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Biomedical subjects

J H Dougherty

Publications and source records attributed to J H Dougherty.

At least 19 recordsLinked to original sources
PubMed1993

Posterior cortical atrophy in Alzheimer's disease: analysis of a new case and re-evaluation of a historical report.

Disturbances of visual function are not uncommon in Alzheimer's disease and several cases with complex impairment of visuospatial abilities have been described. For instance, posterior cortical atrophy has been demonstrated in cases displaying Balint's syndrome as the first symptom of the dementing illness. Such cases showed very high lesion counts in the occipital cortex, as well as in visual association regions in the posterior parietal and posterior cingulate cortex, whereas the prefrontal cortex was consistently less severely involved than usually observed in Alzheimer's disease. This suggests that the distribution of the lesions had been shifted to specific elements of the visual system. In the present study, we report the quantitative analysis of a new case of Alzheimer's disease with possible Balint's syndrome and re-evaluate a case originally described in 1945. The distribution of lesion in these two cases parallels previous observations of Alzheimer's disease cases with early visual impairment. Both cases displayed very high densities of neurofibrillary tangles and senile plaques in the primary visual cortex, secondary visual cortex, visual association areas of the dorsal occipital and posterior parietal lobe and in the posterior cingulate cortex, whereas the prefrontal and inferior temporal regions were comparatively less affected. These cases may define clinical subgroups of Alzheimer's disease and suggest that the breakdown of corticocortical projections that is known to occur in dementia may involve select components of specific functional systems in certain cases. In particular, pathways that subserve motion detection and visuospatial analysis appear to be dramatically affected in these cases presenting with Balint's syndrome.(ABSTRACT TRUNCATED AT 250 WORDS)

Adult↗
PubMed1991

Effect of hypoxia on psychomotor performance during graded exercise.

We evaluated the combined effects of reduced O2 (12%) and graded ergometer exercise (10, 70, and 140 W) on the performance of a psychomotor task. Six men participated in two test sessions each. Each session began with the baseline data (air) and finished with exposure data (12% or 21%, random, unidentified). The gas mixtures were air (control condition) and 12% O2-balance N2 (12% O2 condition). The psychomotor task score was degraded during the 140 W work rate of the 12% O2 condition (p less than 0.05). Reductions of the SaO2 (p less than 0.05) at each work rate proved that hypoxia existed during exercise in the 12% O2 condition. The arterial blood gases indicated that respiratory alkalosis was mixed with metabolic acidosis during the hypoxic exercise. The results differ from previously reported findings of an arousal effect of exercise on psychomotor performance and the decrement of task performance at work rates less than or equal to 50 W. We conclude that hypoxia degraded the performance of the psychomotor task during graded exercise.

Adult↗
PubMed1987

A new technique to improve cortical-evoked potentials in spinal cord monitoring. A ratio method of analysis.

Systemic effects such as anesthesia, hypotension, hypothermia, and hypoxia affect the cortical evoked responses. We propose, that by sequential stimulation of the median and posterior tibial nerves, and the construction of a ratio from the value of their amplitudes, the systemic effects can be eliminated and thus improve the reliability of the cortical evoked responses. Two groups of scoliosis patients who underwent spinal surgery with instrumentation were analyzed retrospectively. Both groups had spinal cord monitoring using peripheral nerve stimulation and cortical recordings of the somatosensory-evoked response (SER). In Group I, 50 patients were analyzed for changes in posterior tibial nerve response before and after distraction. Wide variability in the response suggested this method to be less reliable in predicting spinal cord conduction deficits. Thirty-eight patients in Group 2 were analyzed using both the median and posterior tibial nerve amplitudes. A ratio of the posterior tibial to median nerve wave amplitude was constructed, thus eliminating any systemic variables. A critical value, alerting the surgeons to possible decreases in spinal cord conduction, was calculated by subtracting one standard deviation from the mean of the postdistraction ratios of the posterior tibial to median nerves (1.20-.633 = .567).

Adult↗
PubMed1987

Progression of and recovery from pulmonary oxygen toxicity in humans exposed to 5 ATA air.

Animal studies suggest that pulmonary oxygen toxicity proceeds more slowly in diluted oxygen breathing mixtures than in pure oxygen at the same inspired partial pressure. We exposed 12 healthy subjects to air at 5 ATA (PiO2 = 1.05 ATA) in a hyperbaric chamber for 48 h, and compared the rate of development of symptoms of O2 toxicity to rates seen in previous studies using 100% O2 at 1 ATA. Symptoms consisted of chest tightness, cough, substernal discomfort, exertional dyspnea, anorexia, nausea and vomiting, headache and digital paresthesias starting at about 12 h, and continuing several days into the recovery period. Pulmonary function changes consisted of significant decrements in vital capacity, flow rates, and DLCO. Initial recovery was in a 0.50 ATA oxygen atmosphere, with the majority of subjects showing definite recovery in both symptoms and pulmonary function. Subjects showed complete recovery in about 8 d, although symptoms of fatigue and exertional dyspnea continued for a month in some cases. In contrast, none of the above changes were noted in an additional 6 subjects exposed to a 5 ATA environment with 6% oxygen (PiO2 = 0.30 ATA). No change in resting gas exchange, as indicated by alveolar-arterial oxygen gradients, was detected in either group. Comparison of these data to that for pure oxygen studies reveals no significant difference in the progression or character of pulmonary oxygen toxicity.

Adult↗
PubMed1983

Plasma immunoreactive beta-endorphin levels in depression. Effect of electroconvulsive therapy.

Immunoreactive (ir) plasma beta-endorphin level was assayed in ten symptomatic patients with a unipolar major depressive disorder and in 16 psychiatrically normal controls matched for age and sex. Plasma ir-beta-endorphin level in depressed patients was similar to that in controls. All depressed patients was similar to that in controls. All depressed patients had a transient, approximately threefold increase in ir-beta-endorphin after each use of electroconvulsive therapy (ECT). The increase of plasma ir-beta-endorphin level after ECT parallels the transient elevation of adrenocorticotropic hormone level reported by others and probably reflects a hypothalamic response to ECT.

Adrenocorticotropic Hormone↗
PubMed1982

Experimental cerebral ischemia produced by extracranial vascular injury: protection with indomethacin and prostacyclin.

To determine whether the production of brain ischemia is modified by antiplatelet agents administered at the time of extracranial endothelial injury, we modified a four-vessel occlusion rat model so that an electrogenic platelet thrombus in one carotid artery produced cerebral ischemia. DC current was passed through an anode around the left carotid artery of 11 rats with preoccluded vertebral and contralateral carotid arteries. Five of six untreated rats became unresponsive because of carotid occlusion and resultant cerebral ischemia; none of five animals pretreated with indomethacin and infused with prostacyclin (PGI2) were clinically affected. Light- and electronmicroscopic studies showed arterial platelet-fibrin thrombi and ischemic brain damage in untreated rats. All rats had received radiolabeled platelets; radioactivity was increased in the electrogenically injured left carotid arteries from treated and untreated rats, but counts were reduced by more than 80% in indomethacin/PGI2-treated rats (p less than 0.01).

Animals↗
PubMed1981

Evaluation of acute cerebral ischemia for anticoagulant therapy: computed tomography or lumbar puncture.

Of 217 patients with clinical diagnosis of acute stroke 23% had nonischemic lesions diagnosed by computed tomography (CT) or lumbar puncture (LP). CT demonstrated all 37 cases of intracerebral hemorrhagic lesions; 9 were detected by LP. CT failed to demonstrate 8 of 17 cases of subarachnoid hemorrhage, but only 1 of these lacked headache or stiff neck. In 7 of 342 patients who were treated with anticoagulants after LP, spinal hematoma followed LP ( 5 with paraparesis). CT evaluation reduced the incidence of fatal cerebral hemorrhage during anticoagulant therapy of acute stroke. However, even if patients were evaluated with both CT and LP, the incidence of fatal cerebral hemorrhage resulting from intravenous anticoagulant therapy was 2.4%.

Anticoagulants↗
PubMed1981

Hypoxic-ischemic brain injury and the vegetative state: clinical and neuropathologic correlation.

We studied 10 patients who survived for 2 to 8 weeks in a vegetative state, including 8 with cardiopulmonary failure and 2 with subarachnoid hemorrhage. Within days of onset, they regained brainstem function and awoke, but none had evidence of cognitive awareness. All patients opened their eyes within 2 weeks, and eight had roving conjugate eye movements. Pupillary and corneal responses were intact within 1 week, and seven patients had tonic oculovestibular responses (OVR) within 24 hours. By the end of 1 day, only three patients failed to move limbs in response to noxious stimuli. At postmortem, all patients had widespread ischemic neuronal damage in the cerebral hemispheres. The brainstems lacked morphologic abnormality, except that one patient had a single microinfarct in the superior colliculus.

Adult↗
PubMed1979

Experimental cerebral ischemia produces platelet aggregates.

Human studies indicate that transient platelet abnormalities accompany acute cerebral ischemia. Although these abnormalities may precipitate the ischemi process, ischemia could also alter platelet function. Platelets were therefore studied in gerbils subjected to 1 hour of unilateral carotid artery occlusion. Venous blood from five clinically affected gerbils contained more aggregated platelets (37.8% +/- 6.4) than did blood from eight unaffected animals (11.1% +/- 3.0; p less than 0.01). Platelets labeled with 3H-serotonin were increased in ischemic brain; the ratio of radioactivity in the ipsilateral versus contralateral hemisphere was greater in eight affected (1.09 +/- 0.03) than in 19 unaffected (1.00 +/- 0.01; p less than 0.02) animals. The radioactive serotonin was located predominantly within blood vessels. Cerebral ischemia thus stimulated the formation of platelet aggregates, a response which could contribute to the ischemic process.

Animals↗
PubMed1979

Effect of intermittent exposure to 3% CO2 on respiration, acid-base balance, and calcium-phosphorus metabolism.

One subject was exposed for six days to increasing levels of CO2, rising at a constant rate from 0.03 to 3.0% CO2 within a 15-h period followed by 9 h of air breathing. To assess acid-base parameters, arterialized capillary blood was taken from a finger twice daily (at 8 a.m. and 11 p.m.) at times corresponding to the beginning and end of the intermittent exposure to CO2. Venous blood samples were obtained on alternate days at the same times. Urine specimens were collected twice daily. The subject was on a liquid diet. Resting respiratory minute volume (VE), oxygen consumption (VO2), carbon dioxide excretion (VCO2), alveolar carbon dioxide and oxygen tension (PACO2) and PAO2) were measured twice daily. PACO2 and PAO2 were also determined at the end of breath-holding twice daily; CO2 tolerance tests and lung function tests were also carried out. In contrast to the effects of chronic exposure to 3% CO2, the CO2 tolerance tests showed an increased sensitivity (increase of slope) and breath-holding PACO2 did not change, indicating that acclimatization to CO2 did not develop. The ventilatory response to CO2 was not sufficient to prevent CO2 accumulation in the body; this accumulation was eliminated during the nightly air-breathing periods on the fourth and fifth days, indicated by higher values of PaCO2 and PACO2. The known renal response to hypercapnia, consisting of an increased excretion of titratable acidity, ammonia, and hydrogen ion excretion, occurred but was interrupted after the first day and was triggered again on the fourth and fith days when accumulated CO2 was released from body CO2 stores. The second renal response was associated with a marked calcium excretion, which suggests that bone CO2 stores were involved.

Acid-Base Equilibrium↗
PubMed1978

Neoplastic angioendotheliosis: ultrastructural study and review of the literature.

Neoplastic angioendotheliosis is a rare disorder characterized by progressive multifocal neurological deficit and dementia. The principal pathological findings are multiple infarcts in the brain and spinal cord and the microscopical demonstration of proliferated neoplastic cells, primarily within the lumens of arteries, arterioles, and capillaries. Vessels of the central nervous system are the most severely affected and appear to be the primary site of neoplastic proliferation. Systemic intravascular and focal extravascular proliferation can also be identified. The endothelial origin of the neoplastic cell with a gradation of changes from normal to neoplastic is demonstrated by the electron microscopical study of involved meningeal vessels. Our patient and those reported in the literature all demonstrate involvement of the central nervous system. In addition, an elevated cerebrospinal fluid protein level is present in all patients for whom that information is available, and fever and renal involvement are frequently present. Steroid therapy is generally ineffective. If the disease is suspected clinically, our studies suggest that meningeal biopsy is the diagnostic procedure of choice to help determine whether chemotherapy should be instituted.

Aged↗
PubMed1978

Complications following intraspinal injections of steroids. Report of two cases.

Intrapinal steroids have been recommended for the treatment of sciatica and various other conditions. The procedure is controversial; moreover, evidence suggests that the steroid hormones can be delivered to the site of inflammation more easily by systemic administration. Serious complications that have arisen from the procedure are reviewed. The courses of two women who received intraspinal steroids for the treatment of sciatica and who developed severe meningitis as a consequence are reported. It is suggested that the value of intraspinal steroids in the treatment of disc-related sciatica is unproven and if they are used, one must be alert to the complications.

Adult↗
PubMed1977

Platelet activation in acute cerebral ischaemia. Serial measurements of platelet function in cerebrovascular disease.

Circulating platelet aggregates formed in vivo were serially measured, and platelet-aggregation thresholds were determined in vitro in 82 patients with acute cerebral ischaemia. The percentage of aggregated platelets was increased in 53 patients with completed stroke (30.9% +/- 2.0) and in 29 patients with transient ischaemic attacks (34.1% +/- 2.3), all studied within 10 days of the acute event. These values were higher (P less than 0.001) than levels of aggregated platelets in 30 patients with non-vascular neurological disease (16.8% +/- 2.3). The percentage of aggregated platelets returned to normal 10 days to 6 wk after acute cerebral ischaemia. Aspirin and dipyridamole did not affect either the increase in or subsequent normalisation of circulating-platelet-aggregate levels in these patients. Platelet-aggregation sensitivity to adenosine diphosphate and adrenaline was also increased in patients with acute cerebral ischaemia, but this abnormally resolved during convalescence. Platelet activation is abnormal in acute cerebral ischaemia but usually returns to normal with or without anti-platelet therapy. This activation of platelets may contribute to the clinical manifestations of occlusive vascular disease.

Acute Disease↗
PubMed1976

Use of H2 as an inert gas during diving: pulmonary function during H2-O2 breathing at 7.06 ATA.

A review of the characteristics of hydrogen as an inert gas for use in diving is presented, with special emphasis on the extension of the respiratory limitation in diving by use of this least dense of all gases. Forced vital capacity, FEV1, FEV2, PEFR, PIFR, and MVV were measured on groups of subjects using the following gas mixtures, all at 7.06 ATA: four subjects breathing 97% H2-3% O2, two subjects breathing 97% He-3% O2, and two subjects using 97% N2-3% O2. The MVV while breathing H2-O2 at 7.06 ATA was 14% higher than with air at the surface, and was improved 40% compared with He-O2 and 171% when compared with N2-O2 at 7.06 ATA. Similar findings were obtained for FEV1, FEV2, PEFR, and PIFR. The values in this study for the relationship of relative gas density (rho) to flow are rho-0.41 for MVV, rho-0.44 for PEFR, and rho-0.45 for PIFR (method of Wood and Bryan).

Atmospheric Pressure↗