1/71. Cerebral arterial gas embolism in air force ground maintenance crew--a report of two cases.Two cases of cerebral arterial gas embolism (CAGE) occurred after a decompression incident involving five maintenance crew during a cabin leakage system test of a Hercules C-130 aircraft. During the incident, the cabin pressure increased to 8 in Hg (203.2 mm Hg, 27 kPa) above atmospheric pressure causing intense pain in the ears of all the crew inside. The system was rapidly depressurized to ground level. After the incident, one of the crew reported chest discomfort and fatigue. The next morning, he developed a sensation of numbness in the left hand, with persistence of the earlier symptoms. A second crewmember, who only experienced earache and heaviness in the head after the incident, developed retrosternal chest discomfort, restlessness, fatigue and numbness in his left hand the next morning. Both were subsequently referred to a recompression facility 4 d after the incident. Examination by the diving Medical Officer on duty recorded left-sided hemianesthesia and Grade II middle ear barotrauma as the only abnormalities in both cases. Chest x-rays did not reveal any extra-alveolar gas. Diagnoses of Static Neurological decompression Illness were made and both patients recompressed on a RN 62 table. The first case recovered fully after two treatments, and the second case after one treatment. magnetic resonance imaging (MRI) of the brain and bubble contrast echocardiography performed on the first case 6 mo after the incident were reported to be normal. The second case was lost to follow-up. decompression illness (DCI) generally occurs in occupational groups such as compressed air workers, divers, aviators, and astronauts. This is believed to be the first report of DCI occurring among aircraft's ground maintenance crew.- - - - - - - - - - ranking = 1keywords = brain (Clic here for more details about this article) |
2/71. melioidosis, an environmental and occupational hazard in thailand.melioidosis is a tropical environmental hazard that causes acute and chronic pulmonary disease, abscesses of the skin and internal organs, meningitis, brain abscess and cerebritis, and acute fulminant rapidly fatal sepsis. It is more common among adults, individuals with diabetes, and individuals with chronic renal disease, but it can occur in normal hosts and children. burkholderia pseudomellei is the most prevalent cause of community-acquired pneumonia, liver and splenic abscess, and sepsis in northeastern thailand. melioidosis can reactivate years after primary infection and result in chronic or acute life-threatening disease. With increasing worldwide travel and migration, patients may present in nonendemic countries with reactivation melioidosis decades after leaving an endemic region. We discuss seven selected patients presenting with this disease to a tertiary care facility in Bangkok between 1995 and 1997. awareness should allow early diagnosis and treatment, which can lead to decreased morbidity and mortality.- - - - - - - - - - ranking = 1keywords = brain (Clic here for more details about this article) |
3/71. Acute mercury vapour poisoning in a shipyard worker--a case report.Acute mercury vapour poisoning is a serious, potentially fatal but fortunately rarely encountered problem. It is most commonly due to industrial accidents. The vapour is a direct respiratory tract irritant as well as a cell poison, exerting its greatest effects in the lungs, nervous system, kidneys and liver. We present a case of mercury vapour poisoning in a shipyard workers presenting as an acute chemical pneumonitis, which resolved with aggressive supportive therapy. Further investigations later revealed transient mild neuropsychiatric symptoms, and residual peripheral neuropathy. No chelation therapy was instituted. The detailed investigative work that led to the discovery of the source of mercury is also presented. This case alerts us to the potential hazard to shipyard workers who may work in ships previously carrying oil contaminated with mercury. There have been no previous reports of mercury poisoning in shipyard workers. A high index of suspicion leading to early diagnosis and institution of appropriate supportive measures in suspected cases can be life-saving.- - - - - - - - - - ranking = 3.6398731257249keywords = nervous system (Clic here for more details about this article) |
4/71. Encephalomyeloradiculoneuropathy following exposure to an industrial solvent.A 19-year-old male developed complaints including weakness of the lower extremities and right hand, numbness, dysphagia and urinary difficulties following a 2 month exposure to an industrial solvent constituted mainly of 1-bromopropane, but also containing butylene oxide, 1,3 dioxolane, nitromethane, and other components. Nerve conduction studies revealed evidence of a primary, symmetric demyelinating polyneuropathy. Evidence of CNS involvement came from gadolinium enhanced MRI scans of the brain, showing patchy areas of increased T2 signal in the periventricular white matter, similar scans of the spinal cord revealing root enhancement at several lumbar levels, and SSEP studies. The patient's symptoms had started to resolve following the discontinuation of the exposure, before he was lost to follow-up. Similar findings have been reported following 1-bromopropane exposure in rats. I hypothesize that this patient's symptoms may have been due to 1-bromopropane-induced neurotoxicity.- - - - - - - - - - ranking = 1keywords = brain (Clic here for more details about this article) |
5/71. A possible association between exposure to n-hexane and parkinsonism.Recently, some case-control studies and case reports have shown an association between solvent exposure and parkinsonisms. We present a 55-year-old male parkinsonian patient with chronic exposure to n-hexane for 17 years. The results of neurophysiological (electromyography, evoked potentials), neuroradiological (MRI) and neuropsychological tests performed on the patient suggest a role of this solvent at the level of the central nervous system. Biological susceptibility to neurotoxic compounds is discussed briefly.- - - - - - - - - - ranking = 8.606098354322keywords = central nervous system, nervous system (Clic here for more details about this article) |
6/71. carbon disulfide nephropathy.A 45-year-old nondiabetic man presented with features resembling diabetic triopathy. He worked in a rayon manufacturing plant and was exposed to toxic levels of carbon disulfide (CS(2)). Clinical abnormalities included peripheral and central nervous system abnormalities as well as retinopathy, dyslipidemia, cardiovascular disease, and nephrotic syndrome. He later developed focal sclerosing glomerulonephritis. The latter has not previously been described in cases of CS(2) exposure. Terminally, he developed end-stage renal disease and progressive dementia, both of which were thought to be consequences of CS(2) exposure earlier in life.- - - - - - - - - - ranking = 8.606098354322keywords = central nervous system, nervous system (Clic here for more details about this article) |
7/71. carbon disulfide vasculopathy: a small vessel disease.We present the clinical manifestations of 4 male patients with acute stroke-like symptoms and polyneuropathy after long-term exposure to carbon disulfide (CS2) in a viscose rayon plant. The ages of onset of polyneuropathy ranged from 42 to 45 years with a duration of CS2 exposure between 6 and 21 years. The ages of onset of stroke were from 42 to 48 years. The risk factors for stroke including heart disease and diabetes were denied, except for smoking in 4, hyperlipidemia in 2 and hypertension in 1. At the initial visit in 1992, only 2 patients developed sudden onset of hemiparesis suggesting a lacunar stroke before the diagnosis of CS2 intoxication. Brain computed tomography (CT) scans showed low-density lesions in the basal ganglia in 2 patients, cortical atrophy in 1 and normal in 1. Brain magnetic resonance image (MRI) study disclosed multiple lesions in the corona radiata and basal ganglia on T(2)-weighted images in 3 patients and cortical atrophy in 1. After the diagnosis, they left their jobs for a CS2-free environment, and improvement of the working conditions was noted. During 5 years follow-up period, another 2 patients also developed an acute episode of stroke with hemiparesis. Brain CT and/or MRI follow-up studies in these 2 patients revealed new lesions in the basal ganglia and corona radiata. Intriguingly, a patient with previous stroke also developed new lesions in the bilateral thalami and brainstem. Carotid Doppler scan, transcranial Doppler scan and/or cerebral angiography did not show any prominent stenosis or occlusion in the major intracranial large arteries. We conclude that encephalopathy may occur in patients after long-term CS2 exposure, probably due to impaired cerebral perfusion. The lesions tend to occur in the basal ganglia, corona radiata and even brainstem, particularly involving the small-sized vessels. In addition, the cerebral lesions may progress even after cessation of CS2 exposure. Therefore, we suggest that CS2 exposure may be a risk factor for stroke.- - - - - - - - - - ranking = 2keywords = brain (Clic here for more details about this article) |
8/71. amyotrophic lateral sclerosis in a battery-factory worker exposed to cadmium.A 44-year-old patient died from amyotrophic lateral sclerosis (ALS) after nine years of heavy exposure to cadmium (Cd) in a nickel cadmium (Ni-Cd) battery factory. Two years after starting work he and co-workers had experienced pruritus, loss of smell, nasal congestion, nosebleeds, cough, shortness of breath, severe headaches, bone pain, and proteinuria. Upper back pain and muscle weakness progressed to flaccid paralysis. EMG findings were consistent with motor neuron disease. Cd impairs the blood-brain barrier, reduces levels of brain copper-zinc (Cu-Zn) superoxide dismutase (SOD), and enhances excitoxicity of glutamate via up-regulation of glutamate dehydrogenase and down-regulation of glutamate uptake in glial cells. High levels of methallothionein, a sign of exposure to heavy metals, have been found in brain tissue of deceased ALS patients. The effects of Cd on enzyme systems that mediate neurotoxicity and motor neuron disease suggest a cause effect relationship between Cd and ALS in this worker.- - - - - - - - - - ranking = 3keywords = brain (Clic here for more details about this article) |
9/71. Neuro-ototoxicity in andean adults with chronic lead and noise exposure.Brainstem auditory evoked responses and audiological thresholds were used as biomarkers for neuro-ototoxicity in adults with chronic lead (Pb) intoxication from long-term Pb exposure in ceramic-glazing work. Venous blood samples collected from 30 adults (15 men and 15 women) indicated a mean blood Pb level of 45.1 micrograms/dL (SD, 19.5; range, 11.2 to 80.0 micrograms/dL) and in excess of the world health organization health-based biological limits (men, 46.2 micrograms/dL; SD, 19.6; range, 18.3 to 80.0 micrograms/dL; women, 44.0 micrograms/dL; SD, 20.1; range, 11.2 to 74.2 micrograms/dL). Mean auditory thresholds at frequencies susceptible to ototoxicity (2.0, 3.0, 4.0, 6.0, and 8.0 kHz) revealed sensory-neural hearing loss in men, which may be attributable to occupational noise exposure in combination with Pb intoxication. Bilateral brainstem auditory evoked response tests on participants with elevated blood Pb levels (mean, 47.0 micrograms/dL) showed delayed wave latencies consistent with sensory-neural hearing impairment. The results suggest that environmental noise exposure must be considered an important factor in determining sensory-neural hearing status in occupationally Pb-exposed adults.- - - - - - - - - - ranking = 1keywords = brain (Clic here for more details about this article) |
10/71. Loss of postural reflexes in long-term occupational solvent exposure.inhalation of organic solvents has long been known to damage various nervous systems, including cerebellum, brainstem, and pyramidal tract. However, little is known about the damage of the dopaminergic system. We report two patients with occupational long-term solvent exposure who developed postural instability without other features of parkinsonism. The concentration of HVA in CSF was decreased and the retropulsion was dramatically improved after the administration of levodopa. These findings indicate that the nigrostriatal dopaminergic neurons were disturbed by chronic solvent exposure, resulting in the loss of postural reflexes.- - - - - - - - - - ranking = 4.6398731257249keywords = nervous system, brain (Clic here for more details about this article) |
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