Biomedical subjects

Gary S Gronseth

Publications and source records attributed to Gary S Gronseth.

4 recordsLinked to original sources

PubMed2005

Distal symmetrical polyneuropathy: a definition for clinical research. A report of the American Academy of Neurology, the American Association of Electrodiagnostic Medicine, and the American Academy of Physical Medicine and Rehabilitation.

The objective of this report was to develop a case definition of "distal symmetrical polyneuropathy" to standardize and facilitate clinical research and epidemiologic studies. A formalized consensus process was employed to reach agreement after a systematic review and classification of evidence from the literature. The literature indicates that symptoms alone have relatively poor diagnostic accuracy in predicting the presence of polyneuropathy; signs are better predictors of polyneuropathy than symptoms; and single abnormalities on examination are less sensitive than multiple abnormalities in predicting the presence of polyneuropathy. The combination of neuropathic symptoms, signs, and electrodiagnostic findings provides the most accurate diagnosis of distal symmetrical polyneuropathy. A set of case definitions was rank ordered by likelihood of disease. The highest likelihood of polyneuropathy (useful for clinical trials) occurs with a combination of multiple symptoms, multiple signs, and abnormal electrodiagnostic studies. A modest likelihood of polyneuropathy (useful for field or epidemiologic studies) occurs with a combination of multiple symptoms and multiple signs when the results of electrodiagnostic studies are not available. A lower likelihood of polyneuropathy occurs when electrodiagnostic studies and signs are discordant. For research purposes, the best approach to defining distal symmetrical polyneuropathy is a set of case definitions rank ordered by estimated likelihood of disease. The inclusion of this formalized case definition in clinical and epidemiologic research studies will ensure greater consistency of case selection.

Electrodiagnosis↗

PubMed2005

Gulf war syndrome: a toxic exposure? A systematic review.

Using the strength-of-conclusion scheme enumerated in Box 2, based on two class II studies, there is probably a causal link between deployment to the Persian Gulf theater of operation and the development of the poorly defined multisymptom illness known as GWS (level B). Based on class IV studies, there is insufficient evidence to determine if exposure to toxins encountered during the Persian Gulf war caused GWS (level U). A major limitation of the literature regarding the GWS is the reliance on self-reporting to measure exposure to putative causal toxins. Although objective measures of toxin exposure in GWV generally is unavailable, modeling techniques to estimate exposure levels to low-level nerve agents and smoke from oil well fires have been developed. It would be useful to determine if exposure levels determined by these techniques are associated with GWS. The lack of a clear case definition GWS also hampers research. Some go even further, claiming that the absence of such a definition renders the condition illegitimate. Although an objective marker to GWS would be useful for studies, the absence of such a marker does not make the syndrome any less legitimate. in essence, GWS merely is a convenient descriptive term that describes a phenomenon: GWV reporting suffering from medically unexplained health-related symptoms. In this sense, it shares much with the other medically unexplained syndromes encountered in practice. The real debate surrounding medically unexplained conditions is not whether or not they exist, but defining their cause. In this regard, investigators fall into two camps. One camp insists that the conditions are caused by a yet-to-be-discovered medical problem, rejecting out of hand the possibility of a psychologic origin. The other camp insists the conditions are fundamentally psychogenic rejecting the possibility of an undiscovered medical condition. The evidence shows, however, that the conditions exists, the suffering is real, and the causes are unknown.

Case-Control Studies↗

PubMed2004

From evidence to action.

Despite the availability of vast quantities of evidence from basic biomedical and clinical studies, a gap often exists between the optimal practice suggested by the evidence and actual practice. For many clinical situations, however, evidence is unavailable, of poor quality or contradictory. Out of necessity, clinicians have become accustomed to relying on non-evidence-based tools to make decisions. Out of habit, they rely on these tools even when high-quality evidence becomes available. Growing out of an increasing awareness of this problem, the evidence-based medicine (EBM) movement sought to empower clinicians to find the evidence most relevant to a specific clinical question. Various organizations have used EBM techniques to develop systematic reviews and practice guidelines to aid physicians in making evidence-based decisions. A systematic review follows a process of asking a clinical question, finding the relevant evidence, critically appraising the evidence and formulating conclusions and recommendations. Results are mixed on whether educating physicians about evidence-based recommendations is sufficient to change physician behavior. Barriers to adopting evidence-based best practice remain, including physician skepticism, patient expectations, fear of legal action, and distorted reimbursement systems. Additionally, despite enormous research efforts there remains a lack of high-quality evidence to guide care for many clinical situations.

Evidence-Based Medicine↗

PubMed2003

Challenges in the identification of cobalamin-deficiency polyneuropathy.

BACKGROUND: Diagnosing cobalamin (Cbl) deficiency as a cause of polyneuropathy (PN) is problematic, as the frequency of both disorders increases with age, and serum Cbl levels can be difficult to interpret. OBJECTIVES: To identify unique clinical or laboratory features among PN patients with Cbl deficiency and to examine the role of testing of serum metabolite levels in the identification of Cbl deficiency. DESIGN: Cohort survey comparing patients with Cbl deficiency and cryptogenic PN identified during a 2-year period. Cobalamin deficiency was diagnosed using low serum Cbl levels or elevated serum methylmalonic acid or homocysteine levels. SETTING: Academic neuromuscular clinic. RESULTS: Of 324 PN patients, 27 were diagnosed as having Cbl deficiency. Twelve had Cbl levels within the normal range, but elevated serum metabolite levels. Compared with patients with cryptogenic sensory/sensorimotor PN, those with Cbl deficiency were more likely to have concomitant involvement of the upper and lower extremities and experience symptom onset in the hands and a sudden onset of symptoms (P<.005). These differences were seen regardless of whether Cbl deficiency was defined using low Cbl levels or elevated serum metabolite levels. Autoimmune pernicious anemia was identified in 6 (50%) of 12 Cbl-deficient patients with normal serum Cbl levels. The patients with PN and Cbl deficiency showed little objective improvement after parenteral replacement therapy; however, progression occurred less often in these patients compared with those with cryptogenic sensory/sensorimotor PN (P =.02). CONCLUSIONS: This study highlights the challenges of proving that Cbl deficiency is the cause for PN and identifies clinical features that suggest Cbl-deficiency PN. Testing of serum metabolite levels may identify Cbl deficiency in some patients with normal serum Cbl levels.

Adult↗