Allan H. Ropper
Brigham and Women's Hospital
Network
Latest external collaboration on country level. Dive into details by clicking on the dots.
Publication
Featured researches published by Allan H. Ropper.
Neurology | 1997
Kenneth C. Gorson; Gregory Allam; Allan H. Ropper
Article abstract-We report the clinical and EMG details of 67 consecutive patients with strictly defined chronic inflammatory demyelinating polyneuropathy (CIDP) during a 4-year period and compare responses to treatment in patients with idiopathic CIDP (CIDP-I) and CIDP with monoclonal gammopathy of uncertain significance (CIDP-MGUS). Patients were examined an average of 28 months after first symptoms. There were several variant presentations that still conformed to the clinical and electrophysiologic definitions of CIDP, including a pure motor syndrome (10%), sensory ataxic variant (12%), mononeuritis multiplex pattern (9%), paraparetic pattern (4%), and relapsing acute Guillain-Barre syndrome (16%). Pain was more frequent than in previous studies (42%). Conduction block was the commonest EMG abnormality (detected in at least one nerve in 73% of patients), but only 31% had a pure demyelinating neuropathy and the majority had some degree of axonal change. Patients with CIDP-MGUS had less severe weakness, greater imbalance, leg ataxia, vibration loss in the hands, and absent median and ulnar sensory potentials, but were as likely as CIDP-I patients to respond to plasma exchange. Seventeen of 44 patients (39%) with idiopathic CIDP improved for at least 2 months with an initial therapy. Although the response rates among plasma exchange, IVIG, and steroids were similar, functional improvement (Rankin score) was greatest with plasma exchange. Of 26 patients who failed to respond to an initial therapy, 9 (35%) benefited from an alternative treatment, and of the 11 who required a third modality 3 (27%) improved. Overall, 66% responded to one of the three main therapies for CIDP. NEUROLOGY 1997;48: 321-328
Journal of Clinical Investigation | 2001
Peter Schratzberger; Dirk H. Walter; Kilian Rittig; Ferdinand H. Bahlmann; Roberto Pola; Cynthia Curry; Marcy Silver; Joseph G. Krainin; David H. Weinberg; Allan H. Ropper; Jeffrey M. Isner
The pathogenetic basis for diabetic neuropathy has been enigmatic. Using two different animal models of diabetes, we have investigated the hypothesis that experimental diabetic neuropathy results from destruction of the vasa nervorum and can be reversed by administration of an angiogenic growth factor. Nerve blood flow, as measured by laser Doppler imaging or direct detection of a locally administered fluorescent lectin analogue, was markedly attenuated in rats with streptozotocin-induced diabetes, consistent with a profound reduction in the number of vessels observed. A severe peripheral neuropathy developed in parallel, characterized by significant slowing of motor and sensory nerve conduction velocities, compared with nondiabetic control animals. In contrast, 4 weeks after intramuscular gene transfer of plasmid DNA encoding VEGF-1 or VEGF-2, vascularity and blood flow in the nerves of treated animals were similar to those of nondiabetic control rats; constitutive overexpression of both transgenes resulted in restoration of large and small fiber peripheral nerve function. Similar experiments performed in a rabbit model of alloxan-induced diabetes produced comparable results. These findings support the notion that diabetic neuropathy results from microvascular ischemia involving the vasa nervorum and suggest the feasibility of a novel treatment strategy for patients in whom peripheral neuropathy constitutes a secondary complication of diabetes.
The New England Journal of Medicine | 1986
Allan H. Ropper
Brain-tissue shifts associated with drowsiness, stupor, and coma were studied by clinical examination and CT scanning in 24 patients with acute unilateral cerebral masses. Studies were performed soon after the appearance of the mass to detect the earliest CT changes associated with depression of consciousness. Contrary to traditional concepts, early depression of the level of alertness corresponded to distortion of the brain by horizontal displacement rather than transtentorial herniation with brain-stem compression. Horizontal displacement of the pineal body of 0 to 3 mm from the midline was associated with alertness, 3 to 4 mm with drowsiness, 6 to 8.5 mm with stupor, and 8 to 13 mm with coma. Moreover, drowsy or stuporous patients and some comatose patients had widened cisterns between the tentorial edge and the midbrain on the side of the mass, suggesting that the space was not filled by herniated medial temporal lobe. Downward displacement of the pineal body, indicating central transtentorial herniation, did not occur. Compression of one hemisphere by the other anteriorly (transfalcial herniation) was inconsistently related to alertness, though very large anterior displacements may have caused stupor in some patients. Current concepts of the pathoanatomical nature of depressed consciousness, based on pathological material obtained well after clinical examinations, may require revision, because they do not reflect early brain-tissue distortions.
Nature Medicine | 2000
Peter Schratzberger; Gabriele Schratzberger; Marcy Silver; Cynthia Curry; Marianne Kearney; Meredith Magner; Joseph Alroy; Lester S. Adelman; David H. Weinberg; Allan H. Ropper; Jeffrey M. Isner
Ischemic peripheral neuropathy is a frequent, irreversible complication of lower extremity vascular insufficiency. We investigated whether ischemic peripheral neuropathy could be prevented and/or reversed by gene transfer of an endothelial cell mitogen designed to promote therapeutic angiogenesis. Intramuscular gene transfer of naked DNA encoding vascular endothelial growth factor (VEGF) simultaneously with induction of hindlimb ischemia in rabbits abrogated the substantial decrease in motor and sensory nerve parameters, and nerve function recovered promptly. When gene transfer was administered 10 days after induction of ischemia, nerve function was restored earlier and/or recovered faster than in untreated rabbits. These findings are due in part to enhanced hindlimb perfusion. In addition, however, the demonstration of functional VEGF receptor expression by Schwann cells indicates a direct effect of VEGF on neural integrity as well. These findings thus constitute a new paradigm for the treatment of ischemic peripheral neuropathy.
Journal of Clinical Neuroscience | 2002
Cenk Ayata; Allan H. Ropper
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.
Neurology | 1980
Allan H. Ropper; Roger S. Williams
In patients with Down syndrome, senile plaques and neurofibrillary tangles accumulate in the cortex at an earlier age than in persons of normal karyotype. We studied 20 Down syndrome patients dying after age 30 (average age, 49); all had neocortical plaques and tangles, but only 3 of 20 had been demented. In 12 cases (average age, 531, tissue was available for quantitative study of plaque and tangle densities and estimation of cell loss in the hippocampus. Although at least 8 of these 12 cases had plaque and tangle densities comparable to those previously reported in demented old people, only 1 had dementia. The regional distribution of plaques and tangles in the hippocampus of these Down cases differed from the pattern in senile dementia. Although Alzheimer-like dementia occurs in Down disease, it is less prevalent than the plethoric plaques and tangles in the cortex.
Muscle & Nerve | 2007
Kenneth C. Gorson; Neela Natarajan; Allan H. Ropper; Robert Weinstein
We studied the effect of rituximab in allowing a reduction in dose of intravenous immune globulin (IVIg) in six patients with IVIg‐dependent, relapsing immune polyneuropathy. Rituximab (375 mg/m2 intravenously each week for 4 weeks) was administered in a prospective, open‐label design to two patients with chronic inflammatory demyelinating polyneuropathy (CIDP), two with multifocal motor neuropathy (MMN), one with neuropathy and anti–myelin‐associated glycoprotein (MAG) antibody neuropathy, and one with Sjögren syndrome (SS) ataxic neuropathy. The primary endpoint was a reduced cumulative IVIg dosage by at least 25% at 1 year after rituximab therapy compared to the previous year. Secondary endpoints included an improved summed strength score by at least 5 points on the Medical Research Council scale, an increased sensory score by at least 4 points, or an improved Rankin disability score by at least 1 grade. Total IVIg dosage decreased by greater than 25% in one patient with SS neuropathy and one with MMN; the dosage was unchanged in one with CIDP, slightly reduced in the patient with anti‐MAG neuropathy, and increased in one with CIDP and another with MMN. There was no improvement in secondary endpoints. No adverse events occurred. In this small prospective study, rituximab did not reduce IVIg requirements in the majority of patients with IVIg‐dependent, immune‐mediated polyneuropathies. Muscle Nerve, 2006
Stroke | 1991
E. F. M. Wijdicks; Allan H. Ropper; E. J. Hunnicutt; G. S. Richardson; James A. Nathanson
Background and Purpose The causes of volume depletion and hyponatremia after subarachnoid hemorrhage are not fully understood but may be in part due to natriuresis or “cerebral salt wasting.” Because previous studies using infrequent hormone sampling have given inconsistent results, we determined if elevations in atrial natriuretic factor concentrations preceded negative sodium and fluid balances. Methods We measured diurnal atrial natriuretic factor and vasopressin concentrations and sodium balance for 5 days in 14 consecutive patients after aneurysmal subarachnoid hemorrhage. Results Plasma concentrations of atrial natriuretic factor on admission were elevated in subarachnoid hemorrhage patients (mean±SD 106 ±59 pg/ml) compared with acutely ill controls (39±30 pg/ml). In eight patients, high peak concentrations of atrial natriuretic factor, greater than 300 pg/ml or a twofold increase above baseline, were followed by natriuresis and a negative sodium balance. Three patients, two of whom became hyponatremic, developed cerebral infarcts after natriuresis. Vasopressin concentrations were slightly elevated just after hemorrhage but subsequently declined to normal values. Conclusions A markedly increased atrial natriuretic factor concentration precedes natriuresis in some patients and, with other abnormalities of water handling possibly including a relatively diminished vasopressin concentration, may cause volume depletion. Patients with natriuresis appear to be at increased risk for delayed cerebral infarction after subarachnoid hemorrhage.
Muscle & Nerve | 2000
Kenneth C. Gorson; Allan H. Ropper; Lester S. Adelman; David H. Weinberg
Patients with diabetes occasionally develop clinical and electrodiagnostic features suggestive of chronic inflammatory demyelinating polyneuropathy (CIDP). To clarify the role of diabetes in patients with a CIDP‐like syndrome, we compared the clinical, pathological, and electrodiagnostic features of 14 patients (10 men, 4 women) with diabetes and CIDP (DM‐CIDP) to 60 patients with idiopathic CIDP (I‐CIDP). The average duration of diabetes was 9 years. The patients with DM‐CIDP were older and more often complained of imbalance compared to the idiopathic group, but the frequency of other symptoms and neurologic findings were similar. The mean amplitude of the ulnar compound muscle action potential in the DM‐CIDP group was comparatively reduced, the sural sensory nerve action potential was more often absent, and axonal loss was more commonly observed on nerve biopsy. The response rate to treatment was similar, but the magnitude of functional recovery was greater in patients with I‐CIDP. Thus, our patients with diabetes and CIDP had clinical features similar to those with idiopathic CIDP, but their nerve conduction studies and nerve biopsies showed more severe axonal loss and the degree of improvement following treatment was less favorable. These differences most likely reflect the additive effects of superimposed diabetic axonal polyneuropathy in patients who develop CIDP.
Neurology | 1987
Allan H. Ropper; Susan M. Kehne; Larry Wechsler
Transcranial Doppler examinations (TCD) of 24 brain-dead adult patients demonstrated persistent movement of blood within the middle cerebral arteries in 21. The characteristic pattern of Doppler shift frequencies, seen in 14, was a sharply contoured, brief anterograde systolic envelope with reversed diastolic flow. Five others had variants of this pattern, and two had anterograde flow throughout the cardiac cycle, except at the end of diastole. This suggests that the internal carotid and proximal middle cerebral artery circulation remains patent, but distal resistance to flow in the brain is very high in the majority of brain-dead patients. Three other patients with absent brainstem reflexes but persistent EEG activity had normal TCD patterns. The characteristic pattern on TCD may be a useful ancillary finding in the diagnosis of brain death, and normal TCD patterns probably exclude the diagnosis.