Publications by authors named "Kevin Novak"

Quantitative electroencephalography (qEEG) has been suggested as a biomarker for cognitive decline in Parkinson's disease (PD). Determine if applying a wavelet-based qEEG algorithm to 21-electrode, resting-state EEG recordings obtained in a routine clinical setting has utility for predicting cognitive impairment in PD. PD subjects, evaluated by disease stage and motor score, were compared to healthy controls ( = 20 each).

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Background: The objective of this study was to examine whether an exercise program and standardized operating room positioning protocol (EOPP) would improve surgeon muscle workload and/or surgeon perception of mental/physical workload for nipple-sparing mastectomy (NSM).

Methods: This prospective study analyzed muscle workload by EMG of four surgeons performing NSM before and after an EOPP. Surveys were administered assessing surgeon perception of mental/physical workload.

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In addition to the hallmark muscle stiffness, patients with recessive myotonia congenita (Becker disease) experience debilitating bouts of transient weakness that remain poorly understood despite years of study. We performed intracellular recordings from muscle of both genetic and pharmacologic mouse models of Becker disease to identify the mechanism underlying transient weakness. Our recordings reveal transient depolarizations (plateau potentials) of the membrane potential to -25 to -35 mV in the genetic and pharmacologic models of Becker disease.

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Objective: Myotonia is caused by involuntary firing of skeletal muscle action potentials and causes debilitating stiffness. Current treatments are insufficiently efficacious and associated with side effects. Myotonia can be triggered by voluntary movement (electrically induced myotonia) or percussion (mechanically induced myotonia).

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Background: Pharmacists' role in addressing the opioid crisis continues to expand, but lack of training specifically related to standardized prescription drug monitoring program (PDMP) use and communication strategies for provider and patient interactions remains a significant issue. We developed the Resources Encouraging Safe Prescription Opioid and Naloxone Dispensing (RESPOND) Toolkit to enhance community pharmacists' understanding of their role in addressing opioid safety; improve integration of PDMP into daily workflow; and enhance communication between pharmacists, prescribers, and patients.

Objective: To describe the development of RESPOND Toolkit and summarize findings from initial pilot testing.

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Objective: Pharmacists are well positioned to reduce risks from opioid-prescribing but often lack resources and training to effectively support these activities. The Resources Encouraging Safe Prescription Opioid and Naloxone Dispensing (RESPOND) Toolkit is an educational package developed to provide community pharmacists with a comprehensive education program and practice resources on prescription drug misuse, prescription drug monitoring programs (PDMPs), and naloxone dispensing. Our objective was to evaluate the effectiveness of the RESPOND Toolkit to improve pharmacists' knowledge and assess changes in pharmacists' attitudes and beliefs toward opioid use disorder (OUD) and PDMPs across a diverse pool of Oregon community pharmacists.

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Background: Nipple-sparing mastectomies (NSMs) with reconstruction are believed to be more difficult to perform than skin-sparing mastectomies (SSMs), but there is little quantitative data to support this claim.

Methods: This prospective study analyzed four surgeons performing mastectomies. Electromyography (EMG) electrodes placed on selected muscle groups on each surgeon were used to capture muscle exertion intraoperatively and a percentage of maximum voluntary exertion was calculated (%MVE).

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Objective: Many states have begun implementing enhancements to PDMP patient profiles such as summaries or graphics to highlight issues of concern and enhance comprehension. The purpose of this study was to examine how physicians respond to sample enhanced PDMP profiles based on patient vignettes.

Design: Brief semistructured interviews with physicians.

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Objective: While literature on pharmacists' engagement with prescription drug monitoring programs (PDMPs) is growing, no formal synthesis of findings has been conducted to provide overarching recommendations for research or practice. The objective of this study was to identify and synthesize findings from current literature on community pharmacists' attitudes toward, knowledge of, and registration and utilization behaviors regarding PDMPs.

Data Sources: Electronic databases (MEDLINE, PsychINFO, Cochrane Database of Systematic Reviews, Google Scholar, and the Brandeis University PDMP Center of Excellence) and reference lists from relevant manuscripts were searched for relevant English-language manuscripts.

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Objective: To determine open-label, pilot study whether ranolazine could improve signs and symptoms of myotonia and muscle stiffness in patients with myotonia congenita (MC).

Methods: Thirteen participants were assessed at baseline and 2, 4, and 5 weeks. Ranolazine was started after baseline assessment (500 mg twice daily), increased as tolerated after week 2 (1,000 mg twice daily), and maintained until week 4.

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Hypothesis: Internal jugular vein (IJV) compression before blast injury will lead to reduced risk of traumatic hearing injury following exposure to a blast injury.

Background: IJV compression and its effects on not only intracranial, but also intracochlear pressure may potentiate blast induced hearing injury, therefore, precluding its use as a prophylactic therapy for blast induced traumatic brain injury.

Methods: Twenty Sprague Dawley rats were exposed to a 17.

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Objective: Patients with myotonia congenita have muscle hyperexcitability due to loss-of-function mutations in the chloride channel in skeletal muscle, which causes spontaneous firing of muscle action potentials (myotonia), producing muscle stiffness. In patients, muscle stiffness lessens with exercise, a change known as the warmup phenomenon. Our goal was to identify the mechanism underlying warmup and to use this information to guide development of novel therapy.

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Background: Few studies have systematically investigated the association between PARKIN genotype and psychiatric co-morbidities of Parkison's disease (PD). PARKIN-associated PD is characterized by severe nigral dopaminergic neuronal loss, a finding that may have implications for behaviors rooted in dopaminergic circuits such as obsessive-compulsive symptoms (OCS).

Methods: The Schedule of Compulsions and Obsessions Patient Inventory (SCOPI) was administered to 104 patients with early-onset PD and 257 asymptomatic first-degree relatives.

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Importance: Data on the long-term cognitive outcomes of patients with PARKIN-associated Parkinson disease (PD) are unknown but may be useful when counseling these patients.

Objective: Among patients with early-onset PD of long duration, we assessed cognitive and motor performances, comparing homozygotes and compound heterozygotes who carry 2 PARKIN mutations with noncarriers.

Design, Setting, And Participants: Cross-sectional study of 44 participants at 17 different movement disorder centers who were in the Consortium on Risk for Early-Onset PD study with a duration of PD greater than the median duration (>14 years): 4 homozygotes and 17 compound heterozygotes (hereafter referred to as carriers) and 23 noncarriers.

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Background: During the acute phase of critical illness myopathy (CIM) there is inexcitability of skeletal muscle. In a rat model of CIM, muscle inexcitability is due to inactivation of sodium channels. A major contributor to this sodium channel inactivation is a hyperpolarized shift in the voltage dependence of sodium channel inactivation.

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The processes that trigger severe muscle atrophy and loss of myosin in critical illness myopathy (CIM) are poorly understood. It has been reported that muscle disuse alters Ca(2+) handling by the sarcoplasmic reticulum. Since inactivity is an important contributor to CIM, this finding raises the possibility that elevated levels of the proteins involved in Ca(2+) handling might contribute to development of CIM.

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The cognitive profile of early onset Parkinson's disease (EOPD) has not been clearly defined. Mutations in the parkin gene are the most common genetic risk factor for EOPD and may offer information about the neuropsychological pattern of performance in both symptomatic and asymptomatic mutation carriers. EOPD probands and their first-degree relatives who did not have Parkinson's disease (PD) were genotyped for mutations in the parkin gene and administered a comprehensive neuropsychological battery.

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Objective: To assess the frequency and clinical characteristics of carriers of previously identified mutations in 6 genes associated with early-onset Parkinson disease (PD) and provide empirical data that can be used to inform genetic counseling.

Design: Cross-sectional observational study.

Setting: Thirteen movement disorders centers.

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Background: Mutations in the parkin gene are the most common genetic cause of early-onset Parkinson disease (PD). Results from a multicenter study of patients with PD systematically sampled by age at onset have not been reported to date.

Objective: To determine risk factors associated with carrying parkin mutations.

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While little is known about risk factors for cognitive impairment in early onset Parkinson disease (EOPD), postmortem studies have shown an association between dementia with Lewy bodies (DLB) and glucocerebrosidase (GBA) mutation. We compared Mini-Mental State Examination (MMSE) performance and self-reported cognitive impairment in 699 EOPD participants genotyped for mutations in parkin (PRKN), leucine-rich repeat kinase-2 (LRRK2), and GBA. Logistic regression was used to assess the association between reported cognitive impairment and MMSE score, as well as between GBA group membership and self-reported impairment and MMSE.

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Objective: To determine the motor phenotype of LRRK2 G2019S mutation carriers. LRRK2 mutation carriers were previously reported to manifest the tremor dominant motor phenotype, which has been associated with slower motor progression and less cognitive impairment compared with the postural instability and gait difficulty (PIGD) phenotype.

Design: Cross-sectional observational study.

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Neuropathy and myopathy can cause weakness during critical illness. To determine whether reduced excitability of peripheral nerves, rather than degeneration, is the mechanism underlying acute neuropathy in critically ill patients, we prospectively followed patients during the acute phase of critical illness and early recovery and assessed nerve conduction. During the period of early recovery from critical illness, patients recovered from neuropathy within days.

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Background: Several subcortical structures have been targeted for surgical treatment of dystonia, including motor thalamus, internal segment of globus pallidus (GPi), and more recently, the subthalamic nucleus (STN). Deep brain stimulation of GPi is currently the preferred surgical treatment, but it is unclear if targeting other structures would yield better results. Patients who have already had a pallidotomy yet continue to experience dystonic symptoms may be limited in further treatment options.

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Deep brain stimulation is generally a safe and effective method of alleviating motor impairment in advanced-stage Parkinson's disease patients. However, adverse events of surgery have been noted, such as hemorrhage, infection, seizures, and device failure. In this report, we describe 2 cases of the unusual adverse event of ischemia associated with subthalamic nucleus stimulator implantation.

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