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Neurological differential diagnosis of spinal disorders

Chapter by: Ryan, Devon; Cheriyan, Thomas; Bronfin, Ludmilla
in: Spinal disorders and treatments : the NYU-HJD comprehensive textbook by Errico, Thomas J; Cheriyan, Thomas; Varlotta, Gerard P [Eds]
New Delhi : Jaypee Brothers, 2015
pp. 30-35
ISBN: 9351524957
CID: 2709012

Neuromuscular disorders

Chapter by: Cohen, Jeffrey M; Cohler, Melissa; Bronfin, Ludmilla
in: Medical aspects of disability : a handbook for the rehabilitation professional by Flanagan, Steven R; Zaretsky, Herbert H; Moroz, Alex [Eds]
New York : Springer, c2011
pp. 265-290
ISBN: 0826127843
CID: 5788

Neuromuscular Disorders

Chapter by: Bronfin, Ludmilla
in: Medical aspects of disability : a handbook for the rehabilitation professional by Zaretsky, Herbert H [Eds]
New York, NY, US: Springer Publishing Co, 2005
pp. 383-409
ISBN: 0826179738
CID: 4097

Polyglucosan body myopathy [Meeting Abstract]

Carniciu, S; Kiprovski, K; Levine, DN; ZagZag, D; Bronfin, L; Kolodny, EH
ISSN: 0364-5134
CID: 74939

Assessing microcirculation in familial dysautonomia by laser Doppler flowmeter

Weiser M; Hilz MJ; Bronfin L; Axelrod FB
Microcirculatory vasomotor responses to an alpha-adrenergic agonist and an antagonist were assessed in 11 familial dysautonomia and nine control subjects by laser Doppler flowmetry. Using two iontophoresis machines, blood flow in the midclavicular areas was continuously monitored by two channel laser Doppler flowmeter. Simultaneously, the alpha-antagonist (0.5 mM phentolamine hydrochloride) and a control solution (0.9% saline) were iontophoresed at 200 microA for 15 min. The alpha-agonist (0.5 mM norepinephrine bitartrate) was then iontophoresed (20 microA) to both pretreated areas for progressively longer pulses separated by 3-min observation intervals (15, 30, 60, 90, 120 s). The familial dysautonomia subject group had higher mean baseline perfusion with widely fluctuating baselines, especially on the phentolamine pretreated side (P = 0.03). Saline iontophoresis significantly increased perfusion in the control group, but not in the familial dysautonomia group (ANOVA: P = 0.02 and 0.15, respectively). There was > 100% increase in flow by the end of the saline observation period in seven of nine controls, but in only three of 11 familial dysautonomia subjects. Phentolamine iontophoresis differentiated familial dysautonomia subjects into responders and nonresponders by 7-8 min when all nine control subjects, but only five of 11 familial dysautonomia subjects, had > 200% increase in blood flow. Irrespective of pretreatment type, norepinephrine decreased blood flow in both familial dysautonomia and control groups (ANOVA: P < 0.0001), but the final mean change after saline was greater in the control group, P = 0.02. The final mean changes of flow after phentolamine pretreatment were not different between the two groups and were comparable to the familial dysautonomia group's smaller response after saline pretreatment. Higher baseline perfusion suggests dilation may be intrinsic to familial dysautonomia vasculature. Two populations of familial dysautonomia subjects are noted; those who like controls increase blood flow with iontophoresis of the alpha-antagonist and those who are refractory. In addition, in familial dysautonomia subjects, the microcirculatory constrictive response to alpha-agonist iontophoresis is less than that observed for controls. These data suggest that some familial dysautonomia subjects may have decreased or dysfunctional adrenoceptors as well as decreased innervation
PMID: 9532416
ISSN: 0959-9851
CID: 7846

Overview of diabetic neuropathy

Younger, D S; Bronfin, L
PMID: 8987123
ISSN: 0271-8235
CID: 113978