"Systemic radioisotopic therapy of primary and metastatic bone cancer".
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Animals↗
Biomedical subjects
R G Robinson
Publications and source records attributed to R G Robinson.
Hyperactivity following posterior cortical injury is lateralized, sensitive to lesion size and independent of the nigrostriatal dopamine system.
In a previous study, we reported that a specific size cortical suction lesion of the right posterior cortex in rats produced hyperactivity and increased concentrations of dopamine in the nigrostriatal pathway. The present study extended those findings by addressing whether this phenomenon is lateralized to the right posterior cortex and whether the increases in nigrostriatal dopamine are necessary for the behavioral changes produced by the lesion. Right posterior cortical lesions of 1.8 mm diameter produced spontaneous hyperactivity over a 30-day postoperative period while identically placed 1.3 mm or 2.4 mm diameter lesions did not. Left hemisphere lesions of 1.3 mm, 1.8 mm or 2.4 mm diameter also failed to produce hyperactivity. The hyperactivity response to 1.8 mm diameter lesions of the right posterior cortex was not blocked by 70% depletions in nigrostriatal dopamine produced by bilateral nigral injections of 6-hydroxydopamine two weeks prior to cortical lesions. These findings suggest that hyperactivity following right posterior cortical lesions is lateralized and is not dependent upon changes in the nigrostriatal dopaminergic pathway.
Animals↗
The use of fetal neocortical transplants to treat the hyperactivity resulting from cortical suction lesions in adult rats.
Focal suction lesions of the right frontoparietal cortex in rats produce locomotor hyperactivity. We attempted to reverse these changes by grafting homologous cortex from 16-day-old embryos into the lesion site. Various aspects of activity were measured in computerized photocell chambers until 14 weeks past transplantation. Three groups of animals were tested: sham-operated controls, lesions only (LO), and lesion plus transplant (LT). Hyperactivity was demonstrated for all measures in LO and/or LT groups. There was a partial reversal by the transplants of the increases in vertical activity produced by lesions at 14 weeks after transplant. However, on other measures, such as distance per movement, only LT animals were ever hyperactive, and on others, such as total distance, hyperactivity appeared earlier in the LT group than in LO. Brain chemistry analyses revealed right-sided norepinephrine depletions in posterior cortex in all groups and a bilateral cortical serotonin depletion in LT animals only. Results suggest that transplanted tissue can either ameliorate or exacerbate locomotor changes produced by cortical ablation depending on the particular behavior and on when it is measured.
Animals↗
Developmental and hormonal factors in the sexually dimorphic, asymmetrical response to focal cortical lesions.
The developmental and hormonal determinants of the lateralized response to focal cortical suction lesions were examined in a series of experiments. In an initial study, Sprague-Dawley male rats 25, 30, 55 or 90 days of age, received right unilateral focal frontocortical suction lesions. Only 90-day-old rats developed hyperactivity, suggesting a specific role for maturational factors in the production of this response. Prepubertally castrated adult male rats receiving right frontocortical suction lesions at 90 days also failed to develop hyperactivity, suggesting that sexual maturational factors and/or the presence of testosterone are necessary for the expression of this response. Testosterone implants, producing physiological relevant levels of circulating testosterone reinstated the hyperactivity response to adult cortical lesions in prepubertally castrated male rats. Similar lesions in the left hemisphere, however, did not produce hyperactivity in castrated male rats with testosterone replacement. Finally, in ovariectomized adult female rats, testosterone did not allow the expression of a hyperactivity response to right frontocortical suction lesions. Together, these results demonstrate both an organizational and permissive role for sex steroids in the sexually dimorphic asymmetrical response to cortical injury.
Aging↗
Depression and cognitive impairment in Parkinson's disease.
Neuropsychological deficits including cognitive impairment as well as depression are among the most frequent and important mental disorders found in patients with Parkinson's disease (PD). It has never been determined, however, whether there is a specific relationship between cognitive impairment and depression. A consecutive series of patients with PD was therefore examined for the presence of depression and neuropsychological deficits. Severity of depression was found to be the single most important factor associated with the severity of cognitive impairment. When PD patients with major depression were compared with an age and stage-matched group of nondepressed patients with PD using a neuropsychological battery, major depressed patients performed significantly worse than the nondepressed patients on all aspects of neuropsychological function tested. These impairments were most pronounced on frontal lobe tasks.
Cognition↗
Incidence and severity of rheumatoid arthritis--the view from Australia.
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Arthritis, Rheumatoid↗
Strontium-89: treatment results and kinetics in patients with painful metastatic prostate and breast cancer in bone.
Two hundred and two patients with bone pain from metastatic cancer were treated with 40 microCi/kg of Sr-89. Patients were followed with pain diaries, records of medication taken, sleep patterns, serial bone scans and a Karnofsky Index. One hundred and thirty-seven patients with adequate followup survived at least 3 months, including 100 with prostate and 28 with breast carcinoma. Eighty of the 100 patients with prostate cancer responded, and 25 of the 28 breast cancer patients improved. Ten patients with prostate cancer and five with breast cancer became pain free. Little hematologic depression was noted. Sr-89 kinetic studies showed that strontium taken up in osteoblastic areas remained for 100 days. The tumor-to-marrow absorbed dose ratio was 10:1.
Bone Neoplasms↗
Lateralization of dementia of depression in stroke patients.
In a group of stroke patients with left-hemisphere lesions, those with major depression performed significantly below nondepressed patients on four of nine cognitive domains examined with a neuropsychological test battery. Among patients with right-hemisphere stroke, those with major depression did not perform below nondepressed patients on any of the nine cognitive domains. The differential effect of depression on cognitive performance between left- and right-hemisphere lesion groups could not be accounted for by demographic variables, neurological symptoms, lesion location, or lesion size. Poststroke major depression appeared to produce a decline in cognitive performance or dementia of depression that depended on the laterality of the lesion.
Brain↗
Cognitive impairments in different stages of Parkinson's disease.
A consecutive series of 94 patients with Parkinson's disease (PD) were evaluated for the presence of depression and neuropsychological deficits. Patients were divided into groups based on the severity of their PD symptoms and then further subdivided into depressed and nondepressed groups. Both stage of PD and existence of depression had significant effects on neuropsychological performance. The nondepressed group with severe symptoms showed deficits in cognitive tasks involving motor speed, and the depressed patients with severe symptoms demonstrated impairments in frontal-lobe-related tasks.
Aged↗
Dementia of depression among patients with neurological disorders and functional depression.
Cognitive performance on the Mini-Mental State Examination (MMSE) was assessed in depressed patients (diagnosis of major depression) with cerebrovascular lesions, with Parkinson's disease, or with functional depression (no known brain lesions). Controls for patients with brain lesions or Parkinson's disease were nondepressed patients with the same conditions. Controls for functionally depressed patients were age-matched normal individuals. Depressed patients had significantly lower total MMSE scores than their nondepressed counterparts, but depression did not have an effect on cognitive performance across the three disease groups. The only significant difference between depressed and nondepressed patients shared by all three groups was poorer performance by depressed patients on the delayed-recall task. The findings suggest that major depression may lead to a specific pattern of cognitive deficits independent of coexisting brain pathology.
Brain Damage, Chronic↗
Emotional behavior after a Wada test in a patient with secondary mania.
Soon after treatment of a right basotemporal vascular malformation using an embolization procedure, a 25-year-old patient developed an acute episode of mania. Two months later the patient was still manic, and a second embolization was scheduled. Before it was conducted, a Wada test was carried out to determine speech dominance. No changes in manic symptoms were observed after amytal injections into the left middle cerebral, right frontopolar, or right middle cerebral arteries. This finding suggests that secondary mania may not be the result of "release" of the left hemisphere following a right hemisphere lesion but instead may be related to specific disturbances within the right hemisphere.
Adult↗
Affective disorders and cerebral vascular disease.
Empirical studies have recently demonstrated that major and minor depressive disorders occur in 30-50% of stroke patients, and last more than one year without treatment, although they do respond to tricyclic antidepressants. These mood disorders are not strongly associated with severity of impairment, demographic characteristics, social supports or prior personal history, but major depression is often strongly associated with left frontal or left basal ganglia lesions and pre-existing subcortical atrophy. While the aetiology of these mood disorders remains unknown, serotonergic or noradrenergic dysfunction may play a role. Mania is a rare complication of stroke: the clinical presentation and response to treatment are usually the same as mania without brain injury. Post-stroke mania is strongly associated with both a right hemisphere lesion in a limbic-connected area and a second predisposing factor, such as genetic loading for affective disorder, pre-existing subcortical atrophy or seizure disorder. This disorder may be mediated through frontal lobe dysfunction. The lesion method represents a potentially fruitful technique for investigating the mechanisms of affective disorder.
Bipolar Disorder↗
Mood changes after right-hemisphere lesions.
Ninety-three patients with acute stroke lesions restricted to the right hemisphere were examined for the presence of mood changes. While 46 patients showed no mood changes, 19 were unduly cheerful, 17 had developed major depression, and 11 had developed minor depression. Although there were no significant between-groups differences in other demographic variables, neurological deficits, activities of daily living, cognitive impairment, or quality of social support, patients with major depression had a significantly higher frequency of familial history of psychiatric disorder and lesions of the parietal cortex than patients with either no mood change or major depression following left-hemisphere lesions. On the other hand, undue cheerfulness was significantly associated with lesions of the right frontal operculum. These findings suggest that major depression following right-hemisphere lesions may have a different aetiology and mechanism than major depression following left frontal or basal ganglia lesions.
Activities of Daily Living↗
Depression in patients with early versus late onset of Parkinson's disease.
We examined correlates of depression in patients whose onset of Parkinson's disease (PD) began before age 55 (early-onset group) compared with patients whose onset was after age 55 (late-onset group). The early-onset group showed a significantly higher frequency of depression than the late-onset group. When both groups were matched for duration of the disease, the early-onset group still showed a significantly higher frequency of depression, whereas tremor, akinesia, and rigidity were significantly more severe in the late-onset group. A stepwise regression analysis showed that in the early-onset group, depression scores were significantly correlated with scores of cognitive impairment and duration of the disease, while in the late-onset group, depression scores were significantly correlated with impairments in activities of daily living. These data suggest that depression in patients with early-onset PD may have a different etiology than in patients with late-onset PD.
Aged↗
Mood disorders following stroke: new findings and future directions.
Previous investigations by our group and others have demonstrated that poststroke depressions are not fully explained by the severity of associated impairment. We have consistently found, however, a strong association between development of major depression and left anterior brain injury. Recent studies have demonstrated that either left anterior cortical or subcortical lesions may lead to the development of major depression and that preexisting subcortical atrophy may play an important permissive role in the development of major depression. Patients with a mild degree of ventricular enlargement perhaps related to perinatal damage may be more likely to develop poststroke major depression following a lesion of the left frontal cortex or left basal ganglia than a patient without preexisting atrophy. Poststroke mania, on the other hand, is strongly associated with right hemisphere lesions as well as a preexisting subcortical atrophy and sometimes a family history of affective disorder. Thus, mania following brain injury may require the convergence of two factors: a right hemisphere brain injury and either a preexisting subcortical atrophy or a genetic vulnerability. PET scan findings have suggested that the biochemical response of the two hemispheres to stroke may be different. Right hemisphere stroke produces an increase in serotonin receptor binding, which is not found following comparable left hemisphere strokes. Within the left hemisphere, the lower the serotonin binding, the more severe the depression. This suggests that the right but not the left hemisphere may have an ability to increase serotonin binding in noninjured regions, producing a biochemical "compensation" for damage. This differential biochemical response to injury between the right and left hemisphere may partially explain why left hemisphere injury leads to depression and right hemisphere injury (in special circumstances) lead to mania. There remain, however, numerous unanswered questions and many important areas for future research. Although this area of neuropsychiatry is just beginning to develop, it is hoped that insights gained from studying mood disorders in brain-injured patients may also help to illuminate mechanisms involved in affective disorder in patients without brain injury.
Aged↗
Tricyclic antidepressants in the treatment of poststroke depression.
Depression is a serious complication of stroke. Although tricyclic antidepressants have well-established efficacy in the treatment of functional depression, they are not often used to treat depression following stroke. Studies have identified two types of depression in patients following stroke: major depression and minor depression. Longitudinal studies indicate that untreated major depression may last about 1 year, whereas untreated minor depression may last more than 2 years. Patients with depression who are not treated with antidepressant medication have been found to do more poorly on several measures of physical and cognitive rehabilitation than depressed patients who are treated. Two double-blind drug treatment studies of depression following stroke have been done. Although adverse side effects were reported in both studies, serious side effects were no more common in the active drug group than in the placebo group. Both studies, however, reported significantly better outcome, measured by depression scores or activities of daily living, in patients treated with nortriptyline or trazodone than in placebo-treated controls. Thus, although the use of antidepressant medication requires caution, the recognition and treatment of depression in patients who have had a stroke may result in a significant enhancement of both physical and cognitive recovery as well as emotional state.
Antidepressive Agents, Tricyclic↗
Contributing diagnoses in osteoporosis. The value of a complete medical evaluation.
Osteoporosis often occurs as a consequence of, or is accelerated by, many medical diseases, drug exposures, or other conditions. We called these conditions contributing diagnoses. Although technological advances permit the accurate measurement of bone density, identifying osteoporosis without searching for contributing diagnoses may result in remediable diseases being missed or in the initiation of inadvisable therapy. The value of comprehensive medical evaluation in conjunction with appropriate diagnostic studies was demonstrated in an osteoporosis referral center. We studied 300 consecutive persons who presented to an osteoporosis clinic. Using strict criteria, 180 patients (60%) had osteoporosis. Of these 180 patients, 83 (46%) had one or more contributing diagnosis, ie, a condition thought to accelerate bone loss. The largest single group was composed of persons with past or present exposure to glucocorticoids; the second largest group consisted of women who had undergone premature menopause. In all, 27 different contributing diagnoses were identified. Additionally, in 19 (11%) of the 180 patients with osteoporosis, a contributing diagnosis new to those patients was made. The evaluation of osteoporosis does not only entail measurement of bone density but must also take into consideration a patient's entire medical milieu.
Adult↗
Receptor characteristics and recovery of function following kainic acid lesions and fetal transplants of the striatum. I. Cholinergic systems.
The relationship between striatal muscarinic cholinergic receptor development and locomotor activity/T-maze alternation behavior in adult female rats with kainic acid lesions (kal) and fetal transplants of the striatum (str) was examined. Kal led to a number of deficits under conditions of spontaneous locomotion, including: (1) decreased stereotypical and increased horizontal movements during spontaneous overnight locomotion, (2) decreased spontaneous alternation on a T-maze, and (3) deficits on a sensorimotor neurological exam. Lesion-induced deficits following injection with cholinergic agonists (pilocarpine)/antagonists (scopolamine) included: (1) hypoactivity on vertical activity and stereotypical activity following scopolamine injection, and (2) increased stereotypical activity and decreased horizontal activity following pilocarpine injection. Transplants differentially affected the different types of behavioral deficits. Transplants reversed some of the deficits under conditions of spontaneous locomotion, including the hyperactivity noted during the night period, but only partially reversed the sensorimotor neurological exam and had no effect on spontaneous alternations in the T-maze. The transplants did not reverse the lesion-induced deficits following scopolamine injection, but partially reversed the lesion-induced changes in locomotion following pilocarpine injection. The striatal transplants had reduced numbers of M1 but increased numbers of M2 muscarinic cholinergic receptors. Cholinergic receptor density correlated with scores on the sensorimotor functioning and alternation tasks, but not with the locomotor measures. Conversely, the cross-sectional area of the str correlated strongly with the transplant-induced recovery in the lesion group. These results suggest that the development of cholinergic receptor systems within the transplants proceeds abnormally, and that the abnormal development of the transplant may impact on the transplant's ability to remediate lesion-induced deficits.
Animals↗