Sports-related peripheral nerve injuries of the upper limb.

Peripheral nerve injuries in athletes affect the upper limb more commonly than the lower limb. Common mechanisms include compression, traction, laceration, and ischemia. Specific sports can have unique mechanisms of injury and are more likely to be associated with certain neuropathies. Familiarity with these sport-specific variables and recognition of the common presentations of upper limb neuropathic syndromes are important in assessing an athlete with a suspected peripheral nerve injury. Evaluation may require imaging modalities and/or electrodiagnostic testing to confirm a nerve injury. In some cases, diagnostic injections may be needed to differentiate neuropathic versus musculoskeletal etiology. Early and accurate diagnosis is essential for treatment/management and increases the likelihood of a safe return-to-sport and avoidance of long-term functional consequences. Most nerve injuries can be treated conservatively, however, severe or persistent cases may require surgical intervention. This monograph reviews key diagnostic, management, and preventative strategies for sports-related peripheral nerve injuries involving the upper limb.

Stress Fractures of the Hip and Pelvis.

Stress fractures refer to overuse injuries of bone resulting from repetitive mechanical stress. Stress fractures of the hip and pelvic region, while relatively uncommon, have become increasingly recognized in certain populations, particularly long-distance runners and military recruits. The diagnosis of such injuries can be challenging, often hampered by a nonspecific physical examination and limited sensitivity of plain radiography. Early recognition is important to direct appropriate management, lessen time lost from sport, and avoid potential complications. The present article reviews the epidemiology, diagnosis, and management of bone stress injuries of the hip and pelvis, specifically the sacrum, pubic ramus, and femoral neck.

Medical and Musculoskeletal Concerns for the Wheelchair Athlete: A Review of Preventative Strategies.

Adaptive sports refers to organized sporting activities that are practiced by individuals with disabilities and are worthwhile to maintain physical and psychological health. As adaptive sports participation continues to rise, health care providers must have an enhanced understanding of injury and illness patterns specific to the adaptive athlete. Early recognition and prevention are important to ensure safe and successful participation in sport. The present review aims to provide a framework for diagnosis and prevention of common conditions specific to the wheelchair athlete. In particular, autonomic dysreflexia, impaired thermoregulation, urinary tract infection, and pressure injuries, as well as shoulder pain, upper-extremity entrapment neuropathies, and osteoporotic fractures will be discussed.

Design for Transtibial Modifiable Socket for Immediate Postoperative Prosthesis.

Amputations are long-standing surgical procedures that have been performed for centuries; however, very little attention and urgency have been given to immediate restoration of movement and return to a normal lifestyle. In many cases, the time between amputation and prosthetic fitting can pause recovery and development of new routines. To increase recovery, immediate postoperative prostheses (IPOPs) have been developed yet these are under-utilized because of concerns for wound healing and complications with vascular diseases. Subsequently, we designed a transtibial IPOP that utilizes an ergonomic modifiable socket that allows for examination, wound care, and in situ edema control. Additionally, the IPOP facilitates early weight bearing and protects the amputated limb from external trauma postoperatively. Our purpose is to introduce this technology and describe how its unique design will serve to provide potential benefits and positive effects on patients who have undergone amputations.

Effectiveness of conservative treatment for patellofemoral pain syndrome: A systematic review and meta-analysis.

OBJECTIVE: To evaluate the evidence regarding the effectiveness of conservative treatment in reducing patellofemoral pain. DATA SOURCES: CENTRAL, MEDLINE, CINAHL, and PEDro databases. STUDY SELECTION: Adults with patellofemoral pain, randomized controlled trials only, any conservative treatment compared with placebo, sham, other conservative treatment, or no treatment. Two independent reviewers. DATA EXTRACTION: Data were extracted from the full-text of the articles, based on Cochrane Collaboration recommendations. The outcome of interest was the difference between groups regarding change in pain severity. DATA SYNTHESIS: The majority of studies were underpowered. More than 80% of the 37 trials did not show a clinically significant benefit. Clinically significant effects of different sizes were found for 7 trials (6 studies out of 7 had short follow-ups). These effects were found for: (i) pulsed electromagnetic fields combined with home exercise -33.0 (95% CI -45.2 to -20.8); (ii) hip muscle strengthening -65.0 (95% CI -87.7 to -48.3) and -32.0 (-37.0 to -27.0); (iii) weight-bearing exercise -40.0 (95% CI -49.4 to -30.6); (iv) neuromuscular facilitation combined with aerobic exercise and stretching -60.1 (95% CI -66.9 to -54.5); (v) postural stabilization -24.4 (95% CI -33.5 to -15.3); and (vi) patellar bracing -31.6 (95% CI -35.2 to -28.0). CONCLUSION: There is no evidence that a single treat-ment modality works for all patients with patellofemoral pain. There is limited evidence that some treatment modalities may be beneficial for some subgroups of patients with patellofemoral pain.

Patellofemoral Pain.

Patellofemoral pain is characterized by insidious onset anterior knee pain that is exaggerated under conditions of increased patellofemoral joint stress. A variety of risk factors may contribute to the development of patellofemoral pain. It is critical that the history and physical examination elucidate those risk factors specific to an individual in order to prescribe an appropriate and customized treatment plan. This article aims to review the epidemiology, risk factors, diagnosis, and management of patellofemoral pain.

Update on rehabilitation of patellofemoral pain.

Patellofemoral pain syndrome (PFPS) is a multifactorial disorder with a variety of treatment options. The assortment of components that contribute to its pathophysiology can be categorized into local joint impairments, altered lower extremity biomechanics, and overuse. A detailed physical examination permits identification of the unique contributors for a given individual and permits the formation of a precise, customized treatment plan. This review aims to describe the latest evidence and recommendations regarding rehabilitation of PFPS. We address the utility of quadriceps strengthening, soft tissue flexibility, patellar taping, patellar bracing, hip strengthening, foot orthoses, gait reeducation, and training modification in the treatment of PFPS.

Cortical and hippocampal atrophy in patients with autosomal dominant familial Alzheimer's disease.

BACKGROUND: Both familial and sporadic Alzheimer's disease (AD) result in progressive cortical and subcortical atrophy. Familial autosomal dominant AD (FAD) allows us to study AD brain changes presymptomatically. METHODS: 33 subjects at risk for FAD (25 for PSEN1 and 8 for APP mutations; 22 mutation carriers and 11 controls) and 3 demented PSEN1 mutation carriers underwent T(1)-weighted MPRAGE 1.5T MRI. Using the hippocampal radial distance and cortical pattern matching techniques, we investigated the effects of carrier status and dementia diagnosis on cortical and hippocampal atrophy. All analyses were corrected for age and relative age (years to median age of disease onset in the family). RESULTS: The dementia cases had pronounced cortical atrophy in the lateral and medial parietal, posterior cingulate and frontal cortices and hippocampal atrophy bilaterally relative to both nondemented carriers and controls. Nondemented carriers did not show significant cortical thinning or hippocampal atrophy relative to controls. CONCLUSIONS: FAD is associated with thinning of the posterior association and frontal cortices and hippocampal atrophy. Larger sample sizes may be necessary to reliably identify cortical atrophy in presymptomatic carriers.

Mapping corpus callosum morphology in twin pairs discordant for bipolar disorder.

Callosal volume reduction has been observed in patients with bipolar disorder, but whether these deficits reflect genetic vulnerability to the illness remains unresolved. Here, we used computational methods to map corpus callosum abnormalities in a population-based sample of twin pairs discordant for bipolar disorder. Twenty-one probands with bipolar I disorder (mean age 44.4 ± 7.5 years; 48% female), 19 of their non-bipolar co-twins, and 34 demographically matched control twin individuals underwent magnetic resonance imaging. Three-dimensional callosal surface models were created to visualize its morphologic variability and to localize group differences. Neurocognitive correlates of callosal area differences were additionally investigated in a subsample of study participants. Bipolar (BPI) probands, but not their co-twins, showed significant callosal thinning and area reduction, most pronounced in the genu and splenium, relative to healthy twins. Altered callosal curvature was additionally observed in BPI probands. In bipolar probands and co-twins, genu and splenium midsagittal areas were significantly correlated with verbal processing speed and response inhibition. These findings suggest that aberrant connections between cortical regions--possibly reflecting decreased myelination of white matter tracts--may be involved in bipolar pathophysiology. However, findings of callosal thinning appear to be disease related, rather than reflecting genetic vulnerability to bipolar illness.

Three-dimensional surface maps link local atrophy and fast ripples in human epileptic hippocampus.

OBJECTIVES: There is compelling evidence that pathological high-frequency oscillations (HFOs), called fast ripples (FR, 150-500Hz), reflect abnormal synchronous neuronal discharges in areas responsible for seizure genesis in patients with mesial temporal lobe epilepsy (MTLE). It is hypothesized that morphological changes associated with hippocampal atrophy (HA) contribute to the generation of FR, yet there is limited evidence that hippocampal FR-generating sites correspond with local areas of atrophy. METHODS: Interictal HFOs were recorded from hippocampal microelectrodes in 10 patients with MTLE. Rates of FR and ripple discharge from each microelectrode were evaluated in relation to local measures of HA obtained using 3-dimensional magnetic resonance imaging (MRI) hippocampal modeling. RESULTS: Rates of FR discharge were 3 times higher in areas of significant local HA compared with rates in nonatrophic areas. Furthermore, FR occurrence correlated directly with the severity of damage in these local atrophic regions. In contrast, we found no difference in rates of ripple discharge between local atrophic and nonatrophic areas. INTERPRETATION: The proximity between local HA and microelectrode-recorded FR suggests that morphological changes such as neuron loss and synaptic reorganization may contribute to the generation of FR. Pathological HFOs, such as FR, may provide a reliable surrogate marker of abnormal neuronal excitability in hippocampal areas responsible for the generation of spontaneous seizures in patients with MTLE. Based on these data, it is possible that MRI-based measures of local HA could identify FR-generating regions, and thus provide a noninvasive means to localize epileptogenic regions in hippocampus.

Joint sulcal detection on cortical surfaces with graphical models and boosted priors.

In this paper, we propose an automated approach for the joint detection of major sulci on cortical surfaces. By representing sulci as nodes in a graphical model, we incorporate Markovian relations between sulci and formulate their detection as a maximum a posteriori (MAP) estimation problem over the joint space of major sulci. To make the inference tractable, a sample space with a finite number of candidate curves is automatically generated at each node based on the Hamilton-Jacobi skeleton of sulcal regions. Using the AdaBoost algorithm, we learn both individual and pairwise shape priors of sulcal curves from training data, which are then used to define potential functions in the graphical model based on the connection between AdaBoost and logistic regression. Finally belief propagation is used to perform the MAP inference and select the joint detection results from the sample spaces of candidate curves. In our experiments, we quantitatively validate our algorithm with manually traced curves and demonstrate the automatically detected curves can capture the main body of sulci very accurately. A comparison with independently detected results is also conducted to illustrate the advantage of the joint detection approach.

Semi-automated method for delineation of landmarks on models of the cerebral cortex.

Sulcal and gyral landmarks on the human cerebral cortex are required for various studies of the human brain. Whether used directly to examine sulcal geometry, or indirectly to drive cortical surface registration methods, the accuracy of these landmarks is essential. While several methods have been developed to automatically identify sulci and gyri, their accuracy may be insufficient for certain neuroanatomical studies. We describe a semi-automated procedure that delineates a sulcus or gyrus given a limited number of user-selected points. The method uses a graph theory approach to identify the lowest-cost path between the points, where the cost is a combination of local curvature features and the distance between vertices on the surface representation. We implemented the algorithm in an interface that guides the user through a cortical surface delineation protocol, and we incorporated this tool into our BrainSuite software. We performed a study to compare the results produced using our method with results produced using Display, a popular tool that has been used extensively for manual delineation of sulcal landmarks. Six raters were trained on the delineation protocol. They performed delineations on 12 brains using both software packages. We performed a statistical analysis of 3 aspects of the delineation task: time required to delineate the surface, registration accuracy achieved compared to an expert-delineated gold-standard, and variation among raters. Our new method was shown to be faster to use, to provide reduced inter-rater variability, and to provide results that were at least as accurate as those produced using Display.

Alterations in midline cortical thickness and gyrification patterns mapped in children with 22q11.2 deletions.

The 22q11.2 deletion syndrome (velocardiofacial/DiGeorge syndrome) is a neurogenetic condition associated with visuospatial deficits, as well as elevated rates of attentional disturbance, mood disorder, and psychosis. Previously, we detected pronounced cortical thinning in superior parietal and right parieto-occipital cortices in patients with this syndrome, regions critical for visuospatial processing. Here we applied cortical pattern-matching algorithms to structural magnetic resonance images obtained from 21 children with confirmed 22q11.2 deletions (ages 8-17) and 13 demographically matched comparison subjects, in order to map cortical thickness across the medial hemispheric surfaces. In addition, cortical models were remeshed in frequency space to compute their surface complexity. Cortical maps revealed a pattern of localized thinning in the ventromedial occipital-temporal cortex, critical for visuospatial representation, and the anterior cingulate, a key area for attentional control. However, children with 22q11.2DS showed significantly increased gyral complexity bilaterally in occipital cortex. Regional gray matter volumes, particularly in medial frontal cortex, were strongly correlated with both verbal and nonverbal cognitive functions. These findings suggest that aberrant parieto-occipital brain development, as evidenced by both increased complexity and cortical thinning in these regions, may be a neural substrate for the deficits in visuospatial and numerical understanding characteristic of this syndrome.

Three-dimensional hippocampal atrophy maps distinguish two common temporal lobe seizure-onset patterns.

PURPOSE: Current evidence suggests that the mechanisms underlying depth electrode-recorded seizures beginning with hypersynchronous (HYP) onset patterns are functionally distinct from those giving rise to low-voltage fast (LVF) onset seizures. However, both groups have been associated with hippocampal atrophy (HA), indicating a need to clarify the anatomic correlates of each ictal onset type. We used three-dimensional (3D) hippocampal mapping to quantify HA and determine whether each onset group exhibited a unique distribution of atrophy consistent with the functional differences that distinguish the two onset morphologies. METHODS: Sixteen nonconsecutive patients with medically refractory epilepsy were assigned to HYP or LVF groups according to ictal onset patterns recorded with intracranial depth electrodes. Using preimplant magnetic resonance imaging (MRI), levels of volumetrically defined HA were determined by comparison with matched controls, and the distribution of local atrophy was mapped onto 3D hippocampal surface models. RESULTS: HYP and LVF groups exhibited significant and equivalent levels of HA ipsilateral to seizure onset. Patients with LVF onset seizures also showed significant contralateral volume reductions. On ipsilateral contour maps HYP patients exhibited an atrophy pattern consistent with classical hippocampal sclerosis (HS), whereas LVF atrophy was distributed more laterally and diffusely. Contralateral LVF maps also showed regions of subicular atrophy. DISCUSSION: The HS-like distribution of atrophy and the restriction of HA to the ipsilateral hippocampus in HYP patients are consistent with focal hippocampal onsets, and suggest a mechanism utilizing intrahippocampal circuitry. In contrast, the bilateral distribution of nonspecific atrophy in the LVF group may reflect mechanisms involving both hippocampal and extrahippocampal networks.

Mapping cerebellar degeneration in HIV/AIDS.

Progressive brain atrophy in HIV/AIDS is associated with impaired psychomotor performance, perhaps partly reflecting cerebellar degeneration; yet little is known about how HIV/AIDS affects the cerebellum. We visualized the three-dimensional profile of atrophy in 19 HIV-positive patients (age: 42.9+/-8.3 years) versus 15 healthy controls (age: 38.5+/-12.0 years). We localized consistent patterns of subregional atrophy with an image analysis method that automatically deforms each patient's scan, in three dimensions, to match a reference image. Atrophy was greatest in the posterior cerebellar vermis (14.9% deficit) and correlated with depression severity (P=0.009, corrected), but not with dementia, alcohol/substance abuse, CD4+T-cell counts, or viral load. Profound cerebellar deficits in HIV/AIDS (P=0.007, corrected) were associated with depression, suggesting a surrogate disease marker for antiretroviral trials.

Three-dimensional mapping of hippocampal anatomy in unmedicated and lithium-treated patients with bipolar disorder.

Declarative memory impairments are common in patients with bipolar illness, suggesting underlying hippocampal pathology. However, hippocampal volume deficits are rarely observed in bipolar disorder. Here we used surface-based anatomic mapping to examine hippocampal anatomy in bipolar patients treated with lithium relative to matched control subjects and unmedicated patients with bipolar disorder. High-resolution brain magnetic resonance images were acquired from 33 patients with bipolar disorder (21 treated with lithium and 12 unmedicated), and 62 demographically matched healthy control subjects. Three-dimensional parametric mesh models were created from manual tracings of the hippocampal formation. Total hippocampal volume was significantly larger in lithium-treated bipolar patients compared with healthy controls (by 10.3%; p=0.001) and unmedicated bipolar patients (by 13.9%; p=0.003). Statistical mapping results, confirmed by permutation testing, revealed localized deficits in the right hippocampus, in regions corresponding primarily to cornu ammonis 1 subfields, in unmedicated bipolar patients, as compared to both normal controls (p=0.01), and in lithium-treated bipolar patients (p=0.03). These findings demonstrate the sensitivity of these anatomic mapping methods for detecting subtle alterations in hippocampal structure in bipolar disorder. The observed reduction in subregions of the hippocampus in unmedicated bipolar patients suggests a possible neural correlate for memory deficits frequently reported in this illness. Moreover, increased hippocampal volume in lithium-treated bipolar patients may reflect postulated neurotrophic effects of this agent, a possibility warranting further study in longitudinal investigations.

3D mapping of language networks in clinical and pre-clinical Alzheimer's disease.

We investigated the associations between Boston naming and the animal fluency tests and cortical atrophy in 19 probable AD and 5 multiple domain amnestic mild cognitive impairment patients who later converted to AD. We applied a surface-based computational anatomy technique to MRI scans of the brain and then used linear regression models to detect associations between animal fluency and Boston Naming Test (BNT) performance and cortical atrophy. The global permutation-corrected significance for the maps associating BNT performance with cortical atrophy was p=.0124 for the left and p=.0196 for the right hemisphere and for the animal fluency maps p=.055 for the left and p=.073 for the right hemisphere. The degree of language impairment correlated with cortical atrophy in the left temporal and parietal lobes (BA 20, 21, 37, 39, 40, and 7), bilateral frontal lobes (BA 8, 9, and 44) and the right temporal pole (BA 38). Using a novel 3D mapping technique, we demonstrated that in AD language abilities are strongly influenced by the integrity of the perisylvian cortical regions.

Three-dimensional gray matter atrophy mapping in mild cognitive impairment and mild Alzheimer disease.

BACKGROUND: Alzheimer disease (AD) is the most common form of dementia worldwide. Mild cognitive impairment (MCI) is the recent terminology for patients with cognitive deficiencies in the absence of functional decline. Most patients with MCI harbor the pathologic changes of AD and demonstrate transition to dementia at a rate of 10% to 15% per year. Patients with AD and MCI experience progressive brain atrophy. OBJECTIVE: To analyze the structural magnetic resonance imaging data for 24 patients with amnestic MCI and 25 patients with mild AD using an advanced 3-dimensional cortical mapping technique. DESIGN: Cross-sectional cohort design. Patients/ METHODS: We analyzed the structural magnetic resonance imaging data of 24 amnestic MCI (mean MMSE, 28.1; SD, 1.7) and 25 mild AD patients (all MMSE scores, >18; mean MMSE, 23.7; SD, 2.9) using an advanced 3-dimensional cortical mapping technique. RESULTS: We observed significantly greater cortical atrophy in patients with mild AD. The entorhinal cortex, right more than left lateral temporal cortex, right parietal cortex, and bilateral precuneus showed 15% more atrophy and the remainder of the cortex primarily exhibited 10% to 15% more atrophy in patients with mild AD than in patients with amnestic MCI. CONCLUSION: There are striking cortical differences between mild AD and the immediately preceding cognitive state of amnestic MCI. Cortical areas affected earlier in the disease process are more severely affected than those that are affected late. Our method may prove to be a reliable in vivo disease-tracking technique that can also be used for evaluating disease-modifying therapies in the future.

Joint sulci detection using graphical models and boosted priors.

In this paper we propose an automated approach for joint sulci detection on cortical surfaces by using graphical models and boosting techniques to incorporate shape priors of major sulci and their Markovian relations. For each sulcus, we represent it as a node in the graphical model and associate it with a sample space of candidate curves, which is generated automatically using the Hamilton-Jacobi skeleton of sulcal regions. To take into account individual as well as joint priors about the shape of major sulci, we learn the potential functions of the graphical model using AdaBoost algorithm to select and fuse information from a large set of features. This discriminative approach is especially powerful in capturing the neighboring relations between sulcal lines, which are otherwise hard to be captured by generative models. Using belief propagation, efficient inferencing is then performed on the graphical model to estimate each sulcus as the maximizer of its final belief. On a data set of 40 cortical surfaces, we demonstrate the advantage of joint detection on four major sulci: central, precentral, postcentral and the sylvian fissure.

Structural correlates of apathy in Alzheimer's disease.

BACKGROUND: Apathy is the most common noncognitive symptom in Alzheimer's disease (AD). The structural correlates of apathy in AD have not yet been described. METHODS: We analyzed magnetic resonance imaging data of 35 AD patients with and without apathy. RESULTS: There was a significant linear association between apathy severity and cortical gray matter atrophy in the bilateral anterior cingulate [Brodmann area (BA) 24; r = 0.39-0.42, p = 0.01] and left medial frontal cortex (BA 8 and 9; r = 0.4, p < 0.02). Left mean cingulate cortical thinning predicted the presence/absence of apathy at the trend level of significance. CONCLUSION: Our study demonstrates a strong association between apathy and the integrity of medial frontal regions in AD.