This correspondence is for the author:
I am writing in response to your interview on Radio 4 - aired 20/09/02 and
after having read the abstract for the above research.
My question is simple. You argue that sexual transmission is not the only
cause of MS and instead there are inherited factors that make someone who
already has a sexually transmitted neurotropic agent more susceptible to...
This correspondence is for the author:
I am writing in response to your interview on Radio 4 - aired 20/09/02 and
after having read the abstract for the above research.
My question is simple. You argue that sexual transmission is not the only
cause of MS and instead there are inherited factors that make someone who
already has a sexually transmitted neurotropic agent more susceptible to
the disease, but in doing so, aren't you making the assumption that they
already have a sexually transmitted neurotropic agent?
So if you're not saying that sufferers of MS have contracted it through
sexual contact, are you saying that someone who has MS has a member of
their family who has passed on a neurotropic agent (through sexual
contact) which has now made them susceptable to the disease.
If this is your argument which line are you defending? That MS
sufferers are, or have been, sexually promiscuous or that historically, a
direct descendant of theirs has been.
In your recent summary you seem to mix up two items when discussing
some of our work: The fact (as shown with control groups, Wernig et al.
1995,1998, 1999) that locomotion can significantly be improved by this
specific locomotor training (some call it "body weight assisted", some
call it "locomotion therapy on the treadmill", we call it "Laufband
therapy") and the question where in the CNS the l...
In your recent summary you seem to mix up two items when discussing
some of our work: The fact (as shown with control groups, Wernig et al.
1995,1998, 1999) that locomotion can significantly be improved by this
specific locomotor training (some call it "body weight assisted", some
call it "locomotion therapy on the treadmill", we call it "Laufband
therapy") and the question where in the CNS the learning effect occurs. I wish that you had discussed both separately: here the scientific question
to which degree and which supraspinal centers are involved in incompletely
paralyzed sci persons, and there the benefit for the patient (who does not
primarily care where it happens).
It is of indeed of great interest to learn of the results of the study by
Zeloni et al. (Viewing less to see better). The hemiblinding procedure
seems to effectively improve utilisation of the neglected field and
enhance recovery.
This, no doubt, would be an important technique for rehabilitation of
patients with visuospatial hemineglect.
It is of indeed of great interest to learn of the results of the study by
Zeloni et al. (Viewing less to see better). The hemiblinding procedure
seems to effectively improve utilisation of the neglected field and
enhance recovery.
This, no doubt, would be an important technique for rehabilitation of
patients with visuospatial hemineglect.
In my series of patients (36 patients) who had undergone surgical
decompression for traumatic optic neuropathy, it was initially noticed
that those with single eye vision and traumatic optic neuropathy fared
better than the others. In an attempt to replicate the conditions,
occlusion of the sound eye was attempted for a period of two weeks
following the optic canal decompression. Of the nine patients who received
this treatment, all but one recovered vision to 6/12 or better. Five of
these patients had preoperative vision of light perception or worse.
Following treatment all patients described phenomena similar to the
'gradual widening of a illuminated hole within a black or dark area before
the affected eye' allowing progressivley better vision. The patient with
poor postoperative recovery also commented on the presence of a 'window'
which he could utilise to visualise peripheral objects.
Though the number of patients treated is small, maximising utilisation
does seem to confer an added advantage to the rehabilitation process. A
continued study of the phenomena with controls would perhaps better
illustrate the benefits in traumatic optic neuropathy.
The treatment and its response is interesting also because occlusion is a
known form of vision therapy in Amblopia.
The possibility of the visual system responding similarly to maximal
utilsation in reparative processes following insults of diverse eitilogy
at different levels needs to be considered in the investigation of the
neural basis of visual recovery. The processes with respect to neglect
may be far removed from those with loss of visual function and motor
compensatory phenomena with enhanced contralesional eye movement may be
the major contributory factor in recovery of neglect. However, could
visual perceptive changes in someway contribute to the lasting recovery, a
phenomena perhaps shared at different levels of visual processing? To put
it simply, could it be that if one does not use it, one is condemned to
lose it.
The case presented is of particular interest. Tumour-like MS plaques
present and behave in a delinquent manner, unlike the classic ones.
However, with no evidence of demyelination elsewhere, no paraclinical
support, a somehow meager description of "demyelination with macrophages
etc" wouldn't it be better to call this lesion an "isolated demyelinating
CNS lesion" as proposed by others?
Powell, Heslin and Greenwood[1] are to be commended for their study
reporting the results of community based rehabilitation following
traumatic brain injury. While the effectiveness of rehabilitation
following brain injury has been acknowledged, randomised controlled trials
have not been reported to support this[2]. An especially encouraging result
from Powell, Heslin and Greenwood’s study was the fin...
Powell, Heslin and Greenwood[1] are to be commended for their study
reporting the results of community based rehabilitation following
traumatic brain injury. While the effectiveness of rehabilitation
following brain injury has been acknowledged, randomised controlled trials
have not been reported to support this[2]. An especially encouraging result
from Powell, Heslin and Greenwood’s study was the finding that
multidisciplinary community rehabilitation can produce beneficial results
for individuals several years after sustaining a brain injury[1].
It is often thought that the cognitive, emotional and behavioural
difficulties following brain injury create the greatest barriers to a
favourable outcome[3]. Powell, Heslin and Greenwood’s study used outcome
measures focusing on levels of activity and participation[1]. We report
preliminary results of multidisciplinary community based rehabilitation
utilising an outcome measure focused on cognitive, emotional, behavioural
and social difficulties following brain injury. The European Brain Injury
Questionnaire (EBIQ) consists of two parallel forms related to
difficulties experienced in the previous month and is completed
independently by a patient and a carer[4]. The EBIQ is a routinely used
outcome measure in our Service.
Our preliminary data were retrospectively obtained from 19
participants with an acquired brain injury for who repeated EBIQ measures
were available. All participants received individualised
multidisciplinary community based rehabilitation. Average age was 37.9
years (SD = 12.2); fourteen participants were male. Seventeen sustained a
traumatic brain injury and two a cerebrovascular accident. The average
time between the first and second EBIQ measures was 10.9 months (SD =
3.2). A Wilcoxon comparison revealed a significant improvement in the
subjective self-report of symptoms among participants (T = -25.5, p <
.01), whose mean total EBIQ scores were reduced from 126.7 (SD = 28.7) to
114.7 (SD = 27.4). However, while carers' EBIQ ratings decreased from a
mean score of 123.9 (SD = 31.0) to 119.4 (SD = 33.4), this did not reach
statistical significance.
The average time since injury was 78.7 months (range = 11 to 324
months, SD = 92.2). In most cases, it was unlikely that the EBIQ
improvements were attributable to spontaneous recovery, which often
continues to be observed over the first 24 months. However, as four
participants completed their first EBIQ within two years of injury, we
also compared participants' ratings with their data excluded. The
repeated EBIQ ratings for this sub-group (N=15) continued to show a
significant improvement (T = -11.5,
p<_01. p="p"/> Our preliminary data, while clearly limited, lend further support to
Powell, Heslin and Greenwood’s1 important findings. People with a brain
injury’s subjective experience of cognitive, emotional, behavioural and
social difficulties appear to be amenable to multidisciplinary
rehabilitation in the community. These difficulties may create
significant barriers to a favourable outcome and should always be
addressed in rehabilitation. The finding that carers did not rate
participants as significantly improved may have important implications.
One explanation for this finding could be that they become sensitised and
more aware of the brain injured person’s difficulties over time. This
would be in agreement with previous research[5]. A clear implication would
be that carers should be included in the rehabilitation process to ensure
outcomes that are favourable for the family.
The National Service Framework (NSF) for Long Term Health Conditions,
which will cover brain injury, is expected to appear during 2004. The
research of Powell, Heslin and Greenwood[1] takes on special significance in
view of the NSF. It is hoped that their encouraging results would indeed
stimulate further research and provide some motivation for the development
of more community based rehabilitation services to complement hospital
based services.
B. R. Coetzer & F. L. Vaughan
North Wales Brain Injury Service
Colwyn Bay Hospital
Hesketh Road
Colwyn Bay
LL29 8AY
United Kingdom
References
(1) Powell J, Heslin J, Greenwood R. Community based rehabilitation
after a severe traumatic brain injury: a randomised controlled trial. J
Neurol Neurosurg Psychiatry 2002; 72: 193 – 202.
(2) Cope DN. The effectiveness of traumatic brain injury rehabilitation.
Brain Inj 1995; 9: 649 – 670.
(3) Lishman WA. Organic Psychiatry. The psychological consequences of
cerebral disorder (3rd Ed). Blacwell Science 1998; Oxford.
(4) Teasdale TW, Christensen AL, Wilmes K et al. Subjective experience in
brain-injured patients and their close relatives. A European Brain Injury
Questionnaire Study. Brain Inj 1997; 11: 543 – 563.
(5) Brooks N, Campsie L, Symington C et al. The five year outcome of severe
blunt head injury: a relative’s view. J Neurol Neurosurg Psychiatry 1986;
49: 764 – 770.
The article by Kramer et al [1] suggests that
subcortical ischaemic vascular disease is associated with subtle declines
in executive functioning and visual memory, even in non-demented patients.
The authors compared 27 control subjects and 12 non-demented patients,
which were selected after exclusion of major depression, bipolar affective
disorder, and other DSM-IV I axis disorders. We wish to contribute...
The article by Kramer et al [1] suggests that
subcortical ischaemic vascular disease is associated with subtle declines
in executive functioning and visual memory, even in non-demented patients.
The authors compared 27 control subjects and 12 non-demented patients,
which were selected after exclusion of major depression, bipolar affective
disorder, and other DSM-IV I axis disorders. We wish to contribute with
personal data to this topic suggesting that, even in absence of a clinical
diagnosis of depression, depressive symptoms may modulate executive
dysfunctions in non demented subjects with cerebrovascular disease.
We examined 34 consecutive patients with cognitive impairment-no
dementia (CI-ND) (mean + SD, age: 78.1 + 6.3, range 65-90; years of
education: 4.9 + 1.7, range 3-10; Mini Mental State Examination score:
24.0 + 2.4, range 18-27). The diagnosis of CI-ND was made on the basis of
a standardized multidimensional protocol including history, clinical
examination, detailed neuropsychological testing, and computed tomographic
scan. The presence and severity of cortical, white matter, and deep
subcortical lesions and of leukoaraiosis were assessed on computed
tomographic film with a standardized visual rating scale.[2]
With this method, the patients were quantitatively divided in two groups
(50th percentile) according to the severity of cerebrovascular disease: 17
patients had none or mild, and 17 had moderate or severe cerebrovascular
disease. The 2 groups had similar age (mean + SD, age: 79.1 + 6.5 and 76.9
+ 6.0; p =0.31, t-test), educational level (mean + SD, years of schooling:
4.7 + 1.5 and 5.3 + 1.9; p =0.27 t-test), cognitive impairment (mean + SD,
Mini Mental State Examination score: 24.2 + 2.7 and 23.8 + 2.0; p =0.63 t-
test), functional status (mean + SD, Barthel Index: 85.3 + 18.9 and 80.8 +
21.4; p =0.57, t-test), and comorbidity (mean + SD, Charlson Index: 2.1 +
2.2 and 2.2 + 1.6; p =0.95, t-test). Comparing the neuropsychological
tests, we found that the patients in the group with none or mild
cerebrovascular disease performed better on Babcock (mean + SD, score:
11.3 + 2.3 and 8.6 + 3.0; p =0.01, t-test), on digit symbol (mean + SD,
associations in 90 seconds: 14.3 + 6.8 and 11.7 + 4.9; p =0.24, t-test),
on trail making A (mean + SD, seconds: 143.0 + 82.6 and 228.2 + 157.7; p
=0.05, t-test), but were significantly less depressed (mean + SD number of
symptoms on Center of Epidemiological Studies-depression scale: CES-D,
10.8 + 7.2 and 18.8 + 6.6; p =0.002, t-test). However, when the effect of
cerebrovascular severity on all significant variables was weighted in a
multivariate linear regression model, only depressive symptoms maintained
the statistical significance (CES-D: B: 0.82; confidence intervals [C.I.],
1.2-4.5; p =0.02).
Several studies have demonstrated that depressed patients have a
lower performance than non depressed ones on executive functions[3].
Furthermore, the relationship between cerebrovascular disease and
depression has recently been established.[4] In their study, Kramer and
colleagues performed an extensive neuropsychological evaluation, but
failed to take in consideration that depressive symptoms may be detected
in elderly population even after exclusion of major depression. On the
contrary, we suggest that depressive symptoms need to be considered in the
interpretation of even subtle executive dysfunctions in cerebrovascular
disease patients.
References (1) Kramer JH, Reed BR, Mungas D, et al. Executive dysfunction in
subcortical ischaemic vascular disease. J Neurol Neurosurg Psychiatry
2002; 72:217-220.
(2) Frisoni GB, Beltramello A, Binetti G, et al. Computer tomography
in the detection of the vascular component in dementia. Gerontology 1995;
41:121-128.
(3) Channon S, Green PSS. Executive function in depression: the role
of performance strategies in aiding depressed and non-depressed
participants. J Neurol Neurosurg Psychiatry 1999; 66:162-171.
(4) Alexopoulos GS, Meyer BS, Young RC, et al. “Vascular depression”
hypothesis. Arch Gen Psych 1997; 10: 915-922.
The Beck Depression Inventory (BDI) scores were not correlated with
cortisol levels in our study. In addition, cortisol levels in patients
with BDI score higher than 16 (and 21) were not different from those with
score 16 (and 21) or lower.
We agree hypercortisolemia is a feature of CM with co-morbid
depression, and not CM alone, ho...
The Beck Depression Inventory (BDI) scores were not correlated with
cortisol levels in our study. In addition, cortisol levels in patients
with BDI score higher than 16 (and 21) were not different from those with
score 16 (and 21) or lower.
We agree hypercortisolemia is a feature of CM with co-morbid
depression, and not CM alone, however, depression is present in 80% of CM
patients [1], and CM without depression is, in fact, a small subgroup of
patients.
Reference (1) Mathew NT, Stubits E, Nigam MP. Transformation of episodic
migraine into daily headache: analysis of factors. Headache 1982;22:66-8.
Peres et al (2001) are to be congratulated for advancing the limited
neuroendocrine literature on chronic migraine, a disorder with a
significant attendant morbidity and a poorly understood pathophysiology.
A few points however deserve mention.
In their introduction, the authors rightly highlight that chronic
migraine (CM) and major depression are strongly associated. However, in
this...
Peres et al (2001) are to be congratulated for advancing the limited
neuroendocrine literature on chronic migraine, a disorder with a
significant attendant morbidity and a poorly understood pathophysiology.
A few points however deserve mention.
In their introduction, the authors rightly highlight that chronic
migraine (CM) and major depression are strongly associated. However, in
this study they do not appear to have controlled for this. There is no
mention of a psychiatric interview. Although they allude to the Beck
Depression Inventory in the Methods section, there is no mention in the
results section of the relationship between depression and cortisol in CM.
This is an important omission as overactivity of the hypothalamic-
pituitary-adrenal axis with peripheral hypercortisolemia occurs commonly
in people with major depressive disorder, the rates of overactivity
increasing with increasing severity of depression.[1]
In addition the authors make no mention of the existing literature on
serum cortisol in CM subjects. It was found that 14/48
(29%) subjects with chronic daily headache [2], the majority of whom had
migraine were non-suppressors of cortisol following dexamethasone. In a
second study [3], the same authors found that 44% of
subjects showed either basal cortisol concentrations higher than controls
or non-suppression following dexamethasone. A limitation to these 2 well
designed studies is that depression scores in the CM subjects were in the
depressed range. The present study by Peres et al (2001), by not excluding
or controlling for depression suffers the same limitation.
Thus one can only conclude from the literature to date on CM, that
hypercortisolemia is a feature of CM with co-morbid depression. One cannot
however come to the conclusion that hypercortisolemia is a feature of CM
alone.
References
(1) Dinan, TG (1994) Glucocorticoids and the genesis of depressive illness;
A psychobiological model. British Journal of Psychiatry, 164, 365-371
(2) Martignoni E, Facchinetti F, Manzoni GC, Petraglia F, Nappi G,
Genazzani AR (1986). Abnormal dexamethasone suppression test in daily
chronic headache sufferers. Psychiatry Research 19, 51-7.
(3) Martignoni E, Facchinetti F, Rossi F, Sances AR, Genazzani AR,
Nappi G (1989). Neuroendocrine evidence of deranged noradrenergic
activity in chronic migraine. Psychoneuroendocrinology 14, 357-363
I enjoyed reading the editorial "Getting our Journal to developing
countries".
I think the BMJ Publishing Group is doing a yeoman service to doctors
and patients in developing countries by providing free internet access to
the BMJ journals. As a consultant in a teaching institution with "bare"
library shelves I can attest to the fact that this free internet access to
BMJ journals is a boon to...
I enjoyed reading the editorial "Getting our Journal to developing
countries".
I think the BMJ Publishing Group is doing a yeoman service to doctors
and patients in developing countries by providing free internet access to
the BMJ journals. As a consultant in a teaching institution with "bare"
library shelves I can attest to the fact that this free internet access to
BMJ journals is a boon to doctors in developing countries. I now encourage
my colleagues and students to access these journals online and benefit
from them.
I hope this practice will spread to other parts of the developing
world.
May your tribe increase.
Thanking you,
Yours,
Dr.N.Muthukumar
Department of Neurosurgery
Madurai Medical College
Madurai
India.
I must thank you for making eJNNP free on the net for the
developing countries. I was so excited by this news that I couldn't sleep
the whole night and kept on browsing the JNNP site. It's indeed a great
service to the neurologists of all the developing nations. I sincerely hope
that the American Academy of Neurology follows suit and makes Neurology available on the net for developing nation...
I must thank you for making eJNNP free on the net for the
developing countries. I was so excited by this news that I couldn't sleep
the whole night and kept on browsing the JNNP site. It's indeed a great
service to the neurologists of all the developing nations. I sincerely hope
that the American Academy of Neurology follows suit and makes Neurology available on the net for developing nations. Could you
please suggest this to them when you meet their editor?
Yours truly
Dr. A. Apte
Consultant Neurologist
Surat ,Gujarat
India
Dear Editor
This correspondence is for the author:
I am writing in response to your interview on Radio 4 - aired 20/09/02 and after having read the abstract for the above research. My question is simple. You argue that sexual transmission is not the only cause of MS and instead there are inherited factors that make someone who already has a sexually transmitted neurotropic agent more susceptible to...
Dear Editor
In your recent summary you seem to mix up two items when discussing some of our work: The fact (as shown with control groups, Wernig et al. 1995,1998, 1999) that locomotion can significantly be improved by this specific locomotor training (some call it "body weight assisted", some call it "locomotion therapy on the treadmill", we call it "Laufband therapy") and the question where in the CNS the l...
Dear Editor
It is of indeed of great interest to learn of the results of the study by Zeloni et al. (Viewing less to see better). The hemiblinding procedure seems to effectively improve utilisation of the neglected field and enhance recovery.
This, no doubt, would be an important technique for rehabilitation of patients with visuospatial hemineglect.
In my series of patients (36 patients) w...
Dear Editor
The case presented is of particular interest. Tumour-like MS plaques present and behave in a delinquent manner, unlike the classic ones. However, with no evidence of demyelination elsewhere, no paraclinical support, a somehow meager description of "demyelination with macrophages etc" wouldn't it be better to call this lesion an "isolated demyelinating CNS lesion" as proposed by others?
Dear Editor
Powell, Heslin and Greenwood[1] are to be commended for their study reporting the results of community based rehabilitation following traumatic brain injury. While the effectiveness of rehabilitation following brain injury has been acknowledged, randomised controlled trials have not been reported to support this[2]. An especially encouraging result from Powell, Heslin and Greenwood’s study was the fin...
Dear Editor
The article by Kramer et al [1] suggests that subcortical ischaemic vascular disease is associated with subtle declines in executive functioning and visual memory, even in non-demented patients. The authors compared 27 control subjects and 12 non-demented patients, which were selected after exclusion of major depression, bipolar affective disorder, and other DSM-IV I axis disorders. We wish to contribute...
Dear Dr Eugene Cassidy,
Thanks for your letter and comments.
The Beck Depression Inventory (BDI) scores were not correlated with cortisol levels in our study. In addition, cortisol levels in patients with BDI score higher than 16 (and 21) were not different from those with score 16 (and 21) or lower.
We agree hypercortisolemia is a feature of CM with co-morbid depression, and not CM alone, ho...
Dear Editor
Peres et al (2001) are to be congratulated for advancing the limited neuroendocrine literature on chronic migraine, a disorder with a significant attendant morbidity and a poorly understood pathophysiology.
A few points however deserve mention.
In their introduction, the authors rightly highlight that chronic migraine (CM) and major depression are strongly associated. However, in this...
Dear Editor
I enjoyed reading the editorial "Getting our Journal to developing countries".
I think the BMJ Publishing Group is doing a yeoman service to doctors and patients in developing countries by providing free internet access to the BMJ journals. As a consultant in a teaching institution with "bare" library shelves I can attest to the fact that this free internet access to BMJ journals is a boon to...
Dear Professor Kennard
I must thank you for making eJNNP free on the net for the developing countries. I was so excited by this news that I couldn't sleep the whole night and kept on browsing the JNNP site. It's indeed a great service to the neurologists of all the developing nations. I sincerely hope that the American Academy of Neurology follows suit and makes Neurology available on the net for developing nation...
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