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.
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...
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