Subscapularis Myotendinous Junction Tears Presenting with Posterior Shoulder Pain in Overhead Throwing Athletes.

Objective: Acute inferior subscapularis myotendinous junction injuries are occasionally seen in overhead throwing athletes, and can present with posterior shoulder pain.

Case Reports: Four professional baseball pitchers presented with acute onset of posterior shoulder pain while pitching. After thorough, routine physical examination of the shoulder by the referring orthopaedic surgeon magnetic resonance imaging (MRI) was performed within 7-10 days of the onset of presenting symptoms and interpreted in consensus by 2 fellowshiptrained musculoskeletal radiologists with 9 and 5 years of experience and a musculoskeletal radiology fellow.

Cognitive dysfunction and physical activity after stroke: the Gothenburg cognitive stroke study in the elderly.

This study explored the association between cognitive and executive dysfunction and level of physical activity 1 year after stroke. Cognition before stroke and cognitive and executive function in the acute phase and at 1 year after stroke were assessed in 74 subjects. Physical activity was assessed at 1 year after stroke.

Cognitive function and improvement of balance after stroke in elderly people: the Gothenburg cognitive stroke study in the elderly.

Purpose: The ability to balance is no longer automatic after stroke in patients with motor impairment and needs to be relearned. Learning requires cognitive and executive abilities. It is well known that cognitive and executive impairments are common after stroke, but how these are related to balance has not yet been fully studied.

High frequency of cognitive dysfunction before stroke among older people.

Objectives: We examined cognitive functions before and in acute phase of stroke studying frequency and profile of cognitive impairment and relationships between cognitive status.

Methods: Seventy-four patients with early phase after stroke and 49 healthy controls were included and examined using the Mini-Mental State Examination (MMSE) and a battery of neuropsychological tests. Cognitive status before stroke-onset was investigated using Cognitive Impairment Questionnaire.

Recovery in personal care related to cognitive impairment before and after stroke - a 1-year follow-up.

Objective: To examine whether there were any differences in the recovery in performance of personal activities of daily living (P-ADL) in elderly persons in relation to cognitive impairments pre- and post-stroke from discharge to 6 and 12 months in elderly persons.

Methods: Forty-five elderly persons after stroke were assessed at discharge from hospital and at 6 and at 12 months after stroke onset. A questionnaire posed to the next of kin was used to evaluate the person's pre- and post-stroke cognitive status.

Influence of cognition on personal activities of daily living (P-ADL) in the acute phase: the Gothenburg Cognitive Stroke Study in Elderly.

This study examines how prestroke dementia and cognitive dysfunction after stroke influence the personal activities of daily living (P-ADL) in elderly patients in the acute phase after stroke. Elderly stroke patients (n=60) referred to geriatric rehabilitation were included. Assessments were carried out at admission and evaluated at discharge from the geriatric ward.

Expression of basic fibroblast growth factor mRNA and protein in the human brain following ischaemic stroke.

Our previous work has demonstrated that angiogenesis occurs in the damaged brain tissue of patients surviving acute ischaemic stroke and increased microvessel density in the penumbra is associated with longer patient survival. The brain is one of the richest sources of FGF-2 and several studies have noted its angiogenic and neuroprotective effects in the nervous system. These findings led us to investigate the expression and localisation of both FGF-2 mRNA and protein in brain tissue collected within 12 h of death from 10 patients who survived for between 24 h and 43 days after acute stroke caused by thrombosis or embolus.

Increased intrathecal inflammatory activity in frontotemporal dementia: pathophysiological implications.

Objective: Immunological mechanisms may be part of the pathophysiological mechanisms in frontotemporal dementia (FTD), but hitherto only vague evidence of such mechanisms has been presented. The aim of this study was to compare the cerebrospinal fluid (CSF) levels of the pro-inflammatory cytokines interleukin (IL)-1beta and tumour necrosis factor (TNF)-alpha, and the anti-inflammatory cytokine transforming growth factor (TGF)-beta in patients with FTD and normal controls. Furthermore, serum levels of TNF-alpha, TGF-beta, and IL-1beta were measured in FTD patients.

Cytokines in dementias.

Knowledge regarding putative inflammatory component(s) participating in Alzheimer's disease (AD) and in vascular dementia (VAD) remains scarce. Recently, we have demonstrated the presence of inflammatory components, such as cytokines, in the CSF of demented patients. Although the initial events triggering the neurodegenerative processes in AD versus VAD may be different and thus lead to different neuropathological outcome, they may initiate a similar cascade of cytokine production in response to neuronal injury.

Intrathecal inflammation precedes development of Alzheimer's disease.

Objectives: To analyse the cerebrospinal fluid (CSF) values of the proinflammatory cytokines, interleukin 1beta (IL1beta), tumour necrosis factor alpha (TNFalpha), GM-CSF, of the anti-inflammatory cytokine TGFbeta, of tau protein, a marker for neurodegeneration, and of beta amyloid (Abeta), a protein involved in the formation of senile plaques, in prospectively followed up patients with mild cognitive impairment (MCI).

Methods: Analyses of CSF levels of TNFalpha, IL1beta, GM-CSF, TGFbeta, betaa, and tau protein were performed using ELISA in 56 patients with MCI who were followed up prospectively and in 25 age matched, healthy controls.

Results: Patients with MCI displayed significantly higher levels of TNFalpha and tau protein and significantly lower levels of TGFbeta and Abeta compared with the healthy controls.

Cerebral pattern of pro- and anti-inflammatory cytokines in dementias.

The knowledge regarding putative inflammatory component(s) participating in Alzheimer's disease (AD) and vascular dementia (VAD) is scarce. Recently, we have demonstrated the presence of certain inflammatory cytokines in the cerebrospinal fluid (CSF) of demented patients. Although the initial event(s) triggering the neurodegenerative processes in AD versus VAD may be different and lead to different neuropathological changes, it may initiate a similar cascade of cytokine production in response to neuronal injury.

Normal pressure hydrocephalus triggers intrathecal production of TNF-alpha.

Normal pressure hydrocephalus (NPH) is associated with periventricular white matter lesions and demyelination. The aim of the present study was to examine the cerebrospinal fluid (CSF) levels of tumor necrosis factor-alpha (TNF-alpha), a proinflammatory cytokine mediating myelin damage, in patients with NPH. TNF-alpha levels were analyzed by ELISA and measured before and after shunt operation in 35 patients with NPH.

Correlation between intrathecal sulfatide and TNF-alpha levels in patients with vascular dementia.

Objectives: Subcortical vascular dementia (SVD) is associated with white matter lesions and demyelination. The aim of the present study was to examine the cerebrospinal fluid (CSF) levels of TNF-alpha, a proinflammatory cytokine mediating myelin damage, in SVD patients. The intrathecal TNF-alpha levels were related to the clinical symptoms of dementia, as well as to intrathecal levels of sulfatide, a marker of white matter degradation, and of neurofilament, a marker of neuronal degeneration.

Cytokine response in cerebrospinal fluid from preterm infants with posthaemorrhagic ventricular dilatation.

Aim: Posthaemorrhagic ventricular dilatation (PHVD) is closely associated with white matter damage and neurological disability in the preterm infant. Proinflammatory cytokines have been implicated in the pathogenesis of white matter injury and subsequent cerebral palsy. The aim of this study was to determine the levels of proinflammatory cytokines in cerebrospinal fluid (CSF) from preterm infants with PHVD and to correlate the levels to white matter damage and neurodevelopmental outcome.

Increased intrathecal levels of the angiogenic factors VEGF and TGF-beta in Alzheimer's disease and vascular dementia.

The aim of the present study was to investigate, in patients with Alzheimer's disease (AD), and vascular dementia (VAD), patterns of local release of vascular endothelial growth factor (VEGF) and transforming growth factor-beta (TGF-beta), two cytokines having a pivotal role in hypoxia-induced angiogenesis. The intrathecal levels of these molecules were related to the clinical severity of these diseases and to the intrathecal levels of beta-amyloid protein. Significantly increased cerebrospinal fluid (CSF) levels of both VEGF and TGF-beta were observed in 20 patients with AD and in 26 patients with VAD compared to healthy controls.

Decreased levels of intrathecal interleukin 1 receptor antagonist in Alzheimer's disease.

A growing body of evidence points out the potential role of inflammatory mechanisms in the pathophysiology of brain damage in dementia. In previous studies, we have demonstrated intrathecal production of the proinflammatory cytokine tumor necrosis factor (TNF)alpha in patients with Alzheimer's disease (AD). The aim of the present study was to investigate the downstream products of TNF-alpha expression including interleukin (IL)1beta and its naturally occurring antagonist IL-1 receptor agonist (ra) in patients with AD.

Local and systemic GM-CSF increase in Alzheimer's disease and vascular dementia.

A growing body of evidence points out the potential role of inflammatory mechanisms in the pathophysiology of brain damage in dementia. The aim of the present study was to investigate patterns of local and systemic cytokine release in patients with Alzheimer's disease (AD) and vascular dementia (VAD). The intrathecal levels of cytokines were related to neuronal damage and cerebral apoptosis.

Intrathecal release of nitric oxide in Alzheimer's disease and vascular dementia.

A growing body of evidence points out the potential role of inflammatory mechanisms in the pathophysiology of brain damage in dementia. We have recently demonstrated that patients with Alzheimer's disease (AD) and vascular dementia (VaD) display an intrathecal production of proinflammatory cytokines. TNF-alpha, one of these cytokines, leads to the production of nitric oxide (NO), a potent inflammatory mediator, by induction of inducible NO synthase.

TNF gene polymorphism and its relation to intracerebral production of TNFalpha and TNFbeta in AD.

Objective: To analyze the extent of tumor necrosis factor-alpha (TNFalpha) and TNFbeta gene polymorphism in patients with AD and to relate it to intrathecal levels of these cytokines.

Methods: Analyses of TNFalpha and TNFbeta gene polymorphism were performed using PCR in 52 patients with AD and in 25 control subjects, and the levels of corresponding cytokines were analyzed using ELISA.

Results: Patients with AD displayed significantly higher intrathecal levels of TNFalpha, but not TNFbeta, compared with the control subjects.

Intrathecal release of nitric oxide and its relation to final brain damage in patients with stroke.

The potential role of inflammatory mechanisms in the pathophysiology of ischemic brain damage has intensely been discussed. We have recently demonstrated that stroke patients display an intrathecal production of proinflammatory cytokines early after onset of symptoms. IL-1beta, one of these cytokines, stimulates the production of nitric oxide (NO), a potent inflammatory mediator.

Intracerebral production of tumor necrosis factor-alpha, a local neuroprotective agent, in Alzheimer disease and vascular dementia.

The local pattern of proinflammatory cytokine release was studied in Alzheimer disease (AD) and vascular dementia (VAD), by measuring intrathecal levels of IL-1 beta, IL-6, TNF-alpha, and its naturally occurring antagonists, soluble TNF receptors I and II. The cytokine levels were related to neuronal damage, as measured by the intrathecal tau concentration, to cerebral apoptosis assessed by levels of Fas/APO-1 and bcl-2, and to clinical variables. In vitro analysis was performed to study the effect of TNF-alpha on the production of bcl-2, an antiapoptotic factor, by human neuronal cells.

Intrathecal expression of proteins regulating apoptosis in acute stroke.

Background And Purpose: The neuronal death that accompanies an ischemic stroke has previously been attributed to a necrotic process. However, numerous studies in experimental models of ischemia have recently indicated that programmed cell death, also called apoptosis, may contribute to neuronal death. The aim of the present study was to investigate the intrathecal levels of proteins regulating apoptosis in acute stroke and to relate these levels to brain damage and to production of proinflammatory and anti-inflammatory cytokines.

Cytokine response in cerebrospinal fluid after birth asphyxia.

Experimental studies suggest that cytokine-mediated inflammatory reactions are important in the cascade leading to hypoxic-ischemic brain injury. The purpose was to study the content of pro- and antiinflammatory cytokines in cerebrospinal fluid (CSF) of asphyxiated and control infants. Samples of CSF were obtained from 20 infants who fulfilled the criteria of birth asphyxia and from seven newborn control subjects.

Localization of the brain lesion affects the lateralization of T-lymphocyte dependent cutaneous inflammation. Evidence for an immunoregulatory role of the right frontal cortex-putamen region.

We have previously demonstrated that brain lesions caused by stroke led to the lateralization of T-cell dependent inflammation. The purpose of this study was to assess the impact of localization of the brain lesion on lateralization of immune responsiveness. The delayed-type hypersensitivity (DTH) reaction was used as an in vivo measure of antigen specific T-lymphocyte reactivity.

Intrathecal release of pro- and anti-inflammatory cytokines during stroke.

A growing body of evidence points out the potential role of inflammatory mechanisms in the pathophysiology of ischaemic brain damage. We have recently demonstrated that stroke patients display an intrathecal production of proinflammatory cytokines, such as IL-1beta and IL-6 already within the first 24 h after the beginning of symptoms (Tarkowski et al., 1995).