy.

Hand weakness is a frequent chief concern in neurology practice. We report a case of a 55-year-old woman presenting with a chronic, gradually worsening right hand weakness and atrophy, selectively affecting the thenar muscles, without any sensory symptoms. She had a history of carpal tunnel syndrome and previously underwent surgical carpal tunnel release. This case delves into the differential diagnosis of hand weakness and atrophy, emphasizing the significance of myotomal innervation in intrinsic hand muscles. Furthermore, it outlines a systematic approach to diagnosing an uncommon cause for a common clinical presentation, offering a comprehensive differential diagnosis, and exploring various possible causes.

[THE MUSCULAR COMPONENT OF FIBROMYALGIA PATHOPHYSIOLOGY].

INTRODUCTION: Fibromyalgia syndrome (FMS) is a chronic pain syndrome, prevalent in women more than men. The main symptoms are widespread musculoskeletal pain, fatigue, and weakness. To date, the pathophysiological mechanisms are unclear, and there are several pathogenic theories elucidating this condition. In this review, we summarized articles published in the past few years, regarding the effect of musculoskeletal dysfunction on FMS. We focused on the musculoskeletal system and central nervous system (CNS) disarrays.

Preoperative motor weakness and the impact on patient reported outcomes in lateral lumbar interbody fusion.

This study measures the impact of preoperative motor weakness (MW) on Patient-Reported Outcome Measures (PROMs) in lateral lumbar interbody fusion (LLIF) patients. Retrospectively-sourced data from a prospectively-maintained, single-surgeon database created two cohorts of LLIF patients: patients with/without documented MW. Demographics/perioperative characteristics/PROMs were collected preoperatively and at six-weeks/final follow-up (FF). Studied outcomes were Patient-Reported Outcomes Measurement Information System Physical Function (PROMIS-PF), 12-Item Short Form (SF-12) Physical/Mental Component Score (PCS/MCS), Patient Health Questionnaire (PHQ-9), Visual Analog Scale Back/Leg Pain (VAS-BP/LP), and Oswestry Disability Index (ODI). Multivariable linear/logistic regression calculated/compared intercohort minimum clinically important difference (MCID). Mean postoperative follow-up time was 11.5 ± 7.52 months. In total, 214 LLIF patients from December 2010 to May 2023 were included, with 149 having documented MW. In Table 1, self-reported gender was significant between cohorts (p < 0.025). Other significant demographic characteristics were smoker status (p < 0.002), diabetes (p < 0.016), and CCI score (p < 0.011). Table 2 shows notably significant perioperative characteristics: spinal pathology (degenerative spondylolisthesis/foraminal stenosis/herniated nucleus pulposus) (p < 0.005, all), estimated blood loss/length of stay/postoperative day (POD)-zero narcotic consumption (p < 0.001, all). Table 3 outcomes/MCID achievement percentages demonstrated insignificant intercohort differences besides a weakly significant FF ODI score (p < 0.036). MW, a frequently reported symptom in spine surgery, is poorly studied in LLIF patients. Thus, this study evaluates MW impact on PROMs and notes no significant differences. However, one exception regarding FF disability scores was recorded. MW did not affect MCID achievement for our patient population. Therefore, the preliminary findings suggest preoperative MW imparts minimal influence on PROMs/MCID in LLIF patients.

Acquired hyperkalaemia leading to periodic paralysis: an emergency department perspective.

Hyperkalaemia is one of the common electrolyte imbalances dealt with in the emergency department and is caused by extracellular accumulation of potassium ions above normal limits usually greater than 5.0-5.5 mmol/L. It is found in a total of 1-10% of hospitalised patients usually associated with chronic kidney disease and heart failure. The presentation can range from being asymptomatic to deadly arrhythmias. The appearance of symptoms depends on the rate of change rather than just the numerical values. The rare presentation includes periodic paralysis characterised by the sudden onset of short-term muscle weakness, stiffness or paralysis. Management goals are directed towards reducing potassium levels in emergency settings and later on avoiding the triggers for future attacks. In this case, we present a man in his 50s with the generalised weakness later on diagnosed as hyperkalaemic periodic paralysis secondary to tumour lysis syndrome. Emergency physicians dealing with common electrolyte imbalances should keep a sharp eye on their rare presentation and their precipitating factors and should act accordingly.

Electrophysiological abnormalities of the neuromuscular transmission in two patients with botulism-like syndrome following Botulinum-A muscle injections.

Botulinum neurotoxin serotype A (BoNT-A) has several therapeutic indications such as spasticity and dystonia. Although its use is generally considered safe, a systemic diffusion can lead to systemic complications, and a botulism-like syndrome can occur after intramuscular injections. Herein, two adult cases who developed general muscle weakness after a BoNT-A intramuscular injection are reported. Both presented with a progressive decrement on low-frequency (LF) repetitive nerve stimulation (RNS). It is suggested that a progressive decrement on LF-RNS in muscles distant from the injection site strongly supports the diagnosis of iatrogenic botulism.

Drop Foot With Posterior Tibialis Weakness Treated With Peroneus Longus Transfer in a Child: A Case Report.

CASE: An 8-year-old girl with a history of acute flaccid paralysis presented with chronic valgus drop foot causing tripping and falling. Traditionally surgical correction of this deformity is accomplished by transferring the posterior tibialis tendon to enhance dorsiflexion. The authors describe a new technique which transfers the peroneus longus tendon to the dorsum of the foot in a patient with weakness of the posterior tibialis muscle. The patient's drop foot and gait were improved at the 22-month follow-up. CONCLUSION: Successful transfer of the peroneus longus was accomplished with improved limb clearance during gait and coronal alignment in stance.

Unusual cause of muscle weakness, type II respiratory failure and pulmonary hypertension: a case report of ryanodine receptor type 1(RYR1)-related myopathy.

BACKGROUND: Patients with congenital myopathies may experience respiratory involvement, resulting in restrictive ventilatory dysfunction and respiratory failure. Pulmonary hypertension (PH) associated with this condition has never been reported in congenital ryanodine receptor type 1(RYR1)-related myopathy. CASE PRESENTATION: A 47-year-old woman was admitted with progressively exacerbated chest tightness and difficulty in neck flexion. She was born prematurely at week 28. Her bilateral lower extremities were edematous and muscle strength was grade IV-. Arterial blood gas analysis revealed hypoventilation syndrome and type II respiratory failure, while lung function test showed restrictive ventilation dysfunction, which were both worse in the supine position. PH was confirmed by right heart catheterization (RHC), without evidence of left heart disease, congenital heart disease, or pulmonary artery obstruction. Polysomnography indicated nocturnal hypoventilation. The ultrasound revealed reduced mobility of bilateral diaphragm. The level of creatine kinase was mildly elevated. Magnetic resonance imaging showed myositis of bilateral thigh muscle. Muscle biopsy of the left biceps brachii suggested muscle malnutrition and congenital muscle disease. Gene testing revealed a missense mutation in the RYR1 gene (exon33 c.C4816T). Finally, she was diagnosed with RYR1-related myopathy and received long-term non-invasive ventilation (NIV) treatment. Her symptoms and cardiopulmonary function have been greatly improved after 10 months. CONCLUSIONS: We report a case of RYR1-related myopathy exhibiting hypoventilation syndrome, type II respiratory failure and PH associated with restrictive ventilator dysfunction. Pulmonologists should keep congenital myopathies in mind in the differential diagnosis of type II respiratory failure, especially in patients with short stature and muscle weakness.

Diaphragm weakness in late-onset Pompe disease: A complex interplay between lower motor neuron and muscle fibre degeneration.

BACKGROUND: Late-onset Pompe disease (LOPD) patients may still need ventilation support at some point of their disease course, despite regular recombinant human alglucosidase alfa treatment. This suggest that other pathophysiological mechanisms than muscle fibre lesion can contribute to the respiratory failure process. We investigate through neurophysiology whether spinal phrenic motor neuron dysfunction could contribute to diaphragm weakness in LOPD patients. MATERIAL AND METHODS: A group of symptomatic LOPD patients were prospectively studied in our centre from January 2022 to April 2023. We collected both demographic and clinical data, as well as neurophysiological parameters. Phrenic nerve conduction studies and needle EMG sampling of the diaphragm were perfomed. RESULTS: Eight treated LOPD patients (3 males, 37.5%) were investigated. Three patients (37.5%) with no respiratory involvement had normal phrenic nerve motor responses [median phrenic compound muscle action potential (CMAP) amplitude of 0.49 mV; 1st-3rd interquartile range (IQR), 0.48-0.65]. Those with respiratory failure (under nocturnal non-invasive ventilation) had abnormal phrenic nerve motor responses (median phrenic CMAP amplitude of 0 mV; 1st-3rd IQR, 0-0.15), and were then investigated with EMG. Diaphragm needle EMG revealed both myopathic and neurogenic changes in 3 (60%) and myopathic potentials in 1 patient. In the last one, no motor unit potentials could be recruited. CONCLUSIONS: Our study provide new insights regarding respiratory mechanisms in LOPD, suggesting a contribution of spinal phrenic motor neuron dysfunction for diaphragm weakness. If confirmed in further studies, our results recommend the need of new drugs crossing the blood-brain barrier.

An 11-month-old boy with tuberculous meningitis presenting as progressive limb weakness, fever, developmental retardation, and loss of consciousness: a case report.

BACKGROUND: Tuberculous meningitis (TBM) accounts for about 1% of all tuberculosis cases and about 5% of extrapulmonary tuberculosis cases. However, it poses major importance because approximately half of those affected die or become severely disabled. Herein, the successful treatment of an 11-month-old boy with progressive limb weakness, fever, developmental retardation, and loss of consciousness due to tuberculosis, was reported. CASE PRESENTATION: An 11-month-old (Iranian Turk) boy was referred to Loghman Hakim hospital for progressive limb weakness and loss of previously attained developmental milestones for the past 2 months. He also had persistent fever and loss of consciousness for about 14 to 21 days. Before being referred to our center, the patient had been diagnosed with hydrocephalus at another center due to possible acute bacterial meningitis based on a CT scan and MRI imaging. On physical examination, anterior fontanel bulging and neck stiffness were observed on the admission. His body temperature and heart rate were 38.1 C and 86 beats per minute (bpm), respectively. He had left 6 cranial nerve palsy and spastic quadriparesis with a power of grade 3/5. Other systemic examinations were normal. Endoscopic third ventriculostomy (ETV) (and leptomeningeal biopsy) revealed diffuse thickening of the floor and lateral walls of the 3rd ventricle and also a cobblestone appearance in the form of multiple white patchy lesions was detected on the floor of the 3rd ventricle. CSF analysis and polymerase chain reaction confirmed the TB meningitis. During hospitalization, a temporary EVD (external ventricular drain) was initially inserted. Eventually, defervescence was denoted 5-6 days after initiation of anti-TB medications, and a permanent ventriculoperitoneal shunt was inserted due to hydrocephalus. Gradually his truncal and limb tone and motor function improved, as did his emotional responses to his parents and ability to eat. The patient can walk without help in the 15th month following the operation and resolved hydrocephalus demonstrated on follow-up imaging. CONCLUSION: Over half of treated TB meningitis patients die or suffer severe neurological sequelae, mainly due to late diagnosis. Hence, early diagnosis and prompt initiation of TB treatment offer the best chance of a good neurological outcome.

Practical approach to the child presenting with acute generalised weakness.

Acute generalised muscle weakness in children is a paediatric emergency with a broad differential diagnosis. A careful history and neurologic examination guides timely investigation and management. We review some of the more common causes of acute generalised muscle weakness in children, highlighting key history and examination findings, along with an approach to lesion localisation to guide differential diagnosis and further investigation.

Cancer-associated muscle weakness - From triggers to molecular mechanisms.

Skeletal muscle weakness is a debilitating consequence of many malignancies. Muscle weakness has a negative impact on both patient wellbeing and outcome in a range of cancer types and can be the result of loss of muscle mass (i.e. muscle atrophy, cachexia) and occur independently of muscle atrophy or cachexia. There are multiple cancer specific triggers that can initiate the progression of muscle weakness, including the malignancy itself and the tumour environment, as well as chemotherapy, radiotherapy and malnutrition. This can induce weakness via different routes: 1) impaired intrinsic capacity (i.e., contractile dysfunction and intramuscular impairments in excitation-contraction coupling or crossbridge cycling), 2) neuromuscular disconnection and/or 3) muscle atrophy. The mechanisms that underlie these pathways are a complex interplay of inflammation, autophagy, disrupted protein synthesis/degradation, and mitochondrial dysfunction. The current lack of therapies to treat cancer-associated muscle weakness highlight the critical need for novel interventions (both pharmacological and non-pharmacological) and mechanistic insight. Moreover, most research in the field has placed emphasis on directly improving muscle mass to improve muscle strength. However, accumulating evidence suggests that loss of muscle function precedes atrophy. This review primarily focuses on cancer-associated muscle weakness, independent of cachexia, and provides a solid background on the underlying mechanisms, methodology, current interventions, gaps in knowledge, and limitations of research in the field. Moreover, we have performed a mini-systematic review of recent research into the mechanisms behind muscle weakness in specific cancer types, along with the main pathways implicated.