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Biomedical subjects

Roger E Kelley

Publications and source records attributed to Roger E Kelley.

At least 19 recordsLinked to original sources
PubMed2006

Neuroimaging findings in neurosyphilis.

We report two cases of neurosyphilis with atypical clinical presentations that were compounded by atypical neuroimaging findings. In the first case, MRI brain scan findings were felt to be compatible with mesial temporal sclerosis or herpes simplex encephalitis. The second patient presented with a clinical picture compatible with normal pressure hydrocephalus as well as some degree of ventricular enlargement and prominent periventricular white matter changes by MRI brain scan. He actually underwent ventriculo-peritoneal shunting prior to determination that he had active syphilitic involvement of the central nervous system. Neurosyphilis, "the great imitator," is not only capable of mimicking various other neurological disease clinical presentations, it can also mimic neuroimaging features of various other disease processes as well.

Adult↗
PubMed2006

Role of magnetic resonance spectroscopy in diagnosis and management of multiple sclerosis.

Application of magnetic resonance spectroscopy (MRS) to study the nature, pathogenesis, tissue injury and therapeutic response of MS patients has altered our view of multiple sclerosis (MS) fundamentally. By offering biochemical analysis of demyelinating lesions and axonal injury, MRS generates objective and quantifiable data on central nervous system tissue and metabolism during pathogenesis of MS. Of these biochemical markers, N-acetylaspartate, which serves as an indicator of neuronal and axonal injury and choline (Cho) peaks which demonstrate cell membrane metabolism, provide a plethora of data on the neuropathology of MS. Based on these findings, MRS provides neuroscientists with a unique diagnostic and prognostic tool to follow MS patients and assess their response to treatment with immunomodulators. MRS findings are so significant that consideration should be given to their routine inclusion as secondary outcome measures in clinical trials of MS patients.

Animals↗
PubMed2006

Neurosurgical treatment of multiple sclerosis.

OBJECTIVES: To describe the role of neurosurgical techniques in treatment of symptoms of multiple sclerosis (MS). METHODS: A review of the existing world literature searching (using PubMed, August 22, 2005) for key words 'multiple sclerosis' and multiple symptoms associated with MS including trigeminal neuralgia, pain (pump and rhizotomy), spasticity, intrathecal pump, hydrocephalus and stimulation (brain and spinal). RESULTS: In total, 1,404 articles met selection criteria. These were narrowed based upon uniqueness of technique described, nature of information provided and avoidance of redundancy. Further, the methods listed were classified into groups of cranial and spinal techniques. Indications, brief description of technique and outcome/side effects were noted for each technique. DISCUSSION: A vast, growing body of literature exists for various neurosurgical applications for MS treatment. Older techniques such as rhizolysis for neuralgia and rhizotomy for spasticity have been modified using stereotactic radiosurgery and deep brain stimulation, along with central nervous system stimulation and intrathecal pumps. Other applications continue to be found with varying degrees of success. CONCLUSIONS: Neurosurgical techniques, based upon proper selection criteria, can significantly improve MS-related symptoms with low procedure-associated risk and therefore can substantially improve patients' quality of life.

Deep Brain Stimulation↗
PubMed2006

Ischemic demyelination.

White matter lesions representing ischemic demyelination have evolved in terms of our understanding of their pathogenesis and potential clinical significance. Low density lesions on CT brain scan, most commonly seen in the periventricular region, also frequently seen in the centrum semiovale, have been termed 'leukoaraiosis'. In the past years, it was not uncommon at all to hear the term 'Binswanger's disease' used in an attempt to define the neurological sequelae of such lesions. Further refinement came with the advent of magnetic resonance imaging (MRI) brain scan which is particularly sensitive to such white matter areas of increased signal intensity, which tend to be seen particularly well on T2-weighted and fluid attenuation inversion recovery (FLAIR) scans. The major challenge has been to correlate the clinical attributes with such relatively frequent findings in the elderly population. Recent studies have looked at lesion load in a fashion analogous to that seen with multiple sclerosis. A particularly relevant clinical model for white matter disease is cerebral autosomal dominant arteriopathy with subcortical infarcts and leukoencephalopathy (CADASIL) which combines the potential components of small vessel disease, resulting in progressive neurological deficit, with a common association with migraine which can also be associated with white matter lesions. However, the most common pathogenic factor associated with the microangiopathy, which appears to be at the heart of ischemic demyelination, continues to be hypertension. How well we are able to tie in the various pathological mechanisms associated with this end organ damage of the brain will determine how well we can arrive at effective interventions for a common contributor to neurological deficits in the elderly.

Brain↗
PubMed2005

Soluble HLA measurement in saliva and cerebrospinal fluid in Caucasian patients with multiple sclerosis: a preliminary study.

BACKGROUND: Measurement of soluble HLA in body fluids has a potential role in assessing disease activity in autoimmune disorders. METHODS: We applied a solid phase, enzyme-linked immunoassay to measure soluble HLA class I (sHLA-I) and class II (sHLA-II) molecules in the saliva and cerebrospinal fluid (CSF) in 13 untreated patients with relapsing-remitting form of multiple sclerosis (MS). For comparison purposes, we also studied saliva from 53 healthy subjects. RESULTS: Saliva from normal controls had detectable sHLA-I levels in 41 of 53 individuals studied, with values ranging from 9-100 ng/ml (mean = 41 +/- 2.8 ng/ml). sHLA-I was undetectable in the saliva in 11 of 13 MS patients, and in none of the CSF specimens. In contrast, mean sHLA-II concentration in the saliva of MS patients was significantly increased compared to controls (386 +/- 52 unit/ml vs. 222 +/- 18.4 unit/ml, t = 8.68, P < 0.005). The mean CSF sHLA-II level (369 +/- 16 unit/ml) was equivalent to the mean sHLA-II concentration measured in saliva (mean = 386 +/- 52 unit/ml) (P = 0.7). In patients with brain magnetic resonance imaging (MRI) enhancing lesions (n = 5), reflective of more active disease, CSF sHLA-II averaged 356 +/- 26 unit/ml compared to 380 +/- 51 in saliva. Similarly, in patients with non-enhancing lesions (n = 8), CSF sHLA-II averaged 377 +/- 18 unit/ml compared to 390 +/- 77 unit/ml in saliva. Thus, the mean sHLA-II concentration in saliva and CSF was essentially equivalent for MS patients with or without enhancing plaques. CONCLUSION: Our data suggest that the measurement of soluble HLA in saliva, specifically sHLA-II, correlates with the level found in the CSF. Therefore, if sHLA correlates with disease activity in MS, as has been proposed, saliva measurements provide a noninvasive correlate of CSF measurement.

Journal Article↗
PubMed2005

Update on stroke prevention.

It is now well recognized that stroke-prone individual scan be identified in the majority of instances and that effective preventive therapy is available. Cumulative risk factors enhance the potential for stroke.The challenge is to effectively intervene to substantially reduce stroke risk.

Angioplasty, Balloon↗
PubMed2005

Stroke.

Explore the source record for details and available documents.

Brain↗
PubMed2005

Soluble HLA class I and class II molecules in relapsing-remitting multiple sclerosis: acute response to interferon-beta1a treatment and their use as markers of disease activity.

During relapses in relapsing-remitting multiple sclerosis (RRMS), serum soluble HLA class I surface antigen (sHLA-I) levels are reported to either decrease or remain unchanged, whereas serum sHLA-II levels increase. Interferon-beta1b therapy was recently reported to increase serum sHLA-I in RRMS. In the present prospective study, solid-phase enzyme-linked immunosorbent assay was used to measure sHLA-I and sHLA-II in the sera of 21 RRMS patients during a clinical exacerbation, and then six weeks after treatment with high-dose interferon-beta1a (IFN-beta1a). Pretreatment serum sHLA-I was significantly lower in patients than in normal controls (P < 0.0005). Pretreatment sHLA-II was also significantly lower than in normal controls (P = .003) unless enhancing MRI lesions (objectified relapse) were present; then sHLA-II levels were similar to normal controls (relative increase). Six weeks after initiation of IFN-beta1a treatment, a significant increase in serum sHLA-I was observed in all 21 RRMS patients (P < .0005). Conversely, serum sHLA-II decreased significantly after treatment in the entire patient group (P < .0005). The acute effect of IFN-beta1a on serum sHLA-I and sHLA-II was observed to be the opposite of that occurring during RRMS relapses. Monitoring of both sHLA-I and sHLA-II appears necessary if these molecules are to be developed as RRMS activity markers.

Adult↗
PubMed2004

HIV-associated dementia, Alzheimer's disease, multiple sclerosis, and schizophrenia: gene expression review.

RNA and protein gene expression technologies are revolutionizing our view and understanding of human diseases and enable us to analyze the concurrent expression patterns of large numbers of genes. These new technologies allow simultaneous study of thousands of genes and their changes in regulation and modulation patterns in relation to disease state, time, and tissue specificity. This review summarizes the application of this modern technology to four common neurological and psychiatric disorders: HIV-1-associated dementia, Alzheimer's disease, multiple sclerosis, and schizophrenia and is a first comparison of these diseases using this approach.

AIDS Dementia Complex↗
PubMed2004

CNS vasculitis.

Vasculitis of the central nervous system can be of several varieties depending upon the vessel(s) involved and type of disorder. One can see primary CNS vasculitis as a distinct entity which is primarily manifested as central nervous system injury in a vascular distribution or the vasculitic process can be secondary to a systemic disorder such as systemic lupus erythematosus (SLE) or polyarteritis nodosa (PAN). The inflammation of the CNS vessels can be immune mediated or infectious in nature and a number of "triggers" have been identified including hypersensitivity states. It is quite probable that there is a genetic predisposition in certain individuals and this can lead to an enhanced risk of a vasculitic process when there is exposure to a particular antigen that "sets off" the immune system. The potential for response of the process to antimicrobials and/or immunosuppressants, and the potential for devastating consequences if the process is left untreated, has heightened the urgency in recognizing CNS vasculitis. Key to the recognition and treatment of CNS vasculitis is the evolution of newer insights into the pathogenesis. For example, it is evident that most vasculitides are cell-mediated. Antigen stimulation of CD4+T cells is believed to play a crucial role in giant cell (temporal) arteritis which is the most common type of CNS vasculitis. Identification of genetic susceptibility has also contributed to our understanding of the cascade of events that leads to vascular injury on an inflammatory basis.

Animals↗
PubMed2004

Movement disorders.

Explore the source record for details and available documents.

Essential Tremor↗
PubMed2004

Pathogenesis of brain and spinal cord atrophy in multiple sclerosis.

For more than a century, multiple sclerosis was viewed as a disease process characterized by oligodendrocyte and myelin loss, and research into the pathogenesis of multiple sclerosis was mainly focused on the mechanisms of inflammation. However, with development of more sophisticated neuroimaging and molecular biology techniques, attention has shifted to new aspects of pathogenesis of multiple sclerosis: axonal loss and neurodegeneration. Evidence is increasing that tissue destruction, primarily axonal loss and neurodegeneration, is a key element in the pathogenesis of multiple sclerosis. In addition, it is now known that brain and spinal cord atrophy begins early in the disease process of multiple sclerosis and advances relentlessly throughout the course of the disease. Cumulative data suggest that axonal loss is the major determinant of progressive neurologic disability in patients with multiple sclerosis. Magnetic resonance imaging and magnetic resonance spectroscopy in patients with multiple sclerosis for < 5 years indicate brain atrophy and loss of axonal integrity. Neurodegeneration and axonal loss in patients with multiple sclerosis are initially accompanied by a local response from oligodendrocyte progenitor cells and some remyelination. However, these repair mechanisms eventually fail, and patients typically develop generalized brain atrophy, cognitive decline, and permanent disability. Although the exact mechanisms underlying central nervous system atrophy in patients with multiple sclerosis are largely unknown, evidence exists that atrophy may represent an epiphenomenon related to the effects of dynamic inflammation within the central nervous system, including demyelination, axonal injury, neuronal loss, Wallerian degeneration, and possibly iron deposition. This article summarizes the potential mechanisms involved in central nervous system atrophy in patients with multiple sclerosis.

Apoptosis↗
PubMed2004

Neuroimaging of the complications of epilepsy surgery.

BACKGROUND AND PURPOSE: Stroke-like symptoms can be associated with the invasive evaluation and surgical resection of epileptic foci in patients with intractable epilepsy. Neurological deficits following surgical procedures for epilepsy are not uncommon, but most are relatively minor and transient. The authors investigated the neuroimaging patterns of cerebral tissue insults in patients suffering neurological deficits directly related to procedures performed to evaluate and treat intractable epilepsy. They attempted to discern potential secondary vascular insults from the not unexpected tissue loss that can be associated with various epilepsy procedures. METHODS: The authors prospectively assessed 7 consecutive patients who underwent either the invasive electrocortigraphic monitoring or surgical resection of epileptic foci. All had some degree of neurological deficit postoperatively. The authors evaluated for tissue injury type with postoperative computed tomography and magnetic resonance brain imaging. They also review pertinent medical literature addressing potential complications of epilepsy surgery. RESULTS: Three patients had primarily ischemic tissue injuries, 2 had tissue loss with minor bleeding, and 1 transient deficit appeared to reflect the amount of tissue removed. Another patient had choreiform movements and gait ataxia 1 week after the procedure, but no follow-up neuroimaging was available. The primary ischemic insults appeared to be related to vascular traction or compression or possibly vasospasm. The tissue loss/hemorrhagic insults were presumably related to tissue loss, with seepage of blood or bleeding from a resected cavernous hemangioma. No patients died, but 1 was left with a persistent, moderately severe neurological deficit. CONCLUSIONS: It is important to distinguish the not unexpected neurological deficits associated with inadvertent trauma to normal brain tissue during procedures associated with epilepsy surgery from vascular insults. Postoperative neuroimaging can be useful in this endeavor.

Adolescent↗
PubMed2003

Cardioembolic stroke: an update.

Cardioembolic stroke accounts for approximately 15% of all strokes and is thought to be one of the more preventable types of strokes. Features that have been reported to support cardioembolism as a mechanism for ischemic stroke have included documented cardiac source of embolism, maximal neurologic deficit at onset, multiple cerebrovascular territories involved, enhanced tendency toward hemorrhagic transformation, enhanced risk of syncope or seizure associated with presentation, and lower likelihood of premonitory transient ischemic attacks. Features that tend to make cardioembolic stroke less likely include significant cerebral atherosclerosis, step-wise progression of the neurologic deficit within a finite period of time, vascular distribution such as entire internal carotid artery territory with combined middle cerebral artery and anterior cerebral artery involvement or watershed distribution, and premonitory transient ischemic attacks. A number of cardiac conditions can promote thromboembolism, and there is risk stratification reflective of the specific condition or coexistent conditions. Anticoagulant therapy generally has been found to be the most effective means of preventing cardiogenic brain embolism, but the intensity of anticoagulation needs to be optimized to reflect the risk-to-benefit ratio for the particular patient.

Aged↗
PubMed2003

The Edwin Smith surgical papyrus: description and analysis of the earliest case of aphasia.

The Edwin Smith surgical papyrus, which dates back nearly five millennia, is the oldest known medical text and contains the first written example of the word "brain", as well as the earliest known descriptions of the meninges and the cerebrospinal fluid. The papyrus describes 48 cases and gives the first accounts of several forms of brain injury and their associated complications. The Egyptian author presents an analytical approach to the reported cases and classifies them as favourable, uncertain or intractable, depending on prognosis. The authors believe that case 20 of the papyrus presents the first possible case of aphasia, which occurred following head trauma. The patient, frustrated by his inability to speak, developed nuchal stiffness, which might have been due to meningeal irritation. The case concludes with the advice that a patient with such a grave condition should only be comforted, not treated.

Aphasia↗
PubMed2003

Serum from patients with multiple sclerosis downregulates occludin and VE-cadherin expression in cultured endothelial cells.

Disruption of the blood brain barrier (BBB) and transendothelial migration of inflammatory cells are crucial steps in the development of demyelinating lesions in multiple sclerosis (MS). Occludin and vascular endothelial-cadherin (VE-cadherin) are two major components of the tight junctions (TJs) in the brain microvasculature that help to create the BBB. In the present study, we investigated the effect of serum from MS patients on the expression of these two junctional markers and on the endothelial integrity. Serum from six MS patients in exacerbation, six in remission, and six normal controls (10% by volume) was incubated with cultured endothelial cells, and the expression of occludin and VE-cadherin was measured by immunoblotting. Serum from MS patients in exacerbation significantly reduced the expression of occludin and VE-cadherin compared with patients in remission and normal controls. This disintegrating effect was more pronounced for occludin than for VE-cadherin. We assume that the elevation in cytokines or other serum-soluble factors in MS patients in exacerbation likely provokes downregulation of occludin and VE-cadherin. This downregulation of TJs proteins may, therefore, contribute to the disruption of the BBB in this condition.

Adult↗