Publications by authors named "Julian T Hoff"

Background: The management of idiopathic intracranial hypertension (IIH) depends on a reliable assessment of intracranial pressure (ICP), particularly when visual function measures or ophthalmoscopic indicators are confusing and when invasive surgical procedures are being considered. Although ICP monitoring has been widely applied in many neurologic conditions as a more reliable measure of ongoing ICP than lumbar puncture (LP), it has not often been widely used in the management of IIH.

Methods: We searched the records of the University of Michigan between 2001 and 2008 for patients with IIH who had undergone LP and continuous ICP monitoring with an intraparenchymal Codman ICP Monitoring System and in whom at least 1 year of follow-up information was available.

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Objective: The paraspinal muscles often fail to relax on forward flexion in many persons with low-back pain. The goal of this prospective study was to determine whether this abnormal lack of a flexion-relaxation phenomenon corrects after lumbar diskectomy for symptoms of radiculopathy with low-back pain.

Design: Electromyographic testing was performed on 17 patients before and 30 days after lumbar diskectomy.

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Background: Our previous studies have demonstrated that argatroban, a specific thrombin inhibitor, reduces brain edema and neurological deficits in rat glioma models. The present study investigated whether or not thrombin enhances glioma growth in vivo and in vitro.

Methods: There were two parts in this study.

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Objective: Clinical symptoms associated with lumbar spinal stenosis (LSS) are believed to be due to neurogenic claudication caused by narrowing of the central and lateral spinal canals. However, there is a paucity of published data on these relationships. The purpose of the present study was to examine the relationship between clinical symptoms associated with LSS and osseous anterior-posterior (AP) spinal canal diameter as measured on axial magnetic resonance imaging.

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Background And Purpose: There is an urgent need to develop a model in which to study the mechanism of intracerebral hemorrhage-induced neuronal death in vivo.

Methods: This study was divided into 2 parts: (1) Rats received either an infusion of hemoglobin, ferrous iron, or saline into the right hippocampus; (2) Rats had an infusion of hemoglobin and then were treated with either deferoxamine or vehicle. Rats were killed for hippocampus size, DNA damage, and neuronal death measurements.

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Object: Preconditioning with hyperbaric oxygen (HBO2) reduces ischemic brain damage. Activation of p44/42 mitogen-activated protein kinases (p44/42 MAPK) has been associated with preconditioning-induced brain ischemic tolerance. This study investigated if preconditioning with HBO2 protects against intracerebral hemorrhage (ICH)-induced brain edema formation and examined the role of p44/42 MAPK in such protection.

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Background: Magnetic resonance imaging is commonly used to diagnose lumbar spinal stenosis. Some persons without symptoms have a small lumbar spinal canal. Electrodiagnosis has been used to diagnose spinal stenosis for over sixty years, but we are aware of no masked, controlled trials of the use of electrodiagnosis for that purpose.

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Intracerebral hemorrhage (ICH) is a subtype of stroke with high morbidity and mortality. The mechanisms underlying ICH-induced brain injury have become better understood during the past decade. Experimental investigations have indicated that thrombin formation, red blood cell lysis, and iron toxicity play a major role in ICH-induced injury and that these mechanisms may provide new therapeutic targets.

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Study Design: Longitudinal masked, double-controlled cohort study.

Objectives: To determine prognosis and predictors of function and pain in persons with spinal stenosis.

Summary Of Background Data: The clinical syndrome of spinal stenosis is common and disabling, but not clearly related to anatomic measures.

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Objective: To assess the relations between clinically recognized lumbar spinal stenosis and the conclusions of masked radiologists and electrodiagnosticians.

Design: Prospective, masked, double-controlled trial.

Setting: University spine center.

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Activation of the complement cascade contributes to brain injury after intracerebral hemorrhage (ICH). However, a recent study found that complement C5 deficient mice had enhanced ICH-induced brain injury. The present study, therefore, investigated the role of complement C3 (which is upstream from C5) in ICH.

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Objective: The goals of this study were 1) to determine the effects of intracerebral hemorrhage (ICH) on brain tumor necrosis factor (TNF)-alpha levels, which are still controversial; 2) to investigate the role of TNF-alpha in ICH-induced brain injury; 3) to examine the effects of thrombin on brain TNF-alpha levels; and 4) to elucidate the role of TNF-alpha in thrombin-induced neuroprotection.

Methods: Autologous whole blood and thrombin were injected into the right caudate of rats or mice. Brain TNF-alpha was then determined by enzyme-linked immunosorbent assay and immunohistochemistry.

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Object: Intracerebral hemorrhage (ICH) causes brain atrophy and neurological deficits. The mechanisms of brain atrophy after ICH are poorly understood, although recent evidence suggests that some ICH-induced brain injury results from the products of hemoglobin degradation, including iron. In this study the authors examine the role of iron in brain atrophy and neurological deficits following ICH.

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The past decade has resulted in a rapid increase in knowledge of mechanisms underlying brain injury induced by intracerebral haemorrhage (ICH). Animal studies have suggested roles for clot-derived factors and the initial physical trauma and mass effect as a result of haemorrhage. The coagulation cascade (especially thrombin), haemoglobin breakdown products, and inflammation all play a part in ICH-induced injury and could provide new therapeutic targets.

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Study Design: Prospective, masked, double controlled diagnostic trial.

Objectives: To determine the sensitivity and specificity of electrodiagnostic consultation (EDX) for the clinical syndrome of lumbar spinal stenosis.

Summary Of Background Data: EDX has been used for more than 50 years to diagnose spinal disorders but has not met the new standards of evidence-based medicine.

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Spontaneous intracerebral hemorrhage, from several sources, causes instantaneous mass effect, disruption of surrounding brain, and often an early neurological death. If the patient survives the initial event, the hematoma can lead to secondary brain injury, neurological deficits, and, occasionally, delayed fatality. The mechanisms that trigger pathophysiological changes in and around the hematoma are becoming better understood, offering new therapeutic opportunities.

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Propionibacteria are known to play a part in postneurosurgical infections, primarily those involving ventricular shunts. Nevertheless, little is known about the association between dural allografts and propionibacterium infections. Two patients underwent craniotomy for supratentorial meningiomas and each received a dural allograft.

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Object: The aims of this study were to determine the following: whether there are sex differences in intracerebral hemorrhage (ICH) induced brain injury in rats, whether delayed administration of 17beta-estradiol can reduce ICH-induced brain damage, and whether these effects are estrogen receptor (ER)-dependent.

Methods: Male and female Sprague-Dawley rats received an infusion of 100 microl autologous whole blood into the right basal ganglia. Twenty-four hours later the rats were killed.

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Background And Purpose: Thrombin, heme oxygenase, complement, microglia activation, and leukocyte infiltration are all actively upregulated in intracerebral hemorrhage (ICH). Experimental evidence suggests that all these factors are involved in ICH-induced brain injury. This suggests a scenario whereby ICH actively (through gene and protein upregulation) induces pathways that result in brain injury.

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Our previous studies have demonstrated that DNA injury occurs in the brain after intracerebral hemorrhage (ICH). DNA damage can result from at least two pathways, either endonuclease-mediated DNA fragmentation or oxidative injury. The present study investigated the occurrence of the latter after ICH and the role of iron in such injury.

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Background And Purpose: Previous studies have suggested that delayed release of hemoglobin degradation products, particularly iron, is involved in intracerebral hemorrhage (ICH)-induced brain injury. However, a recent study found evidence of iron-induced brain injury soon after ICH. This study, therefore, examined whether another iron-containing component of blood, holo-transferrin (holo-Tf), might also induce brain injury either alone or in combination with thrombin, another factor involved in early ICH-induced brain injury.

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Study Design: Review of the literature.

Objectives: Review the definition, etiology, incidence, and risk factors associated with as well as potential treatment options.

Summary Of Background Data: The development of pathology at the mobile segment next to a lumbar or lumbosacral spinal fusion has been termed adjacent segment disease.

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Background And Purpose: Intracerebral hemorrhage (ICH) is mostly a disease of the elderly, but most current experimental ICH models have used young animals. Age is an important factor in other forms of brain injury, affecting microglia and astrocyte reactions and plasticity. Therefore, the present study investigated the effects of aging on brain injury after ICH.

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