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From: ironjustice on 29 Jun 2008 21:12
Coincidentally .. ? .. polycythemia causes neuropathy.
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"Neuropathy not necessarily irreversible"

Acta Neurol Scand. 2001 Jun;103(6):386-91. Links
Peripheral neuropathy in systemic lupus erythematosus--a longitudinal
study.Omdal R, Løseth S, Torbergsen T, Koldingsnes W, Husby G,
Mellgren SI.
Department of Clinical Medicine/Neurology, University Hospital of
Tromsø, Oslo, Norway. romdal(a)online.no

OBJECTIVE: Peripheral neuropathy (PN) is reported to occur in 5-27% of
patients with systemic lupus erythematosus (SLE) mostly as a length-
dependent sensorimotor axonopathy. Studies over time have not been
performed. Design - Longitudinal study. Subjects and Methods: Thirty-
three Caucasian SLE patients consented to participate in the study and
were subjected to clinical examination, laboratory tests, and nerve
conduction velocity (NCV) studies. At the follow-up 7 years later, 7
patients (21%) were dead, 4 refused to participate, and 2 did not want
to perform NCV studies. Twenty patients were thus available for
longitudinal study.
RESULTS:
When all SLE patients were considered on a group basis at follow-up, 8
(33%) out of 24 NCV parameters showed significant deterioration
despite correction for time, while 16 (67%) were unchanged. Analysis
of change from baseline showed that, except for F-responses, several
NCV changes were highly dependent (negative regression coefficients)
on baseline levels at start of study. No demographic, laboratory, or
disease associated quantitative factor was associated with these
changes in NCV parameters over time. Nor was a consistent effect on
NCV parameters from any qualitative demographic or disease associated
factor confirmed by Repeated Measures ANOVA analyses.
CONCLUSIONS:
A modest progressive neuropathic process exists in patients with SLE.
Important is also the finding that, over time, the abnormalities of
NCV parameters fluctuate in the individual patients, and the
impairments are not necessarily irreversible. This study also shows no
association to medication, demographic-, or other disease associated
factors.

PMID: 11421851 [PubMed - indexed for MEDLINE]

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Polycythemia DOES cause demyelination.

"Hyperviscosity is the probable pathogenic mechanism"


Sensory ataxic neuropathy with axonal stasis in a case of primary
polycythemia : electrophysiological and morphological study.


AB Taly, SK Shankar, D Nagaraja, T Asha, S Puttaram, C Sagar
Department of Neurology, National Institute of Mental Health and
Neuro
Sciences (NIMHANS), Bangalore - 560 029, India


Correspondence Address:
AB Taly
Department of Neurology, National Institute of Mental Health and
Neuro
Sciences (NIMHANS), Bangalore - 560 029
India


Source of Support: None, Conflict of Interest: None


A case of chronic sensory ataxic neuropathy secondary to primary
polycythemia is reported.
This association, has not been recorded before. Electrophysiological
investigations revealed features consistent with severe sensory and
mild motor axonopathy.
Sural nerve biopsy showed severe fibre loss and Schwann cell
proliferation.
Ultra structurally accumulation of neurofilaments was noted in both
unmyelinated and myelinated fibres.
Low persistent ischaemia of nerves due to hyperviscosity is the
probable pathogenic mechanism for the axonal stasis and nerve damage.
Neurology India, Year : 1996 | Volume : 44 | Issue : 1 | Page :
16--21


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