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Allan H Ropper

Publications and source records attributed to Allan H Ropper.

20 records · Page 2Linked to original sources

Efficacy of intravenous immunoglobulin in patients with IgG monoclonal gammopathy and polyneuropathy.

CONTEXT: The optimal treatment of patients with neuropathy associated with IgG monoclonal gammopathy of undetermined significance is unknown. Plasma exchange has been shown to be effective but alternative therapies have not been systematically evaluated. OBJECTIVE: To report our experience with intravenous immunoglobulin (IVIG) in patients with IgG monoclonal gammopathy of undetermined significance polyneuropathy. DESIGN: Retrospective review of clinical and electrodiagnostic features of 20 consecutive patients treated with IVIG over an 8-year period. SETTING: Academic medical center. MAIN OUTCOME MEASURES: Medical Research Council strength (maximum, 40 points) and sensory (maximum, 26 points) scores, modified Rankin Disability Scale score. RESULTS: There were 14 men and 6 women (mean age, 65 years; age range, 36-82 years). The mean strength score was 35.6 points and the mean sensory score was 15.8 points prior to therapy. After IVIG therapy, the mean strength score increased by 1.1 points (P =.22) and the sensory score increased by 1.7 points (P =.11). Eight patients (40%) improved by 2 points or more in their motor or sensory score and 1 point or more in the modified Rankin Disability Scale score and were considered IVIG therapy responders. They had a shorter duration of symptoms (P =.03), numb hands (P =.02), and falling episodes (P =.02), and had greater proximal leg weakness (P =.02) compared with nonresponders. In IVIG therapy responders, the ulnar motor conduction velocity was slower, ulnar and peroneal distal motor latencies were prolonged, and the frequency of conduction block was higher (13 of 36 motor nerves in responders vs 6 of 53 in nonresponders, P =.008). CONCLUSIONS: Intravenous immunoglobulin therapy was beneficial in 8 (40%) of our 20 patients with polyneuropathy and IgG monoclonal gammopathy of undetermined significance. Proximal leg weakness, short duration of symptoms, and demyelinating features on electrodiagnostic studies were associated with a response to IVIG therapy.

Adult↗

Ischaemic brain oedema.

Ischaemic brain oedema appears to involve two distinct processes, the relative contribution and time course of which depend on the duration and severity of ischaemia, and the presence of reperfusion. The first process involves an increase in tissue Na+ and water content accompanying increased pinocytosis and Na+, K+ ATPase activity across the endothelium. This is apparent during the early phase of infarction and before any structural damage is evident. This phenomenon is augmented by reperfusion. A second process results from a more indiscriminate and delayed BBB breakdown that is associated with infarction of both the parenchyma and the vasculature itself. Although, tissue Na+ level still seems to be the major osmotic force for oedema formation at this second stage, the extravasation of serum proteases is an additional potentially deleterious factor. The relative importance of protease action is not yet clear, however, degradation of the extracellular matrix conceivably leads to further BBB disruption and softening of the tissue, setting the stage for the most pronounced forms of brain swelling. A number of factors mediate or modulate ischaemic oedema formation, however, most current information comes from experimental models, and clinical data on this microcosmic level is lacking. Clinically significant brain oedema develops in a delayed fashion after large hemispheric strokes and is a cause of substantial mortality. Neurological signs appear to be at least as good as direct ICP measurement and neuroimaging in detecting and gauging the secondary damage produced by stroke oedema. The neuroimaging characteristics of the stroke, specifically the early involvement of greater than half of the MCA territory, are, however, highly predictive of the development of severe oedema over the subsequent hours and days. None of the available medical therapies provide substantial relief from the oedema and raised ICP, or at best, they are temporizing in most cases. Hemicraniectomy appears most promising as a method of avoiding death from brain compression, but the optimum timing and manner of patient selection are currently being investigated. All approaches to massive ischaemic brain swelling are clouded by the potential for survival with poor functional outcome. It is possible to manage blood pressure, serum osmolarity by way of selective fluid administration, and a number of other systemic factors that exaggerate brain oedema. Broad guidelines for treatment of stroke oedema can therefore be given at this time.

Brain Edema↗