Steroids Significantly Decrease Postoperative Postural Hypotension in Total Knee Replacement.

Total knee replacement (TKR) is one of the most common orthopaedic procedures performed, and enhanced recovery after surgery (ERAS) has been developed and incorporated into inpatient surgical pathways to improve patient outcomes. Under ERAS recommendations, multimodal prophylaxis has been used to help manage postoperative nausea and vomiting (PONV) following TKR. Dexamethasone is one of the commonly used for this and the anti-inflammatory properties could depress vagal activity, reducing postural hypotension (PH). The hypothesis of this study is that postoperative dexamethasone use is associated with lower rates of early postoperative PH following TKR surgery. In our institution, patients who undergo elective primary TKR are admitted on the day of surgery and follow a standardized ERAS protocol. Data on patients who underwent elective primary TKR under a single adult reconstruction team from September 2017 to March 2020 were reviewed and analyzed. A review of demographic characteristics, surgical data, postoperative medications, and postoperative notes was performed. Binary logistic regression was used to assess the effect of the use of dexamethasone on PH, with an adjusted odds ratio (OR) calculated after accounting for potential confounders. Of the 149 patients were included in the study, 78 had dexamethasone postoperatively, and 71 did not. Patients who had received dexamethasone were statistically less likely to suffer from PH (OR = 0.31, p = 0.03) and less likely to develop PONV (OR = 0.21, p = 0.006). Patients who had received dexamethasone were more likely able to participate in early physiotherapy (OR = 2.42, p = 0.14), and this result was statistically insignificant. The use of postoperative intravenous dexamethasone is significantly associated with lower rates of postoperative PH after TKR. However, more studies are required to assess the optimal dosing amount and frequency, as well as to assess other factors which can enhance early postoperative patient mobilization as part of our goals for ERAS. This therapeutic study reflects level of evidence III.

Post-radiation lower motor neuron syndrome.

UNLABELLED: Objective To describe the clinical features of four patients we encountered with post-radiation lower motor neuron syndromes and to review the related literature BACKGROUND.: Radiation therapy for malignant neoplasms has been associated with a post-radiation lower motor neuron syndrome (PRLMNS). The earliest descriptions date back to World War II. METHODS: We evaluated four patients who developed a lower motor neuron syndrome several years after the completion of radiation therapy to treat malignancies. The clinical and electrophysiological features of these patients are described. RESULTS: Our patients with PRLMNS developed weakness, muscle atrophy, loss of reflexes, and fasciculations in myotomal distributions that corresponded to the regions that had been exposed to radiation The mean time between radiation exposure and onset of motor symptoms was 14 years. Sensory symptoms were either absent or minor. Motor and sensory nerve conduction studies were normal or only mildly affected, Needle electromyography showed varying degrees of active and chronic denervation changes, primarily in the distributions that had received radiation. Magnetic resonance imaging of the spine and myelography were unremarkable. Serum creatine kinase levels were elevated in two patients. The patients followed a stable to slowly progressive course at a mean follow up of 6.5 years. CONCLUSIONS: . Patients presenting with lower motor neuron syndromes should be questioned about prior radiation exposure. A diagnosis of PRLMNS carries a relatively favorable prognosis when compared with amyotrophic lateral sclerosis, another acquired motor neuron disorder.

Multifocal acquired demyelinating sensory and motor neuropathy: the Lewis-Sumner syndrome.

We report 11 patients with multifocal acquired demyelinating sensory and motor (MADSAM) neuropathy, defined clinically by a multifocal pattern of motor and sensory loss, with nerve conduction studies showing conduction block and other features of demyelination. The clinical, laboratory, and histological features of these patients were contrasted with those of 16 patients with multifocal motor neuropathy (MMN). Eighty-two percent of MADSAM neuropathy patients had elevated protein concentrations in the cerebrospinal fluid, compared with 9% of the MMN patients (P < 0.001). No MADSAM neuropathy patient had elevated anti-GM1 antibody titers, compared with 56% of MMN patients (P < 0.01). In contrast to the subtle abnormalities described for MMN, MADSAM neuropathy patients had prominent demyelination on sensory nerve biopsies. Response to intravenous immunoglobulin treatment was similar in both groups (P = 1.0). Multifocal motor neuropathy patients typically do not respond to prednisone, but 3 of 6 MADSAM neuropathy patients improved with prednisone. MADSAM neuropathy more closely resembles chronic inflammatory demyelinating polyneuropathy and probably represents an asymmetrical variant. Given their different clinical patterns and responses to treatment, it is important to distinguish between MADSAM neuropathy and MMN.

Myasthenia gravis activities of daily living profile.

The authors have developed an MG activities of daily living (ADL) profile (MG-ADL)-a simple eight-question survey of MG symptoms. In 254 consecutive encounters with established MG patients, the authors compared scores from the MG-ADL to the quantitative MG score (QMG)-a standardized, reliable scale used in clinical trials. The mean MG-ADL score was 4.89+/-3.63. The mean QMG score was 10.80+/-5.70. Pearson's correlation coefficient was 0.583 (p < 0.001). The MG-ADL is an easy-to-administer survey of MG that correlates well with the QMG and can serve as a secondary efficacy measurement in clinical trials.

Distal myasthenia gravis.

Myasthenia gravis (MG) characteristically involves ocular, bulbar, and proximal extremity muscles. Distal extremity muscles are typically spared or less prominently involved. The authors performed a retrospective chart review of MG patients treated at two university-based neuromuscular clinics. From a total population of 236, nine patients (3%) had distal extremity weakness exceeding proximal weakness by at least one Medical Research Council grade during their illness. Hand muscles, particularly finger extensors, were involved more frequently than were distal leg and foot muscles.

Primary hyperparathyroidism and ALS: is there a relation?

BACKGROUND: An association between primary hyperparathyroidism (PHP) and amyotrophic lateral sclerosis (ALS) has been noted; however, a causal relation between these disorders has not been confirmed. PATIENTS/METHODS: We report five patients (three men, two women) meeting El Escorial criteria for ALS who also had PHP. In three patients, the diagnosis of PHP was made during the laboratory evaluation for motor neuron disease, and in one patient, the diagnosis of PHP preceded the onset of weakness by 5 months and in another by 2 years. Serum calcium levels in all five patients were elevated, ranging from 11.2 to 12.8 mg/dL (normal, <10.4 mg/dL), as were levels of parathyroid hormone (PTH). RESULTS: All five patients underwent parathyroid adenoma resection with subsequent normalization of serum calcium and PTH levels. Each patient had progressive weakness resulting in death 1 to 3 years following parathyroidectomy. CONCLUSION: Resection of parathyroid adenomas in patients meeting El Escorial criteria for ALS did not alter the course of ALS. PHP and ALS appear to be coexisting but unrelated disorders.

Acetylcholine receptor antibodies in the Lambert-Eaton myasthenic syndrome.

Two patients were initially diagnosed with myasthenia gravis with elevated titers of acetylcholine receptor antibodies. Features including weakness that normalized with sustained contraction, areflexia, autonomic symptoms, and low-amplitude baseline compound muscle action potentials with abnormal increments following brief exercise and high-frequency repetitive stimulation, however, suggested that these patients had Lambert-Eaton myasthenic syndrome. One patient had antibodies directed against presynaptic calcium channels, confirming the diagnosis. The second patient was seronegative for these antibodies but had elevated titers of antistriated muscle antibodies. This shows that serologic studies can conflict with clinical and electrodiagnostic findings in patients with Lambert-Eaton syndrome. These cases also point out that acetylcholine receptor antibodies are not necessarily diagnostic of myasthenia gravis in patients with Lambert-Eaton syndrome. Instead, these antibodies could represent a nonpathogenic epiphenomenon.

Inclusion body myositis: clinical and pathological boundaries.

Inclusion body myositis, polymyositis, and dermatomyositis are three distinct categories of inflammatory myopathy. Some authorities commented on the selective early weakness of the volar forearm muscles, quadriceps, and ankle dorsiflexors in inclusion body myositis. The most important feature distinguishing inclusion body myositis from the other two inflammatory myopathies is the lack of responsiveness to immunosuppressive treatment. Although most patients with inclusion body myositis have characteristic muscle biopsy findings, some cannot be distinguished histologically early from polymyositis. Predicting responsiveness to immunosuppressive medications, independent of muscle histology, would be valuable to clinicians. We retrospectively reviewed the pattern of weakness and other clinical features of 46 patients newly diagnosed with either inclusion body myositis, polymyositis, or dermatomyositis. Asymmetrical muscle weakness with prominent wrist flexor, finger flexor, and knee extensor involvement was specific for inclusion body myositis and unresponsive polymyositis. Male sex, lower creatine kinase levels, slower rate of progression, and peripheral neuropathy were also more common in inclusion body myositis and unresponsive polymyositis than in responsive polymyositis and dermatomyositis patients. Repeat muscle biopsy in 2 patients in the unresponsive polymyositis group demonstrated histological features of inclusion body myositis. We suspect that patients with clinical features of inclusion body myositis but lacking histological confirmation may nonetheless have inclusion body myositis. Our study supports the recently proposed criteria for definite and possible inclusion body myositis.

Denervated human skeletal muscle: MR imaging evaluation.

Because determination of neurologic integrity after severe limb trauma is crucial in patient care, the authors assessed magnetic resonance (MR) imaging as a tool to map denervated motor units of skeletal muscle in patients with traumatic peripheral neuropathy. Denervation was confirmed in 22 patients with use of electromyography, surgery, or both. MR imaging was performed with moderately T1- and T2-weighted spin-echo and short-tau inversion-recovery (STIR) sequences. MR imaging was unreliable in depicting acute denervation. Muscles of patients with subacute denervation had prolonged T1 and T2, which contributed to conspicuous hyperintensity on STIR images. Chronically denervated muscles showed marked atrophy, variable changes on STIR images, and conspicuous fatty infiltration on T1-weighted images. Normal variants in motor unit anatomy were seen in denervated muscle volumes outside the expected distribution of the injured nerve. MR imaging is promising for the noninvasive mapping and monitoring of denervated muscle in subacute and chronic phases of peripheral neuropathy.

MRI-guided biopsy in inflammatory myopathy: initial results.

The purpose of this report is to describe our initial experience with techniques employing magnetic resonance imaging (MRI) to guide the choice of muscle to be biopsied in patients suspected of having inflammatory myopathy. Five patients with a clinical diagnosis of inflammatory myopathy (IM) were studied. Four were imaged prior to biopsy. Four had repeated examinations, either immediately following biopsy or to evaluate disease progression. Use of MRI to localize muscle lesions was associated with abnormal pathologic findings in all cases, including histopathologic demonstration of lymphocyte infiltration in three cases of idiopathic polymyositis; nonspecific myopathic changes were seen in one patient with probable dermatomyositis and in one patient with chronic inflammatory polyneuropathy and high serum creatine kinase levels (> 45,000 IU/ml). The precise location of the area sampled by biopsy was visible in only one of four postbiopsy images. MRI shows promise in identifying pathologic muscle in patients suspected of having one of the inflammatory myopathies; however, further refinement of localization techniques may be needed to optimize histopathologic diagnoses.