Biomedical subjects

David S. Saperstein

Publications and source records attributed to David S. Saperstein.

3 recordsLinked to original sources

PubMed2003

Chronic Inflammatory Demyelinating Polyneuropathy.

Although there are close to 10 randomized trials showing efficacy for prednisone, intravenous immunoglobulin, or plasmapheresis in chronic inflammatory demyelinating polyneuropathy (CIDP), large differences in cost, side effect profiles, and ease of use create controversy over the therapy that is best. Most clinicians use intravenous immunoglobulin or prednisone as first-line therapy. Unfortunately, the clinical trials performed to date are not easily extrapolated to answer, "which agent is best for clinical practice" because they have used varying doses and duration of therapy, different diagnostic criteria for CIDP, and mixtures of patients who have failed previous therapy versus those with newly diagnosed disease. There are a number of small case series describing the efficacy of immune-modulating agents, such as azathioprine, cyclophosphamide, cyclosporine A, interferon-alpha, and mycophenolate mofetil. These studies generally use these medications as second-line agents for patients who failed corticosteroids or intravenous immunoglobulin. In the authors' practice, this lack of robust knowledge still relegates these to second-line or prednisone-sparing agents.

Journal Article↗

PubMed2002

Peripheral Neuropathy Due to Cobalamin Deficiency.

Vitamin B12, or cobalamin (Cbl), deficiency can produce a number of neurologic complications, including myelopathy, peripheral neuropathy, optic neuropathy, and dementia. The myelopathy, combined systems disease, is probably the most well known manifestation, and is usually readily recognized. The frequency with which peripheral neuropathy is the sole presenting feature of Cbl deficiency is a point of controversy. The prevalence and the clinical and electrophysiologic features of Cbl deficiency peripheral neuropathy have not been well characterized. In addition, there is evidence that the commonly used assays of serum Cbl are not adequately sensitive. Testing the serum metabolites methylmalonic acid and homocysteine can increase the identification of Cbl deficient patients. Treatment with parenteral Cbl injections may not produce improvement of neurologic deficits, but might prevent worsening. In some patients with Cbl deficiency, oral Cbl may be an effective therapy.

Journal Article↗

PubMed2001

Asymmetric Acquired Demyelinating Polyneuropathies: MMN and MADSAM.

More than a half a century after Austin's initial description of chronic inflammatory demyelinating polyradiculoneuropathy (CIDP), the clinical spectrum of chronic acquired demyelinating polyneuropathies has expanded. Currently there are a number of entities that can be put under the heading of chronic acquired demyelinating neuropathy (CADP) based on differing clinical presentations. In this scheme, CIDP is used only to refer to patients with demyelinating neuropathies and generalized symmetric weakness. In contrast, multifocal motor neuropathy (MMN) and multifocal acquired demyelinating sensory and motor neuropathy (MADSAM) fall into the category of asymmetrical, multifocal forms of CADP. These are distinguished from each other only by the presence of sensory involvement. In our opinion, there are pragmatic reasons for splitting these clinical presentations into distinct entities. Although each of these clinical subtypes shares some basic similarities, there are important differences. MMN is usually considered resistant to corticosteroid therapy and the first line agent in this disorder is intravenous immunoglobulin (IVIg). MADSAM neuropathy can be responsive to prednisone or IVIg, and has a profile more analogous to classic CIDP with regards to its laboratory features and treatment response.

Journal Article↗