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Showing posts with label Unable. Show all posts
Showing posts with label Unable. Show all posts

Thursday, July 11, 2013

Primary Care Physicians Unable to Form Early Diagnosis of Cervical Spondylotic Myelopathy


This is an important finding, because previous studies have shown that early diagnosis and treatment of CSM lead to better outcomes. The majority of patients initially sought a diagnosis for their symptoms from family physicians, who arrived at a correct diagnosis in only 4.8% of cases and never at the first clinic visit. Many other patients initially consulted community-based orthopedic surgeons, only one of whom suspected CSM at the first visit. Detailed findings of this study are reported and discussed in the article "Delayed diagnosis of cervical spondylotic myelopathy by primary care physicians," by Eyal Behrbalk, M.D., Khalil Salame, M.D., Gilad J. Regev, M.D., Ory Keynan, M.D., Bronek Boszczyk, Dr. Med., and Zvi Lidar, M.D., published today, in the July 2013 issue of Neurosurgical Focus.

Cervical spondylotic myelopathy (CSM) has been called the most common form of spinal cord dysfunction in older adults, although it can occur in younger people due to injury. As we age, vertebral joints in our necks begin to show wear (cervical spondylosis) and cervical spine ligaments thicken. These changes cause the spinal canal to narrow, which can lead to compression of the spinal cord. As spinal cord compression increases, nerve cells die, resulting in symptoms of cervical myelopathy that range from mild neck pain to motor weakness, sensory loss, impaired walking, and, in cases of advanced disease, loss of bladder and bowel control. CSM is a progressive disease. Surgery is indicated when there is neurological impairment. Studies have shown that outcomes of surgery are best when the operation is performed during the early stages of the disease, when neurological impairment is minimal.

Between January 2009 and December 2010, 146 patients underwent surgery for CSM at The Spine Unit of Tel-Aviv Medical Center, a tertiary care center. All cases of degenerative pathological conditions of the cervical spine were included. Complete medical records (from both the Center and community-based physicians' offices) were available for 42 patients, and these patients comprised the study population. The researchers collected data from the time the first signs or symptoms of CSM were documented until the date of surgery. The diagnosis of CSM was based on the following: 1) symptoms consistent with CSM; 2) neurological findings suggestive of myelopathy; and 3) MRIs showing compression of the cervical spinal cord. In addition to the review of medical records, phone interviews with patients were conducted to obtain any missing clinical data.

Behrbalk and colleagues found that 69% of patients initially sought a diagnosis for their symptoms from family physicians and 21.4% from community-based orthopedic surgeons. The remaining patients consulted other physicians, none of whom was a neurologist or neurosurgeon, the most likely to recognize the disease. The researchers state that this follows the normal pattern of physician visits in Israel, where patients can directly schedule appointments with family physicians and orthopedic surgeons but require referrals to see neurologists or neurosurgeons. During the first physician visit, only one doctor?an orthopedic surgeon?suspected that CSM could be the underlying cause of the patient's symptoms.

At the second physician visits, most patients went to orthopedic surgeons (48.8%) and family physicians (26.8%); far fewer saw neurologists (9.8%) or neurosurgeons (2.4%). At the third physician visit, patients continued to consult orthopedic surgeons most frequently (38.5%), but more patients sought out neurologists (25.6%) and neurosurgeons (18%) than before; 12.8% of patients returned to family physicians.

In this study, Behrbalk and colleagues found that it took a mean of 5.2 ? 3.6 physician visits to obtain the correct diagnosis of CSM. In the end, the diagnosis was made most often by neurosurgeons (38.1%) and neurologists (28.6%), and less frequently by orthopedic surgeons (19%), family physicians (4.8%), and a variety of other specialists (9.5%). The delays in diagnosis in this study, according to the researchers, rest primarily on a lack of awareness of CSM on the part of family practitioners and community-based orthopedic surgeons, who did not conduct full neurological examinations that could indicate myelopathy.

Given that CSM is a progressive disease, the researchers point out that delays in diagnosis can mean that "patients are referred to surgery at an advanced stage of the disease, at which point they are suffering from severe, often irreversible neurological damage."

Behrbalk and colleagues call for continued education of family practitioners and community-based orthopedic surgeons to make them more aware of CSM and promote early referrals for surgery when patients present with CSM symptoms.

Source-Eurekalert


View the original article here

Thursday, June 6, 2013

Highly Respected Research Teams Unable to Confirm High-profile Alzheimer's Study


Those results, presented online Feb. 9, 2012, suggested that the drug bexarotene (marketed as Targretin?) could rapidly reverse the buildup of beta amyloid plaques (Aβ) ? a pathological hallmark of Alzheimer's disease ? in the brains of mice. According to the authors of the 2012 report, drug treatment quickly removed most of the plaques and brought rapid reversal of the pathological, cognitive and memory deficits related to the onset of Alzheimer's.

However, the new reports from extensive and carefully controlled studies did not show any reduction in the number of plaques or total area occupied by the plaques during or after treatment. These results are described in three "technical comments" ? one of which comes from researchers at the University of Chicago, Northwestern University, Massachusetts General Hospital, Washington University in St Louis and University of Tubingen in Germany ? to be published in the May 24, 2013, issue of Science.

"The drug has no impact on plaque burden in three strains that exhibit Aβ amyloidosis," according to that group's comment. "We have failed to support earlier findings by Cramer et al that Targretin is efficacious in reducing plaque burden in transgenic mouse models of cerebral Aβ deposition."

Comment co-author Sangram Sisodia, PhD, professor of neurosciences at the University of Chicago, said he and his colleagues were curious about the initial report in 2012.

"We were surprised and excited, even stunned, when we first saw these results presented at a small conference," said Sisodia. "The mechanism of action made some sense, but the assertion that they could reduce the areas of plaque by 50 percent within three days, and by 75 percent in two weeks, seemed too good to be true."

"We all went back to our labs and tried to confirm these promising findings," Sisodia added. "We repeated the initial experiments ? a standard process in science. Combined results are really important in this field. None of us found anything like what they described in the 2012 paper."

The researchers found no effects on plaque burden in three different strains of mice that were treated with bexarotene.

The discrepancy, besides being disappointing, also raises concerns about patient safety. The Food and Drug Administration approved bexarotene in December 1999 for a very specific use: treatment of refractory cutaneous T-cell lymphoma, a type of skin cancer. Once approved, the drug became legally available by prescription for "off-label" uses as well.

"Anecdotally, we have all heard that physicians are treating their Alzheimer's patients with bexarotene, a cancer drug with severe side effects," said co-author Robert Vassar, PhD, professor of cell and molecular biology at Northwestern University Feinberg School of Medicine. "This practice should be ended immediately, given the failure of three independent research groups to replicate the plaque-lowering effects of bexarotene."

Bexarotene has never been tested as a treatment for Alzheimer's disease in humans, not even to determine the optimal dose or duration of treatment. This drug has significant side effects, including major blood-lipid abnormalities, pancreatitis, liver function test abnormalities, thyroid axis alterations, leucopenia, headaches, fatigue, weight gain, depression, nausea, vomiting, constipation and rash.

The two other technical comments came from research teams led by Kevin Felsenstein, Todd Golde, David Borchelt and colleagues at the University of Florida and by Bart DeStrooper and colleagues at the University of Leuven, Belgium.

There is no cure or effective treatment for Alzheimer's disease, which is a progressive type of dementia that occurs when nerve cells in the brain die. When Alzheimer's was first identified in 1906, it was considered a rare disorder. Today, Alzheimer's is the most common cause of dementia. An estimated 5.3 million Americans have the disease.

Source-Eurekalert


View the original article here