I read with interest your review of "Internet resources for psychiatry and neuropsychiatry".[1]
I would agree that "[there] are rather fewer resources specifically dedicated to neuropsychiatry [...]. This reflects the nature of the beast - after 50 or more years of sometimes rather heavy-handed attempts to separate neurology from psychiatry (and sometimes, vice-versa) there is now a fair amount of co...
I read with interest your review of "Internet resources for psychiatry and neuropsychiatry".[1]
I would agree that "[there] are rather fewer resources specifically dedicated to neuropsychiatry [...]. This reflects the nature of the beast - after 50 or more years of sometimes rather heavy-handed attempts to separate neurology from psychiatry (and sometimes, vice-versa) there is now a fair amount of confusion in the medical and the lay public about what exactly neuropsychiatry means. Although discussed together with neuropsychology in your article, it has little to do with the latter. Also, neuropsychology (sic) resources abound, on and off the Internet. It is, unlike neuropsychiatry, a sharply defined discipline.
I would like to bring to your attention, somewhat self-referentially, my new web site, http://www.psychiatryneurology.com, that attempts to illustrate the newly rediscovered interface of neurology and psychiatry at length. It is to my knowledge, the only physician run web site dedicated to neuropsychiatry. A discussion of how re-integrating aspects of neurology and psychiatry would improve patient care can be found in the BMJ, at http://bmj.com/cgi/eletters/324/7352/1468#28326
Reference
(1) Internet resources for psychiatry and neuropsychiatry
J Stone and M Sharpe. J Neurol Neurosurg Psychiatry 2003; 74: 10-12.
This is a very nicely done study. I agree with the authors that the
lack of multivariable significance of the straight leg (SLR) sign is
disturbing. The authors propose a physiologic explanation for the lack of
association; however, I think the results support the usefulness of the
SLR.
I urge the authors to analyze their results with recursive
partitioning with weighted marginals to emphasize...
This is a very nicely done study. I agree with the authors that the
lack of multivariable significance of the straight leg (SLR) sign is
disturbing. The authors propose a physiologic explanation for the lack of
association; however, I think the results support the usefulness of the
SLR.
I urge the authors to analyze their results with recursive
partitioning with weighted marginals to emphasize sensitivity. In the
univariate analysis, the SLR was significant and by far the most sensitive
sign. If the clinician uses the physical examination to decide which
patients need imaging, then the clinician wants a sensitive examination.
Logistic regression and the gain in certainty of Connell and Koepsell both
optimize overall diagnostic accuracy. A reanalysis using weighted
recursive partitioning may reveal that the SLR does have a role when the
clinician wants a sensitive physical examination.
We have a 47 year old female who has spinal myoclonus with segmental
myoclonus of the legs involving the L5 and S1 myotomes. She exhibited
spinal jerking and leg tremors after herniation of L5-S1 intervertebral
disc. Even after decompression and fusion of the segment the spinal and
segmental myoclonus remains.
1. We are looking for treatment approaches for the myoclonus and would
appreci...
We have a 47 year old female who has spinal myoclonus with segmental
myoclonus of the legs involving the L5 and S1 myotomes. She exhibited
spinal jerking and leg tremors after herniation of L5-S1 intervertebral
disc. Even after decompression and fusion of the segment the spinal and
segmental myoclonus remains.
1. We are looking for treatment approaches for the myoclonus and would
appreciate any recommendations.
2. There appears to be central sensitization present to explain the
hypersensitivity and low tremor threshold. Any other pathophysiological
processes to explain the myoclonus after peripheral nerve injury?
The findings published in this article are very interesting. They bring about two questions:
1 - Does the triptans, being vasoconstrictors, make a migraine
related stroke more likely? If so, we are doing a disservice to our
patients. We need to know it now.
2 - Do women with classical migraine need primary stroke prophylaxis?
Does the prophylaxis against migraine also work for stroke?
The findings published in this article are very interesting. They bring about two questions:
1 - Does the triptans, being vasoconstrictors, make a migraine
related stroke more likely? If so, we are doing a disservice to our
patients. We need to know it now.
2 - Do women with classical migraine need primary stroke prophylaxis?
Does the prophylaxis against migraine also work for stroke?
I read with pleasure the paper of Garrard et al.[1] outlining the cognitive
sequels in patients with a more or less isolated brain stem lesion.
Nevertheless, their results might be hampered by several potential
pitfalls.
First, a lesion is not a lesion; it depends on the pathological
substrate. So the inclusion of cavernomas might be misleading, as even MRI
can’t exclude the presence of a...
I read with pleasure the paper of Garrard et al.[1] outlining the cognitive
sequels in patients with a more or less isolated brain stem lesion.
Nevertheless, their results might be hampered by several potential
pitfalls.
First, a lesion is not a lesion; it depends on the pathological
substrate. So the inclusion of cavernomas might be misleading, as even MRI
can’t exclude the presence of a second or even multiple lesions, as it can
be the case in cavernomatosis. Furthermore, the presence of extensive
vasogenic oedema might make a difference when comparing to brain stem
stroke.
The discussion on the neuropsychological sequels of MS remains
difficult: it is probable that even clinically and radiologically non-
existent lesions might be there due to technical reasons, and thus may not
be taken into account for the interpretation of the neuropsychological
results. It is noteworthy that the full extent of brain stem lesion is not
always visualised, and sometimes might only be proven by means of
electrophysiology (Thömke and Hopf 1998 [2], Thömke et al. 2002[3]). This implies
the importance of the pathophysiology of the stroke. Is it
microangiopathic or embolic? It is possible to find a brainstem stroke as
a first-ever stroke, but unlikely. If the stroke was embolic, it could be
that other structures of the brainstem are compromised escaping
visualisation. I oberserved a patient who had a pontine stroke following
basilar artery embolism of unknown origin. He had a auditory deficit
localised to the superior olivary complex on the right, but with the
auditory brainstem spared following MRI criteria. The wave III of the AEP
had initially disappeared, and reappeared with significant delay within
the course of several months. Psychoacoustic testing showed left-ear
advantage instead of right-ear advantage, which resolved in parallel with
the AEP. Clinically, the patient had important susceptibility to auditory
interference (unpublished observation).
The described deficits include almost constantly dysexecutive syndrome and
diminuished attention. There doesn’t seem to be a localizing value of the
neuropsychological findings. Could it be that the authors described
pathology similar to the cerebellar cognitive affective syndrome of
Schmahman, but as a disconnection syndrome (Schmahman and Sherman 1998 [4]).
"Frontal executive functions" is a misleading term. In fact, executive
functions were introduced, as description of functions that were thought
be associated with frontal lobe functioning. But using the term use in the
context of diaschisis and an isolated brain stem lesion might be
misleading and is contradictory.
It is surprising that seemingly every brain stem stroke in this series had
cognitive trouble. In the series of Miyazawa et al[5], the Xenon-CT was
suggestive of diaschisis in only 36 of 105 patients, but
neuropschyological testing was lacking (Miyazawa et al., 1999). The study
of Hoffmann and Watts [6] prospectively examined five patients by means of
SPECT and neuropschyology, and their results were confirmed in the present
study (Hoffmann and Watts 1998).
References
(1) P Garrard, D Bradshaw, H R Jäger, A J Thompson, N Losseff, and D PlayfordCognitive dysfunction after isolated brain stem insult. An underdiagnosed cause of long term morbidity. J Neurol Neurosurg Psychiatry 2002;73: 191-194
(5) Miyazawa N, Uchida M, Fukamachi A, Fukasawa I, Sasaki H, Nukui H. Xenon
contrast-enhanced CT imaging in patients with brain stem infarction. AJNR
1999;20: 1858-62.
(6) Hoffmann M, Watts A. Cognitive dysfunction in isolated brainstem stroke: a
neuropsychological and SPECT study. J Stroke Cerebrovasc Dis7 (1); 24-31.
Dr McCorry makes an intriguing point that has indeed occurred to us
before. It is theoretically possible that a positive PCR HSV result in the
CSF could reflect asymptomatic HSV latency in the sensory ganglia and/or
CNS and not viral reactivation causing encephalitis. However, it would be
difficult to explain how the virus reaches the CSF from the ganglia or
brain in the absence of reactivation. Also, i...
Dr McCorry makes an intriguing point that has indeed occurred to us
before. It is theoretically possible that a positive PCR HSV result in the
CSF could reflect asymptomatic HSV latency in the sensory ganglia and/or
CNS and not viral reactivation causing encephalitis. However, it would be
difficult to explain how the virus reaches the CSF from the ganglia or
brain in the absence of reactivation. Also, in practical terms, the PCR
test has been shown in several studies to have a very high specificity ie
a very low false positive rate, this being based on testing of large
numbers of CSF samples from individuals with conditions other than herpes
simplex encephalitis. So in practice this possibility seems not to be a
problem. In order to answer this question unequivocally it would be
necessary to correlate CSF positivity or negativity for HSV with known
ganglionic positivity. But this is not possible in practice since the
demonstration of HSV latency in ganglia has been based on autopsy studies,
such tissues not being accessible in live individuals.
The assumption is that if PCR for HSV in the CSF is positive this
then confirms the diagnosis of Herpes Simplex Encephalitis, yet it is
known that the HSV genome is found in 85-90% of patients at unselected
necroscopy in the trigeminal ganglion and so do we know whether HSV DNA
can be found in healthy individuals? Could it be that some positive PCR
results are truely positive, and not due to con...
The assumption is that if PCR for HSV in the CSF is positive this
then confirms the diagnosis of Herpes Simplex Encephalitis, yet it is
known that the HSV genome is found in 85-90% of patients at unselected
necroscopy in the trigeminal ganglion and so do we know whether HSV DNA
can be found in healthy individuals? Could it be that some positive PCR
results are truely positive, and not due to contamination, but do not
reflect Herpes simplex encephalitis. If this were the case then PCR tests
for patients with 'atypical' or 'mild' disease would carry a significant
false positive rate.
Reply to Heidi Watson
What I suggested is that some people are born with gene(s)that confer
susceptibility to a sexually transmissible agent, perhaps a retrovirus. If
and when they come into contact with the agent then the disease may
develop. This principle is well known and applies to other non-sexually
tranmitted infections such as TB, leprosy, leishmaniasis and
poliomyelitis....
Reply to Heidi Watson
What I suggested is that some people are born with gene(s)that confer
susceptibility to a sexually transmissible agent, perhaps a retrovirus. If
and when they come into contact with the agent then the disease may
develop. This principle is well known and applies to other non-sexually
tranmitted infections such as TB, leprosy, leishmaniasis and
poliomyelitis.
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).
Dear Editor
I read with interest your review of "Internet resources for psychiatry and neuropsychiatry".[1]
I would agree that "[there] are rather fewer resources specifically dedicated to neuropsychiatry [...]. This reflects the nature of the beast - after 50 or more years of sometimes rather heavy-handed attempts to separate neurology from psychiatry (and sometimes, vice-versa) there is now a fair amount of co...
Dear Editor
This is a very nicely done study. I agree with the authors that the lack of multivariable significance of the straight leg (SLR) sign is disturbing. The authors propose a physiologic explanation for the lack of association; however, I think the results support the usefulness of the SLR.
I urge the authors to analyze their results with recursive partitioning with weighted marginals to emphasize...
Dear Editor
We have a 47 year old female who has spinal myoclonus with segmental myoclonus of the legs involving the L5 and S1 myotomes. She exhibited spinal jerking and leg tremors after herniation of L5-S1 intervertebral disc. Even after decompression and fusion of the segment the spinal and segmental myoclonus remains.
1. We are looking for treatment approaches for the myoclonus and would appreci...
Dear Editor
The findings published in this article are very interesting. They bring about two questions:
1 - Does the triptans, being vasoconstrictors, make a migraine related stroke more likely? If so, we are doing a disservice to our patients. We need to know it now.
2 - Do women with classical migraine need primary stroke prophylaxis? Does the prophylaxis against migraine also work for stroke?
...Dear Editor
I read with pleasure the paper of Garrard et al.[1] outlining the cognitive sequels in patients with a more or less isolated brain stem lesion. Nevertheless, their results might be hampered by several potential pitfalls.
First, a lesion is not a lesion; it depends on the pathological substrate. So the inclusion of cavernomas might be misleading, as even MRI can’t exclude the presence of a...
Dear Editor
Dr McCorry makes an intriguing point that has indeed occurred to us before. It is theoretically possible that a positive PCR HSV result in the CSF could reflect asymptomatic HSV latency in the sensory ganglia and/or CNS and not viral reactivation causing encephalitis. However, it would be difficult to explain how the virus reaches the CSF from the ganglia or brain in the absence of reactivation. Also, i...
Dear Editor
The assumption is that if PCR for HSV in the CSF is positive this then confirms the diagnosis of Herpes Simplex Encephalitis, yet it is known that the HSV genome is found in 85-90% of patients at unselected necroscopy in the trigeminal ganglion and so do we know whether HSV DNA can be found in healthy individuals? Could it be that some positive PCR results are truely positive, and not due to con...
Dear Editor
Reply to Heidi Watson
What I suggested is that some people are born with gene(s)that confer susceptibility to a sexually transmissible agent, perhaps a retrovirus. If and when they come into contact with the agent then the disease may develop. This principle is well known and applies to other non-sexually tranmitted infections such as TB, leprosy, leishmaniasis and poliomyelitis....
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...
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