In their interesting paper Bower and colleagues report results of a
study employing manual amygdala volumetry to imaging-negative patients
with refractory temporal lobe epilepsy (TLE).[1] They identify 7 out of 11
patients in whom they diagnose amygdala enlargement and postulate this
might be attributable to developmental abnormality or low grade tumor.
In their interesting paper Bower and colleagues report results of a
study employing manual amygdala volumetry to imaging-negative patients
with refractory temporal lobe epilepsy (TLE).[1] They identify 7 out of 11
patients in whom they diagnose amygdala enlargement and postulate this
might be attributable to developmental abnormality or low grade tumor.
However, in discussing their interesting observation the authors do not
mention the extensive literature on amygdala enlargement in different
neuropsychiatric conditions. Significant amygdala enlargement has been
reported in patients with unipolar [2] and bipolar depression,[3] and in fact
in patients with refractory TLE and depression and psychosis of
epilepsy.[4,5] Amygdala volumes are increased in first episode major
depression and seem to „normalise“ in the course of the disease.[2]
Finally,
there is some evidence that amygdala volumes might be affected by
psychotropic medication.6 While the mechanism of amygdala enlargement in
all these cases is unknown and open to discussion most of the authors
quoted favour more dynamic mechanisms compared to developmental
abnormalities or tumors. The fact that initial amygdala enlargement seems
to normalise in the course of depression [2] or in case of antipsychotic
medical treatment supports a dynamic underlying mechanism. The fact that
patients with TLE were classified as imaging-negative implies that no
lesional pathology was recognisable on standard MRI investigations.
However, when amygdala enlargement is noted on volumetric findings alone
it is very likely that mechanisms other than developmental abnormalities
or low grade tumours are involved. The investigators should control for
psychiatric morbidity when assessing amygdala volumes. Further more,
Furthermore, one should be very cautious with basing a decision for or
against surgery purely on volumetric findings of the amygdala.
Reference
1. Bower SP, Vogrin SJ, Morris K, et al. Amygdala volumetry in
"imaging-negative" temporal lobe epilepsy. J.Neurol.Neurosurg.Psychiatry
2003;74:1245-9.
2. Frodl T, Meisenzahl EM, Zetzsche T, et al. Larger amygdala
volumes in first depressive episode as compared to recurrent major
depression and healthy control subjects. Biol Psychiatry 2003;53:338-44.
3. Strakowski SM, DeBello MP, Sax KW, et al. Brain magnetic
resonance imaging of structural abnormalities in bipolar disorder. Arch
Gen Psychiatry 1999;56:254-60.
4. Tebartz vE, Woermann FG, Lemieux L, et al. Amygdala enlargement
in dysthymia--a volumetric study of patients with temporal lobe epilepsy.
Biol Psychiatry 1999;46:1614-23.
5. Tebartz vE, Baeumer D, Lemieux L, et al. Amygdala pathology in
psychosis of epilepsy: A magnetic resonance imaging study in patients with
temporal lobe epilepsy. Brain 2002;125:140-9.
6. Tebartz van Elst L, Baeumer D, Ebert D, et al. Chronic
antidopaminergic medication might affect amygdala structure in patients
with schizophrenia. J Clin Psychopharmacology (In Press)
We read with attention the report of Adler and colleagues.[1]
By studying 20 patients with Alzheimer’s
disease (AD) assigned to rivastigmine, the authors found that baseline
short-term memory performances and EEG data are useful for predicting
response to treatment at 6 months.
We would like to contribute to this topic with our own personal data on 24
AD subjects treated for 9 months w...
We read with attention the report of Adler and colleagues.[1]
By studying 20 patients with Alzheimer’s
disease (AD) assigned to rivastigmine, the authors found that baseline
short-term memory performances and EEG data are useful for predicting
response to treatment at 6 months.
We would like to contribute to this topic with our own personal data on 24
AD subjects treated for 9 months with rivastigmine. Subjects were on
average old (mean age = 79.0+5.5 years), predominantly females (n= 16,
65.2%), with a mild cognitive (mean Mini Mental State Examination, MMSE
score =19.5+3.4) and functional (mean number of activities of daily
living, ADL lost = 1.3+1.6) decline. None of them had been previously
treated with other cholinesterase inhibitors or rivastigmine.
As a whole, subjects showed a slight improvement in MMSE score from
baseline to 3 months (mean MMSE score = 19.9+4.4) and the return close to
baseline levels by 9 months (mean MMSE score = 19.4+5.2). However, 9
patients decreased 1 or more MMSE points (non-responders), while 15 did
not change MMSE score or increased 1 or more MMSE points (responders) at 9
months. In order to evaluate whether some specific MMSE items were
predictive of response to treatment at 9 months, the variation of the
scores for each MMSE items from baseline to 3rd month was calculated. In a
stepwise regression model, after adjusting for all potential confounders
(age, gender, duration of disease, and ADL at baseline) and covariates
(total and single items MMSE scores at baseline), the variation at 3rd
month in the score of the MMSE item “delayed recall” was the only
independently and significantly associated with the variation of global
MMSE score at 9th month (B=2.50, 95% confidence intervals 1.28-3.72;
p=.000).
Our data suggest that the variation in a specific MMSE item (i.e. “delayed
recall”) at 3rd month may represent a useful marker of cognitive
improvement at 9th month, indicating that a peculiar neurobiological
structure, responsible of a selective neuropsychological domain, should be
a preferential target of rivastigmine therapeutic action.
References
1. Adler G, Brassen S, Chwalek K, Dieter B and Teufel M. Prediction of
treatment response to rivastigmine in Alzheimer’s dementia. J Neurol
Neurosurg Psychiatry 2004; 75:292-294.
Dodson [1] described the successful and “novel” use of cold-water
caloric ear irrigation in a manic woman, stating that the effect of this
procedure on psychiatric symptomatology has not been reported. In fact,
there is nothing new [2] about shock measures that overstimulate, exhaust, or
generally reset the vestibular system, including cold water poured onto
the head, swings to induce vertigo, emetics t...
Dodson [1] described the successful and “novel” use of cold-water
caloric ear irrigation in a manic woman, stating that the effect of this
procedure on psychiatric symptomatology has not been reported. In fact,
there is nothing new [2] about shock measures that overstimulate, exhaust, or
generally reset the vestibular system, including cold water poured onto
the head, swings to induce vertigo, emetics to produce nausea and
vomiting, and electrical stimulation of the head and labyrinth.
It is, of course, fashionable nowadays to patronise the mad doctors,
labelling them credulous fools, mercenary quacks, state torturers,
religious bigots or moral zealots. However, the simplest explanation, and
the scientifically most productive, is to assume that doctors then and
indeed now offer treatments that they think benefit patients. Of course
they could be, and often are, mistaken about this. It is implausible that
these mad doctors administered these expensive and unpleasant treatments
using complicated apparatus unless they saw, or thought they saw, benefits
in their patients. Ironically, Dodson had his article published based on
results from a single patient!
I suggest people adopt an open mind about these treatments, and read
the primary sources. Meanwhile, Dodson’s finding can easily be followed up
in a broader range of patients. Perhaps someone can take some psychotics
for a ride on a roller coaster.
Reference
1. Dodson MJ. Vestibular stimulation in mania: case report. J Neurol
Neurosurg Psychiatry 2004;75:168-9.
.
2. Hunter R, Macalpine I. Three hundred years of psychiatry: 1535-1860.
London: Oxford University Press,1963.
The report by Hausmann et al.[1] adds to negative experiences with
rTMS as an add-on strategy in patients with major depression.[2] However,
again, the evidence is not completely convincing. In this study, only
"slight" effects were expected, but the sample size did not appear to
account for that. 25 vs. 13 patients may not suffice to detect - and even
less to refute - slight effects.
The report by Hausmann et al.[1] adds to negative experiences with
rTMS as an add-on strategy in patients with major depression.[2] However,
again, the evidence is not completely convincing. In this study, only
"slight" effects were expected, but the sample size did not appear to
account for that. 25 vs. 13 patients may not suffice to detect - and even
less to refute - slight effects.
This study contributes to disproving the
existence of large antidepressant effects of add-on rTMS, but conclusions
regarding smaller effects should be avoided. A careful analysis of the
statistical power would have been helpful.
References
1. Hausmann A, Kemmler G, Walpoth M, Mechtcheriakov S, Kramer-
Reinstadler K, Lechner T, Walch T, Deisenhammer E, Kofler M, Rupp C,
Hinterhuber H, Conca A. No benefit derived from repetitive transcranial
magnetic stimulation in depression: a prospective, single centre,
randomised, double blind, sham controlled "add on" trial. Journal of
Neurology, Neurosurgery and Psychiatry 2004;75:320-322.
2. Garcia-Toro M, Pascual-Leone A, Romera M, Gonzalez A, Mico J,
Ibarra O, Arnillas H, Capllonch I, Mayol A, Tormos JM. Prefrontal
repetitive transcranial magnetic stimulation as add on treatment in
depression. J Neurol Neurosurg Psychiatry. 2001 Oct;71(4):546-8.
Williams and colleagues underscore the non-specific relationship
between depression and pain in patients seen early at neurology clinics in
wide range of unconnected disorders; patients with primary headaches
constituted a substantial cohort in this study.[1] This clinical study makes
an important contribution to maintain perspective in primary headache
research.
Williams and colleagues underscore the non-specific relationship
between depression and pain in patients seen early at neurology clinics in
wide range of unconnected disorders; patients with primary headaches
constituted a substantial cohort in this study.[1] This clinical study makes
an important contribution to maintain perspective in primary headache
research.
Several epidemiological studies have concluded that a bidirectional
link exists between migraine and depression that, in turn, suggests a
shared pathogenesis.[2,3] In primary headache research it has been assumed
that:
(i) Migraine is the outcome of brain serotonergic hyperactivity; and
(ii) Brain serotonergic antagonism is the probable mechanism of action of
migraine prophylactic agents such as beta-blockers, calcium channel
antagonists, and antidepressants. What has, nevertheless, as yet not been
acknowledged is that both serotonergic antagonists [4] and serotonin agonists
offer effective migraine prophylaxis. Amitriptyline is a proven agent for
preventive therapy of migraine.[4] In psychiatry, amitriptyline is an
acknowledged brain serotonin agonist. The prophylactic activity of drugs
with opposing brain serotonergic influences indicates that – in contrast
to depression – brain serotonergic dysfunction is not central to migraine
pathogenesis. Second, while propranolol is an established prophylactic
agent for migraine, it is best avoided in depression. Furthermore,
atenolol is included in the list of drugs of first choice for migraine
prophylaxis.[5] Atenolol does not freely cross the blood-brain barrier and,
therefore, cannot critically influence brain neuronal function.[6] Also,
headache remitting influence of neither propranolol nor amitriptyline
correlates with decrease in anxiety or depression.[7] Finally, carbamazepine
effectively manages depression [8] but is of no value in migraine therapy.[9]
This study [1] helps to address the apparent disconnect between
epidemiological evidences that suggest an aetiological link between
depression and migraine and pharmacological evidences that do not.
References
1. Williams LS, Jones WJ, Shen J , Robinson RL, Weinberger M, Kroenke
K. Prevalence and impact of depression and pain in neurology
outpatients. J Neurol Neurosurg Psychiatry 2003;74:1587-9.
2. Low NCP, du Fort GG, Cervantes P. Prevalence, clinical correlates, and treatment of migraine in bipolar disorder. Headache 2003;43:940-49.
3. Breslau N, Lipton RB, Stewart WF, Schultz LR, Welch KMA. Comorbidity of migraine and depression. Investigating potential etiology and
prognosis. Neurology 2003;60:1308-12.
4. Goadsby PJ, Lipton RB, Ferrari MD. Migraine – current understanding and treatment. N Engl J Med 2002;346:257-70.
5. Emilien G, Maloteaux JM. Current therapeutic uses and potential of beta-adrenoceptor agonists and antagonists. Eur J Clin Pharmacol 1998;53:389-404.
6. Gupta VK. Migraine following haemorrhage in brain stem cavernous angioma: pathophysiological considerations [electronic response to Afridi S and Goadsby PJ, New onset migraine with a brain stem cavernous angioma] jnnp.com 2003http://jnnp.bmjjournals.com/cgi/eletters/74/5/680#55
7. Ziegler DK, Hurwitz A, Preskorn S, Hassanein R, Seim J. Propranolol and amitriptyline in prophylaxis of migraine. Pharmacokinetic and
therapeutic effects. Arch Neurol 1993;50:825-30.
The authors' proposed physiological models of the relationship
between arterial blood pressure (ABP) and cerebral blood flow (CBF)
illustrated in Figures 1 and 2 are not entirely correct. In particular,
as depicted in each figure the apparent average radius of the vascular bed
and CBF appear to increase linearly with ABP during passive vasodilation.
Since flow is laminar and vascular resistance is i...
The authors' proposed physiological models of the relationship
between arterial blood pressure (ABP) and cerebral blood flow (CBF)
illustrated in Figures 1 and 2 are not entirely correct. In particular,
as depicted in each figure the apparent average radius of the vascular bed
and CBF appear to increase linearly with ABP during passive vasodilation.
Since flow is laminar and vascular resistance is inversely related to the
fourth power of the radius of the vessel, the relationship between CBF and
ABP should be approximately proportional to the product of ABP times the
average radius to the fourth power. Thus during passive vasodilation, the
relationship between CBF and ABP should be saliently non-linear. This
criticism of the proposed models does not negate the conclusions of the
authors' work but is intended to further clarify our abstract
understanding of the nature of CBF during passive vasodilation.
I have read with interest the article written by Finsterer et al.
However, I do have several concerns and remarks in relation to it.
First, the authors describe a stenotic lesion at the L-ICA that I do not
actually see in the diagnostic angiogram. Moreover, this lesion was
treated wih a stent-graft.
Second, the image of the R-ICA corresponds to a classic carotid artery
dissection, probabl...
I have read with interest the article written by Finsterer et al.
However, I do have several concerns and remarks in relation to it.
First, the authors describe a stenotic lesion at the L-ICA that I do not
actually see in the diagnostic angiogram. Moreover, this lesion was
treated wih a stent-graft.
Second, the image of the R-ICA corresponds to a classic carotid artery
dissection, probably related to a minor trauma (abortion is referred in
the text, thus consider intubation, cervical hyperextention, coughing,
vomiting as etiological factors). The clinical presentation is classic of
a repetitive embolic phenomena.
Third, The pattern of fibromuscular dyaplasia is questionable.
Fourth, I do not agree with the implantation of stent graft for a disease
that can be easily managed with self expandable bare stents.
And last, the cervical surgical access to the carotid artery in order to
implant a stent in a young patient (straightforward arteries)seems
uneccessary when compared to the endovascular transfemoral route has been
the route of choice for years.
We thank Dr Celio Levyman for his supportive comments.[1]
We fully agree
with him that, in patients with baroreflex failure, it is necessary to
adopt approaches to combat orthostatic hypotension without increasing
supine hypertension. It is also important to follow up an open study with
a blinded study. We expect to complete, within the next month, a double-
blind placebo controlled study, funded by...
We thank Dr Celio Levyman for his supportive comments.[1]
We fully agree
with him that, in patients with baroreflex failure, it is necessary to
adopt approaches to combat orthostatic hypotension without increasing
supine hypertension. It is also important to follow up an open study with
a blinded study. We expect to complete, within the next month, a double-
blind placebo controlled study, funded by NIH, on this subject. The study
has 4 arms: pyridostigmine; pyridostigmine + subthreshold dose of
midodrine (2.5 mg); and pyridostigmine + low dose (5 mg) midodrine;
placebo, in the treatment of neurogenic orthostatic hypotension.
Reference
(1) Levyman C. A new light to orthostatyc hypotension [electronic response to Singer et al Acetylcholinesterase inhibition: a novel approach in the treatment of neurogenic orthostatic hypotension] jnnp.com 2003http://jnnp.bmjjournals.com/cgi/eletters/74/9/1294#68
The issue of orthostatic hypotension is a very common an important
diseable picture of many diseases, as Singer et al. points. Parkinson
disease and diabetic neuropathy are the most common clinical situation of
these cases, and even the very well controlled patient, with tilt-test
table measures to the choice of therapeutic strategies in most cases shows
frustanting results.
The issue of orthostatic hypotension is a very common an important
diseable picture of many diseases, as Singer et al. points. Parkinson
disease and diabetic neuropathy are the most common clinical situation of
these cases, and even the very well controlled patient, with tilt-test
table measures to the choice of therapeutic strategies in most cases shows
frustanting results.
This novel approach, with pyridostigmine, in this open study, is a
very important way to enlight the paths of this cases:I have used the
similar approach in a few patients, with all methods of observation and
control of side effects, and the results were similar of the paper
presented.
We need more research like those, with well-designed statistical and
evidence-based sources, to prescribe acetylcholinesterase inibition as the
prime indication.
Of course, this paper open a novel view of treatment of this kind of
hypotension, perhaps with other measures and/or drugs.
As it is well known, endorphin levels change in different circumstances, for example, in injury, illness, or as a result of circadian influences, among
others.[1-7] It would be helpful to know which was the primary stimulus for
endorphin level changes in MS patients. Perhaps a further experiment can
show that it is or is not circadian.
As it is well known, endorphin levels change in different circumstances, for example, in injury, illness, or as a result of circadian influences, among
others.[1-7] It would be helpful to know which was the primary stimulus for
endorphin level changes in MS patients. Perhaps a further experiment can
show that it is or is not circadian.
References
(1) Covelli V,
Massari F, Fallacara C, Munno I, Jirillo E, Savastano S,
Tommaselli AP, Lombardi G. Interleukin-1
beta and beta-endorphin circadian rhythms are inversely
related in normal and stress-altered sleep.
Int J Neurosci. 1992 Apr;63(3-4):299-305.
(2) Iranmanesh A,
Lizarralde G, Johnson ML, Veldhuis JD. Circadian,
ultradian, and episodic release of beta-endorphin in men,
and its temporal coupling with cortisol.J Clin
Endocrinol Metab. 1989 Jun;68(6):1019-26.
(3) Sekiya K, Nawata H, Kato K, Motomatsu T,
Ibayashi H. Diurnal rhythms of
proopiomelanocortin-derived N-terminal peptide,
beta-lipotropin, beta-endorphin and adrenocorticotropin in
normal subjects and in patients with Addison's disease and
Cushing's disease. Endocrinol Jpn. 1986 Oct;33(5):713-9.
(4) Melmed S. Series Introduction: The immuno-neuroendocrine interface. J Clin Invest, December 2001, Volume 108, Number 11, 1563-1566
(5) Barreca T, Siani C, Franceschini R, Francaviglia N, Messina
V, Perria C, Rolandi E. Diurnal beta-endorphin changes in human cerebrospinal fluid. Life Sci. 1986 Jun 16;38(24):2263-7.
(6) Shanks MF, Clement-Jones V, Linsell
CJ, Mullen PE, Rees LH, Besser GM. A study of 24-hour profiles of plasma
met-enkephalin in man. Brain Res. 1981 May 18;212(2):403-9.
(7) Gil-Ad I, Dickerman Z, Amdursky S, Laron Z.
Diurnal rhythm of plasma beta endorphin, cortisol and growth
hormone in schizophrenics as compared to control subjects.
Psychopharmacology (Berl). 1986;88(4):496-9.
Dear Editor
In their interesting paper Bower and colleagues report results of a study employing manual amygdala volumetry to imaging-negative patients with refractory temporal lobe epilepsy (TLE).[1] They identify 7 out of 11 patients in whom they diagnose amygdala enlargement and postulate this might be attributable to developmental abnormality or low grade tumor.
However, in discussing their interesting o...
Dear Editor
We read with attention the report of Adler and colleagues.[1]
By studying 20 patients with Alzheimer’s disease (AD) assigned to rivastigmine, the authors found that baseline short-term memory performances and EEG data are useful for predicting response to treatment at 6 months.
We would like to contribute to this topic with our own personal data on 24 AD subjects treated for 9 months w...
Dear Editor
Dodson [1] described the successful and “novel” use of cold-water caloric ear irrigation in a manic woman, stating that the effect of this procedure on psychiatric symptomatology has not been reported. In fact, there is nothing new [2] about shock measures that overstimulate, exhaust, or generally reset the vestibular system, including cold water poured onto the head, swings to induce vertigo, emetics t...
Dear Editor
The report by Hausmann et al.[1] adds to negative experiences with rTMS as an add-on strategy in patients with major depression.[2] However, again, the evidence is not completely convincing. In this study, only "slight" effects were expected, but the sample size did not appear to account for that. 25 vs. 13 patients may not suffice to detect - and even less to refute - slight effects.
Thi...
Dear Editor
Williams and colleagues underscore the non-specific relationship between depression and pain in patients seen early at neurology clinics in wide range of unconnected disorders; patients with primary headaches constituted a substantial cohort in this study.[1] This clinical study makes an important contribution to maintain perspective in primary headache research.
Several epidemiological studies...
Dear Editor
The authors' proposed physiological models of the relationship between arterial blood pressure (ABP) and cerebral blood flow (CBF) illustrated in Figures 1 and 2 are not entirely correct. In particular, as depicted in each figure the apparent average radius of the vascular bed and CBF appear to increase linearly with ABP during passive vasodilation. Since flow is laminar and vascular resistance is i...
Dear Editor
I have read with interest the article written by Finsterer et al. However, I do have several concerns and remarks in relation to it.
First, the authors describe a stenotic lesion at the L-ICA that I do not actually see in the diagnostic angiogram. Moreover, this lesion was treated wih a stent-graft. Second, the image of the R-ICA corresponds to a classic carotid artery dissection, probabl...
Dear Editor
We thank Dr Celio Levyman for his supportive comments.[1]
We fully agree with him that, in patients with baroreflex failure, it is necessary to adopt approaches to combat orthostatic hypotension without increasing supine hypertension. It is also important to follow up an open study with a blinded study. We expect to complete, within the next month, a double- blind placebo controlled study, funded by...
Dear Editor
The issue of orthostatic hypotension is a very common an important diseable picture of many diseases, as Singer et al. points. Parkinson disease and diabetic neuropathy are the most common clinical situation of these cases, and even the very well controlled patient, with tilt-test table measures to the choice of therapeutic strategies in most cases shows frustanting results.
This novel...
Dear Editor
As it is well known, endorphin levels change in different circumstances, for example, in injury, illness, or as a result of circadian influences, among others.[1-7] It would be helpful to know which was the primary stimulus for endorphin level changes in MS patients. Perhaps a further experiment can show that it is or is not circadian.
References
(1) Covelli V, Massari F, Falla...
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