Diffuse Sclerosis

Question: I have been experiencing blurred vision, eye pain and feeling unstable whenever I look around.? I have been experiencing blurred vision, eye pain and feeling unstable whenever I look around and change eyesight direction. This has been happening sporadically but today is the worst it has been. I feel pressure in my eyes, anyone have any suggestions as to the cause? I am worried I may actually have Multiple Sclerosis, I have almost every symptom but have never been tested. I have been to a neurologist and had my spine examined and an MRI done. The Dr said my chronic pain and symptoms of nerve damage are caused by my spine (tests done in the office) but the MRI showed nothing significant to explain the back pain, nerve pain and muscle spasms leaving them to just call it fiblomyalgia and call it a winner. I am on methadone for the pain, with a prescrition for Soma for the spasms. The Soma (when I take it) does hardly anythng for my pain, which is diffuse and "moves" around with no rhyme or reason.

Answer: I don't have any medical expertise but I have MS and have learned a lot about optic neuritis. I highly recommend seeing an eye doctor asap! Ask him about Optic Neuritis. I hope this helps. Don't give up until you figure out what is going on.

Question: MS Cause? What causes it? From the publishers of The New England Journal of Medicine December 7, 2006 Past Lead Exposure and Brain Lesions A dose-response relation was found between past lead exposure and brain lesions on MRI scans. Despite decades of research on lead poisoning, few data are available on the effects of occupational exposures on brain structures. In 532 former organolead workers (mean age, 56; mean time since last exposure, 18 years), researchers evaluated the associations between cumulative lead dose and MRI measures of white matter lesions and of total and region-specific brain volumes. They measured tibia lead levels, which reflect long-term stores but decline over time after exposure ends. They estimated peak tibia level (PTL) from the time since last exposure. PTL was significantly associated with both the prevalence and the severity of white matter lesions. Higher PTL was significantly related to reduced volumes in 6 of 20 areas measured: total brain, total gray matter, parietal white matter, frontal gray matter, insula, and cingulate gyrus. Final models were adjusted for age, education level, APOE genotype, and height, although numerous other potential confounders were considered, including smoking, alcohol use, and race. The authors conclude that past exposures to lead resulted in persistent global and region-specific brain lesions, perhaps mediating the progressive decline that they had previously observed in the workers on tests of verbal memory and learning, visual memory, and executive function. Comment: Accumulating data suggest that lead exposure contributes to age-related cognitive decline and neurodegeneration. Among the relevant pathogenetic processes in which lead has been implicated are mitochondrial dysfunction, oxidative stress, deregulation of protein turnover, and brain inflammation. Limited evidence suggests that the APOE 4 allele increases susceptibility to lead neurotoxicity (Environ Health Perspect 2002; 110:501), and elevated brain lead levels have been found in patients with diffuse neurofibrillary tangles with calcification (Neuroreport 2001; 12:3887). In rodents and primates, developmental lead exposure produces delayed overexpression of the amyloid precursor protein and aggregated beta-amyloid peptides (Rev Neurosci 2005; 16:325). To date, most attention has focused on the effects of lead on children. Apparently, much remains to be learned about the effects of lead on our aging population. - David C. Bellinger, PhD Dr. Bellinger is Senior Research Associate in Neurology, Children's Hospital; Professor, Department of Environmental Health, Harvard School of Public Health; and Professor of Neurology, Harvard Medical School, Boston. Published in Journal Watch Neurology December 5, 2006 Citation(s): Stewart WF et al. Past adult lead exposure is linked to neurodegeneration measured by brain MRI. Neurology 2006 May 23; 66:1476-84. [Original article][Medline abstract] --------------------------------------… Multiple Sclerosis and the Petrochemical industry have been linked in many studies -- and as our gasoline used to contain lead, and my first symptoms started when I was cleaning out the Gulf oil refinery in North Burnaby in 1974, just a little numbness in my right hand' s fingertips, I thought that perhaps there are other people who could connect their MS with petrochemicals. The gunk I was cleaning out, the sludge at the bottom of those huge white tanks you see in refineries, contained lead and a lot of other toxic chemicals that were added to gasoline in the 1970s. There are a lot of other symptoms which I have that are connected, or could be connected, with toxic chemicals particularly lead. I had my blood level lead analyzed recently -- and it's okay now. And I haven't progressed for at least six years -- all the lead has been flushed out by now. But the damage remains. And just because they eliminated lead in gasoline, doesn't mean that they've rid our environment of environmental poisons -- in fact they've probably added more than they've taken out! A friend of a friend of mine, suffers from MCS -- Multiple Chemical Sensitivity -- he really does, it's been confirmed by the UBC neurology clinic, well anyways, he says that Febreeze was derived from Agent Orange of the Vietnam era -- and he confronted, via telephone, the lab that had developed Febreeze and asked why??? "Why are you doing this when you know it's dangerous???" And the answer was a mumbled explanation that "The consumers wanted a product like Febreeze." We've come a long way in the last 50 years -- but for every gain, there are sacrifices. As an afterthought, I think Multiple Sclerosis should be renamed "demyelination of unknown etiology" -- but I don't think I'll get anywhere. __________________ richardlong@telus.net Vancouver, BC, Canada Telephone: 604 301 1606

Answer: I haven't come across anything conclusive with regard to MS and I did an assignment/presentation on the topic while studying for my science degree. The best I can do is point you in the direction of some websites that might be helpful.

Question: What is the cause of death? I'm not able to slove this case(I'm a student,and this ia not homework,my teacher offers me a challenge) a 71 year old woman, who spent the last two days of her life in hospital having been admitted from a nursing home with diffuse abdominal pain and increasing temperature. Upon admission, she was treated with oral antibiotics, but continued to deteriorate rapidly until suffering a respiratory arrest in the early hours of the morning. In accordance with her own and the family's wishes, resuscitation was not attempted and she died. The nursing home records show that the patient had been investigated for Multiple Sclerosis but this diagnosis was not confirmed. She had spent the last two years as a full-time resident in the nursing home as the family did not live locally and she found it difficult to manage on her own. CENTRAL NERVOUS SYSTEM The scalp, skull and meninges were normal, with no evidence of internal bruising or bleeding. The brain weighed 1100g and appeared norm with no evidence of cerebral oedema or infarction. No focal lesions were identified. ENDOCRINE SYSTEM The adrenals were very small, but appeared otherwise normal. The thyroid appeared normal, with no evidence of tumour or enlargement. CARDIOVASCULAR SYSTEM The pericardium was normal. The heart weighed 350g and the atria and ventricles appeared normal on sectioning (see images below). All cardiac valves were normal; there was a small amount of calcification in the pulmonary valve. There was a minimal amount of atheroma present in the coronary arteries. Uncomplicated atheroma was present in the aorta and other large systemic arteries, but none of the vessels affected were narrowed or occluded in any way. RETICULO-ENDOTHELIAL SYSTEM The spleen was small, but otherwise normal, with a nodular external appearance and normal cut surface Lymph nodes, where found, appeared normal. EXTERNAL EXAMINATION The body was of an elderly woman of medium build. No scarring Distended abdomen Pitting oedema of the ankles MUSCULO-SKELETAL SYSTEM There was marked wasting of the muscles of the hands, with flexion contractures of the muscles of the upper arms - not to be confused with rigor mortis, which disappears a few days after death. The bone of the ribs, vertebral bodies and spine was easily cut through and very fragile, indicating long-standing osteoporosis. No fractures were noticed anywhere. GENITO-URINARY SYSTEM Both kidneys weighed 160g and had smooth capsular surfaces, which stripped easily. Both kidneys had a normal appearance on cut surfaces, with a well- defined cortico-medullary junction. The ureters and bladder appeared normal. GASTROINTESTINAL SYSTEM The mouth and tongue were normal. The oesophagus was normal, but there was some evidence of gastric reflux in the lower third. On cutting into the peritoneal cavity, foul-smelling gas escaped under some pressure. As you can clearly see in the image below (left), there was approximately three litres of foul-smelling, green-brown liquid in the peritoneal cavity; this seems to have covered the whole of the abdominal contents, and caused the omentum to become green and stick to the abdominal wall in several areas. The image on the below (right) shows the peritoneal cavity once the fluid was removed. The stomach showed evidence of gastritis, and the duodenum was inflamed about 10cm from the pyloric sphincter. A small hole, about 1.5cm in diameter, was found at the centre of the inflamed area; there was a streaky area of fat necrosis around the hole on the external surface of the duodenum. The rest of the small intestine was adherent to the omentum. The liver weighed 1200g and had a normal external appearance and cut surface A large (2cm diameter) stone was present in the extrahepatic bile duct (image below-left); the gall bladder itself was distended and contained several large gallstones The pancreas was normal. RESPIRATORY SYSTEM The larynx and trachea were normal. Both lungs appeared very small; as you can see, both of the lungs are much smaller than the pericardial sac - they would normally extend either end of the pericardial sac if the heart and lungs were taken out together in a normal specimen. The right lung weighed 370g and the left lung weighed 330g. They were also rather dense and floppy. On sectioning, the lungs appeared free from fluid and other secretions; the bronchi were also clear of secretions. There were no emboli or stenoses in the pulmonary vessels. There was a small bilateral pleural effusion of about 50mls on each side. I contacted my Teacher some moments ago stating that I suspect that her cause of death is Perforated duodenal ulcer. However he replied that I'm close, but not quite there.He said that the duodenal ulcer was the underlying cause of death in this patient; gastric contents escaped through into the peritoneal cavity via the perforation. However, the ulcer in itself didn't kill the patient.He gave me a clue,what would three litres of bacteria-laden intestinal contents do to the peritoneum assuming the ulcer wasn't picked up the moment it perforated?

Answer: Did her appendix burst?