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Biomedical subjects

R G Robinson

Publications and source records attributed to R G Robinson.

At least 73 records · Page 4Linked to original sources
PubMed1996

Self-reported aggressive behavior in patients with stroke.

This study represents a first attempt to identify some of the clinical and pathoanatomical correlates of violent outbursts in patients with cerebrovascular accident. Subjects were selected from a population of patients hospitalized with acute stroke. Although we did not have behavioral measures of violent behavior, patients who reported having had violent outbursts were identified based on clinical ratings on a structured interview. Subjects were asked if they had experienced episodes of anger accompanied by behaviors ranging from shouting to violence during the time since their stroke. These patients were compared with controls matched for demographic variables. Violent patients had higher total Present State Exam and Hamilton-D scores. The percentage of patients with cognitive impairment in the angry outburst group (66%) was greater than the control group (22%). Outburst patients had a higher frequency of left-hemisphere lesions (46.7%) compared with controls (29.4%). When lesion volumes were statistically equated, proximity of lesion to the frontal pole was one of the factors related to the self-reported irritable/violent behavior. To determine whether depression explained our findings, we carried out two-way analyses of variance with angry outburst and major depression group membership as factors. Effects of left anterior lesion location and cognitive impairment on violence remained present. These findings suggest that the potential for anger and violence in patients with stroke has multiple clinical and neuropathological correlates, including greater cognitive impairment and left anterior hemisphere lesions.

Aggression↗
PubMed1996

Lesion characteristics and depressed mood in the stroke data bank study.

This study examined the relationship between post-stroke lesion size and location and depressed mood by using data from the multicenter National Stroke Data Bank. For in patients with first-ever cerebral infarction, lesions were characterized by location and size from CT scans. Forty-seven (24%) of the 193 patients studied were depressed. In the complete sample, neither lesion size nor location was associated with depression. However, among patients with comparable small-sized lesions (n = 124), depression was more frequent among those with left hemisphere stroke than those with right hemisphere stroke (31% vs. 16%; P = 0.04). Among patients with larger lesions, brain edema was common and may have obscured lateralized findings. Different biogenic amine neurotransmitter responses to right and left hemisphere brain injury may underlie this mood asymmetry.

Aged↗
PubMed1996

Lesion location and poststroke depression.

This study examined whether stroke lesions involving left hemisphere prefrontal or basal ganglia structures are associated with poststroke depression. A consecutive series of first-ever stroke patients with single small lesions on CT scan were examined for the presence and severity of poststroke depressive disorder. Lesions involving left prefrontal or basal ganglia structures were compared with other left hemisphere lesions and all right hemisphere lesions. Forty-one patients were examined. Patients with lesions involving left hemisphere prefrontal or basal ganglia structures had a higher frequency of depressive disorder (9/12; 75%) than other left hemisphere lesions (1/12; 8%) or those with right hemisphere lesions (5/17; 29%), P = 0.002. These findings suggest that damage to neural pathways within left hemisphere prefrontal or basal ganglia structures is associated with depressed mood following stroke.

Aged↗
PubMed1996

Suicidal plans following spinal cord injury: a six month study.

Suicidal plans were examined among patients with spinal cord injury. Suicidal plans during the acute period may be related to inadequacy of support. Suicidal plans during the chronic period may be related to a depressive disorder provoked by prolonged severe impairment.

Adult↗
PubMed1996

Dysthymia in neurological disorders.

Dysthymia is characterized by long-lasting periods of lowered mood. Epidemiological studies in the USA and Europe have demonstrated that the prevalence of dysthymia is at least 3% of the general population. Its pervasive occurrence makes dysthymia a public health problem worldwide. One feature of this disorder is its co-occurrence with medical and neurological disorders. A World Health Organization meeting on dysthymia in neurological disorders was held in Geneva, 1-3 July 1996 to address this topic. Some of the major goals of this meeting were to clarify the definition of dysthymia in the presence of neurological disorders and to evaluate current research in the field, to point out new areas for investigation, and to discuss current psychological and pharmacological treatments for dysthymia in neurological disorders. The potential roles of neuroendocrine and molecular mechanisms in dysthymia were identified through specific problems related to dysthymia occurring in disorders such as Parkinson's disease, Alzheimer's disease, stroke, multiple sclerosis and epilepsy. This meeting provided direction and opportunity for future studies in the under-recognized and under-investigated relationship between dysthymia and neurological disorders.

Dysthymic Disorder↗
PubMed1995

Strontium 89 therapy for the palliation of pain due to osseous metastases.

OBJECTIVE: To present the current state of systemic radiopharmaceutical therapy for the palliation of pain in individuals with metastatic cancer and to evaluate the palliative effect and degree of hemotoxicity of strontium chloride 89 (89Sr) in patients with painful osteoblastic metastases primarily from prostate and breast cancer. DATA SOURCES AND STUDY SELECTION: A MEDLINE search through December 1994 was performed to identify English-language studies that met the following criteria. All eligible studies reported treatment of patients with painful osteoblastic bony metastases primarily from prostate or breast cancer treated with intravenous 89Sr. For study eligibility, evaluation of clinical response as assessed by the Karnofsky index, need for pain medication, or changes in mobility or sleep patterns was required. Hemotoxicity data were a requirement. A minimum of 10 prostate cancer cases was necessary for study inclusion. Only those studies assessing clinical response following one injection of 89Sr were included. Preliminary reports of cooperative studies were not included. Doses of 89Sr ranged from 0.6 MBq/kg (16 microCi/kg) to 400 MBq (10.8 mCi) per patient. Evaluation of patients for at least 3 months following 89Sr treatment was required. In addition, two studies examining issues of cost with regard to 89Sr treatment were identified. DATA EXTRACTION: Baseline pain assessment and periodic pain estimates as measured by the Karnofsky index, medication diaries, changes in mobility, sleep patterns, and/or ability to work were the basis for assessment of response. Baseline and periodic complete blood cell counts were the basis for hemotoxicity evaluation. DATA SYNTHESIS: Palliation and hemotoxicity data were analyzed separately for each study. Some improvement occurred in as many as approximately 80% of patients. Several studies demonstrated complete relief of pain in at least 10% of patients The nadir of platelet and white blood cell counts appears at approximately 4 to 8 weeks following injection, with a partial return to baseline by 12 weeks. As many as 10 injections spaced 3 months apart have been given to some patients with repeated palliative effect and without serious hemotoxicity. Reinjection may be limited by a platelet count below 60 x 10(9)/L, a white blood cell count below 2.4 x 10(9)/L, or the absence of osteoblastic skeletal metastasis as seen on bone scan. Studies examining treatment costs suggest that 89Sr may decrease costs associated with palliation of pain due to metastatic disease. CONCLUSIONS: As many as 80% of selected patients with painful osteoblastic bony metastases from prostate or breast cancer may experience some pain relief following 89Sr administration. In addition, as many as 10% or more may become pain free. Duration of clinical response may average 3 to 6 months in some cases. Hemotoxicity is mild. A decrease in treatment costs with administration of 89Sr to patients with painful osteoblastic bony metastases from prostate cancer may occur. These observations reflect the preliminary nature of knowledge in this field and point to the need for larger clinical trials of the use of 89Sr palliation.

Bone Neoplasms↗
PubMed1995

Mechanism of action and antitumor activity of (S)-10-(2,6-dimethyl-4-pyridinyl)-9-fluoro-3-methyl-7-oxo-2,3-dihydro-7 H- pyridol[1,2,3-de]-[1,4]benzothiazine-6-carboxylic acid (WIN 58161).

(S)-10-(2,6-Dimethyl-4-pyridinyl)-9-fluoro-3-methyl-7-oxo-2,3-dihydro-7H - pyrido[1,2,3-de][1,4]benzothiazine-6-carboxylic acid (WIN 58161) is an enantiomerically pure quinolone with outstanding bacterial topoisomerase II (DNA gyrase, EC 5.99.1.3) inhibitory and antibacterial activity. Unlike most quinolones, WIN 58161 also exhibits significant inhibitory activity against mammalian topoisomerase II (EC 5.99.1.3). DNA gyrase and topoisomerase II inhibitory activities are enantioselective. Consequently, WIN 58161 and its enantiomer (WIN 58161-2) provide useful tools to probe the contribution of topoisomerase II inhibition to the mechanism of cytotoxicity of quinolones and the potential utility of quinolone-topoisomerase II inhibitors as antitumor agents. WIN 58161 inhibited both highly purified Escherichia coli DNA gyrase and HeLa cell topoisomerase II by the promotion of enzyme-DNA covalent complexes. WIN 58161 did not bind stably to DNA via intercalation and did not enhance the formation of topoisomerase I (EC 5.99.1.2)-DNA covalent complexes. At drug concentrations that are cytotoxic to P388 murine leukemia cells, WIN 58161 promoted intracellular DNA single-strand breaks (SSBs) that exhibited the hallmarks of being mediated by topoisomerase. DNA fragments were complexed with protein, and SSBs were readily resealed at 37 degrees following drug removal. WIN 58161-2 was neither cytotoxic nor did it promote intracellular SSBs in P388. These observations suggest that the mechanism of cytotoxicity of WIN 58161 is predominantly, if not exclusively, a result of topoisomerase II inhibition. When studied in tumor-bearing mice, WIN 58161 exhibited a significant antitumor effect against each of five tumors tested, whereas neither toxicity nor antitumor activity was observed with WIN 58161-2. We conclude from these studies that WIN 58161 represents the prototype of a novel chemical class of topoisomerase II inhibitor with potential clinical utility in treating cancer.

Animals↗
PubMed1995

Comparison between acute and delayed onset major depression after spinal cord injury.

Sixty patients with spinal cord injury were examined to assess major depression during the in-hospital period and at 3- and 6-month follow-up. Thirteen patients had depression during the initial in-hospital evaluation (acute onset depression) and eight had depression first diagnosed at either 3- or 6-month follow-up (delayed onset depression). Acute onset depression was related to the severity of impairment and premorbid history of psychiatric disorder, suggesting a psychological reaction to impairment or premorbid vulnerability as a possible mechanism for developing depression. Delayed onset depression was not related to severity of physical impairment but was associated with more rostral spinal injury, suggesting the possibility that neurophysiological response to injury more proximal to the brain may play a role in delayed onset depression. These data also suggest that the etiology and pathophysiology of these two types of depression may be different.

Adult↗
PubMed1995

The heterogeneity of temporal lobe epilepsy. Neurology, neuropsychology, and psychiatry.

The present paper introduces the reader to the behavioral variability of patients with temporal lobe epilepsy. The neurobiological variability is evidenced by reviewing neurological, neurophysiological, and neuropsychological investigations. The behavioral variability of persons affected by epilepsy with a temporal focus is proposed to be an expression of the neurobiological complexity of temporal lobe epilepsy. The aim of this paper is to encourage endeavors in behavioral taxonomy. Efforts to foster homogeneity through improved classification are considered fundamental in behavioral science and should be applied to epilepsy. The achievement of a behavioral taxonomy may help in both understanding the mechanism(s) of these behavioral disorders and targeting more specific treatments.

Brain↗
PubMed1995

Clinical correlates of early-onset and late-onset poststroke generalized anxiety.

OBJECTIVE: The authors' goal was to determine if generalized anxiety diagnosed while a patient was hospitalized for stroke (early onset) had the same clinical correlates as anxiety beginning 3 months or more after the stroke (late onset). METHOD: Patients with acute stroke (N = 142) were examined while they were in the hospital and 3, 6, 12, and 24 months later for the presence of anxiety symptoms. Patients underwent a structured psychiatric interview as well as assessment of cognitive, physical, and social function at each visit. Patients with early-onset and late-onset poststroke generalized anxiety were identified and compared to patients without poststroke generalized anxiety. RESULTS: The frequency of early-onset poststroke generalized anxiety was 27% and that of late-onset poststroke generalized anxiety was 23%. Three-quarters of the anxious patients had comorbid major or minor depression. Patients who developed early-onset or late-onset poststroke generalized anxiety were no more socially, cognitively, or physically impaired than patients who did not develop anxiety. Early-onset but not late-onset anxiety was associated with a previous history of psychiatric disorder. The median duration of late-onset anxiety was 3.0 months, and that of early-onset anxiety was 1.5 months. The presence of anxiety was significantly associated with depression; onset of depression and onset of anxiety occurred at approximately the same time. CONCLUSIONS: These findings suggest that although early-onset and late-onset poststroke generalized anxiety are phenomenologically similar, they may be the result of different pathophysiological mechanisms.

Anxiety Disorders↗
PubMed1995

Hereditary late-onset chorea without significant dementia: genetic evidence for substantial phenotypic variation in Huntington's disease.

We examined five individuals and obtained information concerning six other members from two unrelated families, nearly all of whom developed chorea after age 50 (one patient developed chorea at age 40). The severity of chorea progressed in all patients and became disabling in some individuals approximately 15 years after onset. Cognitive impairment was absent or minimal. All five examined patients were cognitively normal, even 10 to 30 years following the onset of chorea. Formal neuropsychometric testing demonstrated mild cognitive impairment in two individuals. Nevertheless, all patients were able to maintain employment or carry on with their usual household tasks until chorea was severe. One individual first became demented 30 years after the onset of chorea. Neuroimaging (with CT or MRI) in four patients failed to demonstrate significant caudate or putaminal atrophy 8 to 15 years following the onset of chorea. Three other family members (who were not available for examination) were said to have suffered chorea (without any mental decline) beginning after age 50, with subsequent survival of 20 years (in one) and 30 years (in two). Given this constellation of history and findings, three experienced neurologists and two medical geneticists concluded that these patients had a familial chorea syndrome distinct from Huntington's disease (HD). However, genetic analysis of the trinucleotide (CAG) repeat length associated with HD (in 4p16.3) determined repeat lengths of 44 and 46 in four patients tested (within the HD range). We conclude that these patients have HD and that such families represent further convincing examples of significant phenotypic variation for HD.

Age of Onset↗
PubMed1995

Personality neuroticism and depression after stroke.

AIM: The aim of this study was to determine whether personality neuroticism or extroversion traits are associated with post-stroke depression. METHOD: Ninety-four stroke inpatients undergoing rehabilitation were examined two months post-stroke for the presence and severity of depression and a retrospective assessment was made of life-time neuroticism and extroversion. RESULTS: Depressed patients (N = 35) had higher neuroticism scores than non-depressed patients. Neuroticism was correlated positively with depressive symptomatology. Extroversion was not associated with depression diagnosis or depressive symptomatology. CONCLUSION: We conclude that personality neuroticism may be a risk factor for depression following stroke.

Aged↗
PubMed1995

DNA sequence preferences at sites cleaved by human DNA topoisomerase II in response to novel quinolone derivatives.

We have examined the DNA cleavage site specificity of human type II DNA topoisomerase in the presence of each of five novel quinolone derivatives. Each quinolone derivative inhibited the human enzyme, inducing double-strand breaks with a four-base stagger. Break sites generated in response to each derivative had a predominance of C in the 3'-terminal position. Consensus sequences derived for cleavage sites induced by each derivative were strikingly similar, not only at the 3'-terminal position, but also at additional positions on either side of the broken phosphodiester bond. Analysis of these consensus sequences yielded information about possible interactions of specific substituents on the quinolone derivatives with DNA and/or topoisomerase. Comparison of the quinolone-based consensus sequences with those derived for cleavage sites generated by the human type II topoisomerase in the presence of either m-AMSA or VM-26, or in the absence of drug, provided compelling evidence that DNA cleavage sites include two domains: one which interacts with drug and a second, larger domain which interacts with topoisomerase.

Amsacrine↗
PubMed1994

The strength and stiffness of thoracic implant anchors in osteoporotic spines.

OBJECTIVE: To gain a better understanding of factors affecting dorsal implant pull-out strength and stiffness so thoracic spinal implant fixation can be improved. METHODS: Posterior pull-out testing of six thoracic implant anchor types was performed on 54 osteoporotic human vertebra, T2-10, with an average bone mineral density of 0.67 g/cm2. RESULTS: The mean loads at neural arch failure were similar (296 to 382 N). Pedicle strength was greatest at T2 and least at T3. Hook claws were stiffer than sublaminar wires (121 N/mm and 180 N/mm versus 42 N/mm and 52 N/mm, respectively). Facet hook and pedicle hook claws were comparable, as were subpars wires. Bone mineral density of the vertebral bodies correlated with the stiffness of the sublaminar wire anchors only. CONCLUSION: To optimize the strength and stiffness of implant constructs designed to resist forward flexion, this study supports using hook-claws rather than sublaminar wires and extension of fixation to T2 when clinically realistic.

Aged↗
PubMed1994

The effects of implant stiffness on the bypassed bone mineral density and facet fusion stiffness of the canine spine.

STUDY DESIGN: Effects of spinal implant stiffness and removal/retention on bypassed bone mineral density and column/fusion stiffness were studied in dogs. METHODS: After facet fusion and bicortical peripedicle screw placement, one group of eight dogs received 6.35 mm and another 4.76 mm rod instrumentation at L3-L5. At 12 weeks, four in each group had implants removed. Bone mineral density was analyzed by dual energy x-ray absorptiometry at 1 to 24 weeks. Axial compressive stiffness of the L3-L5 construct, spinal column, fused facets, and instrumentation were measured. Percent load through the vertebral column was predicted. RESULTS: Five observations were made for this canine model. First, stiffer implants resulted in more bypassed bone mineral loss at 6 and 12 weeks, plateauing and not different at 24 weeks. Second, after implant removal, a significant and similar rebound in bone mineral density occurred. Third, 4.76 mm rod instrumentation (initially 71% load through column) resulted in stiffer posterior fusions and vertebral columns than 6.35 mm rod instrumentation (initially 57% load through column). Fourth, marked stiffening of the anterior-middle columns (apparently disks) occurred. Fifth, percent load borne by the vertebral column increased with time. CONCLUSIONS: There appears to be a range of percent load through the vertebral column that creates optimum fusion/column stiffening while limiting bone stress shielding effects. The 6.35 mm rod constructs were predicted to allow greater than 70% axial load through the adult human thoracic/lumbar spine, implying biologic responses similar to 4.76 mm rods in dogs.

Absorptiometry, Photon↗