subacute combined systems disease

Mcharris · 09-30-2007, 01:30 AM

Hello Everyone:

would it be safe to assume (arghhh.... dangerous I suppose) that IF you have been deficient in B12 for some considerable time (literature says neuro symptoms show before blood work does) that it could have progressed to subacute combined systems disease?

These problems have been slowly accruing for over 7 years that I can definitely remember. I am on PPI and have been for over 7 years, before that other gastric acid reducers for about twenty years, but no one has ever put two and two together........ I mean I am supposing PPI's could be a reason for malabsorbtion or killing off of stomach cells etc?

Reason I ask this is because I have some white matter changes showing in recent MRI's that docs say is DEFINITELY NOT MS, and I have heaps of neuro signs, like tingling/burning legs and feet, arms and hands, light headedness and dizziness, thought problems and remembering problems etc etc etc...... walking is becoming difficult for me too now, my hips are hurting, and xrays show them and knees to be 'normal'.

I am asking you who are more knowledgable to help me out here, give me reading to do, links to follow etc.... where you can.

I am awaiting results of Hcy and MMA..... B12 levels have fallen (in 5 months) from 548 to 362. I have started giving myself IM B12 every other day, when my supply runs out this week I have sublingual methyl 5mg ready to take.

Thanks for considering my question.

Cheer's

rose · 10-01-2007, 05:52 PM

If a person has been deficient for quite a while, depending on how quickly their B12 is being depleted, it would be likely that the spinal cord is being affected at least somewhat.

If caught before real damage is done (function can be affected long before lesions will show on an MRI), a lot of improvement can take place.

From the looks of your rapidly falling B12 level, it is very likely that B12 deficiency is your problem.

Of course other things can accompany it, precede it, or even be caused by it. But taking care of that is a very good start!

I'm in a rush, but will try to get back here and supply some links.

rose

rose · 10-02-2007, 01:14 PM

I haven't re-read this, but usually people are not followed very long (not even enough months, let alone years). And very seldom are people given methylcobalamin in these studies.

Quote:

J Neurol Neurosurg Psychiatry 1998;65:822–827

Subacute combined degeneration: clinical,
electrophysiological, and magnetic resonance
imaging findings

B Hemmer, F X Glocker,M Schumacher, G Deuschl, C H Lücking
Abstract

Objective—Vitamin B12 deficiency is a systemic
disease that often affects the nervous
system. One of the most prevalent
manifestations is subacute combined degeneration
(SCD) of the spinal cord. To
access the clinical, electrophysiological,
and structural abnormalities associated
with SCD, a study was conducted in nine
patients.
Methods—Clinical, electrophysiological
(electroneurography, somatosensory and
motor evoked potentials), and MRI evaluations
were performed in patients before
and after treatment.
Results—The most prominent clinical and
electrophysiological findings in all patients
were dysfunctions of the posterior
column. Corresponding hyperintense lesions
in the posterior column of the spinal
cord were found in two patients by T2
weighted MRI. Damage to the central
motor pathway was identified in four
patients. Demyelinating neuropathy was
present in one patient and axonal neuropathy
in four. All patients showed
improvement of their symptoms after
treatment with cobalamin. Abnormalities
of the spinal cord on MRI disappeared
early in recovery.Motor evoked potentials
and median somatosensory evoked potentials
typically normalised after treatment,
whereas tibial somatosensory evoked potentials
remained abnormal in most patients.
Conclusions—Clinical, electrophysiological,
and MRI findings associated with
SCD in vitamin B12 deficiency are diverse.
Thus vitamin B12 deficiency should be
considered in the differential diagnosis of
all spinal cord, peripheral nerve, and neuropsychiatric
disorders.
(J Neurol Neurosurg Psychiatry 1998;65:822–827)
Keywords: vitamin B12 deficiency; subacute combined
degeneration; myelopathy
Vitamin B12 deficiency causes a wide range of
haematological, gastrointestinal, psychiatric,
and neurological disorders.1 Megaloblastic
anaemia is a common early symptom leading to
the diagnosis, although neurological symptoms
may occur in the absence of haematological
abnormalities.2 The neurological syndromes
associated with vitamin B12 deficiency include
myelopathy, neuropathy, neuropsychiatric abnormalities,
and less often, optic nerve atrophy.
The spinal cord affliction called subacute combined
degeneration (SCD) is clinically characterised
by symmetric dysaesthesia, disturbance
of the position sense, and spastic paraparesis or
tetraparesis.1 Although most patients respond
well to cobalamin treatment, residual neurological
abnormalities persist in most.3 Studies
involving limited numbers of patients with
cobalamin deficiency have shown various
abnormal electrophysiological findings4–9 and
more recently lesions of the cervical spinal cord
by MRI.10–12
Here, we present clinical, electrophysiological,
and MRI findings of nine patients affected
by SCD. Seven of these patients were followed
up after treatment.

Quote:

Evoked potentials in subacute combined degeneration of the spinal cord

Neurophysiologie Clinique (France), 1997, 27/1 (59-65)

We describe visual, brain stem auditory, and somatosensory evoked potentials (VEP, BAEP, SEP) in a 49-year old male patient presenting with subacute degeneration of the spinal cord due to vitamin B12 deficiency. Neurological signs included tetraplegia with a C4-C5 spinal cord compression that was unchanged after surgical decompression. Before treatment, the duration of the bilateral VEP was slightly increased, though their amplitude and morphology were not modified. BAEP were normal. However, abnormalities of SEP with loss of cortical potentials were noticed. Two months after initiation of the treatment, both VEP and SEP recorded in response to median nerve stimulation had improved, but there was still no cortical response to tibial nerve stimulation. Eighteen months later, VEP were normal and recovery of SEP in response to tibial nerve stimulation was observed; however, alterations of peripheral sensory and motor action potentials were still present. These findings are in good agreement with previously reported pathological changes in patients presenting with subacute combined degeneration. Similar abnormalities have been described in patients with multiple sclerosis. Evoked potentials in this case proved to be useful for the diagnosis and the evaluation of the efficacy of the treatment. These findings also suggest that demyelination of the posterior part of the spinal cord and peripheral axonal degeneration might be the main pathological changes related to vitamin B12 deficiency. The former, but not the latter, were clearly responsive to the treatment.

Here's one they caught pretty early:

Quote:

MRI in Subacute Combined Degeneration of Spinal Cord :
A Case Report and Review of Literature

S.G. Srikanth, P.N. Jayakumar, M.K. Vasudev, A.B. Taly,* H.S. Chandrashekar
Departments of Neuroimaging & Interventional Radiology and Neurology*
National Institute of Mental Health and Neurosciences
Bangalore – 560 029, India.

Summary
A 56 year old man presented with acute onset posterior column and lateral spinothalamic tract
dysfunction over a period of 15 days. MRI showed diffuse hyperintensity on T2WI involving the
posterior columns.A diagnosis of subacute combined degeneration (SCD) of the spinal cord was
considered and confirmed by laboratory findings. The patient showed complete recovery on B12
therapy. MRI lesion also compeletely resolved.

rose · 10-05-2007, 11:13 AM

Just wanted to make sure you saw my answer.

rose

Site Navigation

NeuroTalk Online Support Groups

subacute combined systems disease

NeuroTalk Forums