Publications by authors named "Crystal L MacLellan"

Few certainties exist regarding the optimal type, timing, or dosage of rehabilitation after stroke. Despite differing injury mechanisms and recovery patterns following ischemic and hemorrhagic stroke, most translational stroke research is conducted after ischemia. As we enter the era of personalized medicine, exploring subtype-specific treatment efficacy is essential to optimizing recovery.

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Objective: To evaluate the efficacy of upper cervical joint mobilization and/or manipulation on reducing pain and improving maximal mouth opening (MMO) and pressure pain thresholds (PPTs) in adults with temporomandibular joint (TMJ) dysfunction compared with sham or other intervention.

Data Sources: MEDLINE, CINAHL, EMBASE, and Cochrane Library from inception to June 3, 2022, were searched.

Study Selection: Eight randomized controlled trials with 437 participants evaluating manual therapy (MT) vs sham and MT vs other intervention were included.

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Background: Student-led clinics (SLCs) offer unique clinical placement experiences and address unmet community rehabilitation needs. There is growing evidence that SLCs provide high-quality experiential practice and adequate quality of patient care. The purpose of this study was to evaluate patient satisfaction with student-led care and students' perception of their learning experiences in a student-led physiotherapy clinic.

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Background: After hemiplegic stroke, people often rely on their unaffected limb to complete activities of daily living. A component of residual motor dysfunction involves learned suppression of movement, termed learned nonuse.

Objective: To date, no rodent stroke model of persistent learned nonuse has been described that can facilitate understanding of this phenomenon and test interventions to overcome it.

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Hypothermia is an effective neuroprotectant for cardiac arrest and perinatal ischemic injury. Hypothermia also improves outcome after traumatic brain injury and stroke. Although the ideal treatment parameters (duration, delay, and depth) are not fully delineated, prolonged cooling is usually more effective than shorter periods.

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The likelihood of translating therapeutic interventions for stroke rests on the quality of preclinical science. Given the limited success of putative treatments for ischemic stroke and the reasons put forth to explain it, we sought to determine whether such problems hamper progress for intracerebral hemorrhage (ICH). Approximately 10% to 20% of strokes result from an ICH, which results in considerable disability and high mortality.

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Background: Enriched rehabilitation (ER; environmental enrichment plus skilled reaching) improves recovery after middle cerebral artery occlusion (MCAo) in rats. Fundamental issues such as whether ER is effective in other models, optimal rehabilitation intensity, and underlying recovery mechanisms have not been fully assessed.

Objective: The authors tested whether the efficacy of ER varies with ischemia model and assessed the importance of rehabilitation intensity and brain-derived neurotrophic factor (BDNF) in recovery.

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Background: Rehabilitation improves recovery after intracerebral hemorrhage (ICH) caused by collagenase infusion into the striatum of rats by promoting dendritic growth and reducing brain injury in this model.

Objective: Effective preclinical testing requires multiple models because none, including the collagenase model, perfectly mimics human ICH. Thus, the authors assessed enhanced rehabilitation (ER), a combination of environmental enrichment and task-specific motor training, on skilled reaching, lesion size, and dendritic plasticity after whole blood-induced, striatal ICH.

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The collagenase and whole blood intracerebral hemorrhage (ICH) models are widely used to identify mechanisms of injury and to evaluate treatments. Despite preclinical successes, to date, no treatment tested in phase III clinical trials has benefited ICH patients. These failures call into question the predictive value of current ICH models.

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The incidence of infection among stroke patients is alarmingly high and both acute and delayed infections increase morbidity and mortality. Experimental studies support the acute clinical data, but little attention has focused on delayed systemic infections. Here, we investigated the effects of prolonged systemic inflammation either before or 24-h after ischemia.

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Stroke and traumatic brain injuries often lead to cerebral edema and persistent elevations in intracranial pressure (ICP) that can be life threatening. Thus, rodent models would benefit from a simple and reliable method to measure ICP in awake, mobile animals. Up to now most techniques have been limited to anesthetized or immobile animals, which is not practical for following the prolonged elevations in ICP that follow stroke and traumatic brain injury.

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Therapeutic (induced) hypothermia (TH) has been extensively studied as a means to reduce brain injury following global and focal cerebral ischemia, intracerebral hemorrhage (ICH), and subarachnoid hemorrhage (SAH). Here, we briefly review the clinical and experimental evidence supporting the use of TH in each condition. We emphasize the importance of systematically evaluating treatment parameters, especially the duration of cooling, in each condition.

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Background And Purpose: Brain-derived neurotrophic factor (BDNF) is involved in neuronal survival, synaptic plasticity, learning and memory, and neuroplasticity. Further, exogenous treatment with BDNF or exposing animals to enrichment and exercise regimens, which also increase BDNF, enhances behavioral recovery after brain injury. Thus, the beneficial effects of rehabilitation in promoting recovery after stroke may also depend on BDNF.

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Preclinical studies must rigorously assess whether putative therapies improve motor and cognitive function following brain injury. Intracerebral hemorrhage (ICH) causes significant sensory-motor and cognitive deficits in humans. However, no study has evaluated cognition in rodent ICH models.

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The potential for using stem cells to treat stroke has garnered much interest, but stem cell therapies must be rigorously tested in animal models before transplantation studies progress to clinical trials. An enriched environment enhances transplanted subventricular zone (SVZ) cell migration and functional benefit following stroke in rats. However, the ability of SVZ cells to survive, migrate, differentiate and promote functional recovery at protracted survival times (e.

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Many therapies have shown promise in preclinical stroke studies, but few benefit patients. A greater understanding of stroke pathophysiology is needed to successfully develop therapies, and this depends on appropriate animal models. The collagenase and blood infusion models of intracerebral hemorrhage (ICH) are widely used; yet, investigators often prefer using one model for a variety of reasons.

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The infusion of autologous blood into the brain of rats is a widely used model of intracerebral hemorrhage (ICH). Careful assessment of functional recovery is an essential part of preclinical testing (e.g.

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Background And Purpose: Late hypothermia (HYPO) reduces injury after collagenase-induced intracerebral hemorrhage (ICH), whereas early HYPO does not because it exacerbates the protracted bleeding that occurs in this model. We hypothesized that early HYPO would not increase bleeding after whole blood infusion and thus expected early HYPO to improve outcome through reducing secondary consequences of ICH (eg, inflammation).

Methods: Autologous blood (100 microL) was infused into the striatum.

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Successful clinical translation of prospective cytoprotectants will likely occur only with treatments that improve functional recovery in preclinical (rodent) studies. Despite this assumption, many rely solely on histopathologic end points or the use of one or two simple behavioral tests. Presently, we used a battery of tests to gauge recovery after a unilateral intracerebral hemorrhagic stroke (ICH) targeting the striatum.

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Hyperthermia worsens outcome in clinical and experimental studies of ischemic stroke. Thus, we tested whether hyperthermia aggravates intracerebral hemorrhage (ICH) in rats. A striatal hemorrhage was produced via an infusion of bacterial collagenase.

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The hippocampal CA1 sector is especially vulnerable to brief forebrain ischemia. Excitotoxicity is widely thought to contribute to this cell death. Accordingly, drugs that presumably counteract excitotoxicity, such as GABAergic agonists, have been repeatedly tested and found to reduce CA1 cell loss.

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Prolonged hypothermia reduces ischemic brain injury, but its efficacy after intracerebral hemorrhagic (ICH) stroke is unresolved. Rats were implanted with core temperature telemetry probes and subsequently subjected to an ICH, which was produced by infusing bacterial collagenase into the striatum. Animals were kept normothermic (NORMO), or were made mildly hypothermic (33-35 degrees C) for over 2 days starting 1 hour (HYP-1), 6 hours (HYP-6), or 12 hours (HYP-12) after collagenase infusion.

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Background: Inadequate preclinical testing (e.g., rodent studies) has been partly blamed for the failure of many cytoprotectants to effectively treat stroke in humans.

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