We thank Dr. Gupta [1] for his interest in our article [2]. His comments [1]
are very interesting when we consider how complex the postdural puncture
headache (PDPH) physiopathology can be.
Different and multiple factors
contribute in a resulting PDPH, which can justify the differences in the
intensity and duration of the headache. Factors such as technique [3-6],
doctor’s experience, patien...
We thank Dr. Gupta [1] for his interest in our article [2]. His comments [1]
are very interesting when we consider how complex the postdural puncture
headache (PDPH) physiopathology can be.
Different and multiple factors
contribute in a resulting PDPH, which can justify the differences in the
intensity and duration of the headache. Factors such as technique [3-6],
doctor’s experience, patient’s medical history and the surroundings of the
surgical procedure or the neurological diagnosis. The dura-arachnoid
lesion (DAL) and the cerebrospinal fluid (CSF) leakage are only isolated
influencing factors among the whole involved.
The DAL features, size and later sealing will depend on the needle
used, its tip design and its manufacture properties. Needles of the same
diameter and tip design made by different manufacturers cannot behave in
the same way. We also find from practice that brand new needles can also
have its tip damaged or even metallic split edges on its surface [7].
These inadvertent defects are widely evident when the same microscopy
technique used to study the DAL lesion is employed.
The viscosity and elasticity properties of the dural and arachnoid lamina
might not be the same on every patient therefore affecting the final
sealing of the lesion.
In general, the arachnoid lesion takes longer to
close than the dural lesion. In some patients, it is also possible that a
small fragment of the arachnoid lamina can get displaced when performing
the puncture, making more difficult its closure and being more likely to
result in a PDPH.
The hypothesis based on the arachnoid inflammatory response to the
puncture, mentioned by Gupta, can be an accepted hypothesis to explain the
arachnoid lesion closure. The same argument can be used to explain the
fact that pencil point needles result in less frequency of PDPH than
Quincke needles of same diameter although the size of the lesion is
similar in both [3].
Whitacre needles result in lesions with more
irregular edges when compared to the “C” shaped clean edge lesions caused
by Quincke needles. The irregular and torn edges may develop to a local
inflammation helping to effectively seal the DAL [3].
When considering the arachnoid and dural lamina lesion, the complete
sealing of the arachnoid lesion could be the most important. The dural
laminae are very permeable and they are made of collagen and some elastic
fibres that provide mechanical support to the dural sac. The arachnoid
lamina, on the other hand, is mainly made of arachnoid cells, its
mechanical resistance is poor but it behaves as a semi permeable membrane
[8-10]. Its sealing would stop the CSF to leak out into the dural sac.
Another aspect to consider is the formation of small cranial subdural
haematomas after CSF hypotension following a lumbar puncture [11]. When
CSF is lost the encephalon becomes less floating, it is pulled down
tractioning the cranial arachnnoid lamina. The exerted traction can result
in rupture of the small blood vessels crossing the subdural compartment
that leads to small haematoma formation that can be missed on the MRI,
although they could be important enough to affect the intensity and
duration of the PDPH.
When the needle crosses the dural sac at spinal level, it can also
perforate small vessels of the inside of its thickness. Apart from
considering the distance between the vessels, puncture site and needle
gauge, fortune will play decisive in puncturing the blood vessels. If so,
a small haematoma results along the same DAL that will contribute to its
closure [12-13].
Changes on the encephalon position during a CSF hypotensive episode will
also affect the normal cerebrospinal fluid hydrodynamics. CSF leakage is
associated with encephalon prolapse and a reduced size of the subarachnoid
cisterns. Under these circumstances, different encephalic areas such as
the aqueduct of Sylvius can slightly change their location and modify the
tissue distribution. In some patients, these changes might alter the
normal CSF circulation. We do not really know if that could modify the
headache’s nature.
Another possible factor in relation with the PDPH is the vasodilatation of
some encephalic areas secondary to CSF loss (Monroe-Kelly’s theory). The
degree of reactive vasodilatation can vary between patients and may depend
on previous medical history.
Both cerebral MRI and Doppler Ultrasound are non-invasive methods to study
the PDPH physiopathology and the effectiveness of its treatment. MRI
provides images such as meningeal enhancement with gadolinium captation in
all sections, changes on the aqueduct of Sylvius and cerebellar amygdala
position, hygromas and subdural haematomas, increased size on the
hypophysis, decreased size of the arachnoid cisterns and cerebral
ventricles [14].
There is a close relationship between the clinical signs
and the radiological features. In fact, these features disappear once the
PDPH is resolved. Doppler Ultrasound, on the other hand, provides
information on the flow dynamics. Determination of the velocity of the
ophthalmic vein flow might be useful in assessing clinical responses to
different PDPH treatments [15].
The development of PDPH remains an ongoing problem. The incidence of
PDPH is greater after diagnostic lumbar puncture when 20G or 22G needles
are used in order to measure CSF pressure and to obtain great volume
samples. The incidence is lower after spinal anaesthesia using 25G or 27G
needles. In some cases, the arachnoid injection of local anaesthetic
agents together with opioid analgesics might contribute as well.
Many unresolved questions about PDPH that still need further research.
(2). Reina MA, Lopez A, Badorrey V, De Andres JA, Martin S. Dura-
arachnoid lesions produced by 22 gauge Quincke spinal needles during a
lumbar puncture. J Neurol Neurosurg Psychiatry 2004; 75: 893-7.
(3). Reina MA, de Leon-Casasola OA, Lopez A, De Andres J, Martin S,
Mora M.
An in vitro study of dural lesions produced by 25-gauge Quincke and
Whitacre needles evaluated by scanning electron microscopy. Reg Anesth
Pain Med 2000; 25: 393-402.
(4). Reina MA, Lopez A, Manzarbeitia F, Amador V, Goxencia I, Olmedilla
MC. Skin fragments carried by spinal needles in cadavers. Rev Esp
Anestesiol Reanim 1995; 42: 383-5.
(5). Reina MA, Lopez-Garcia A, Dittmann M, de Andres JA, Blazquez MG.
Iatrogenic spinal epidermoid tumors. A late complication of spinal
puncture. Rev Esp Anestesiol Reanim 1996; 43: 142-6.
(6). Reina MA, Lopez Garcia A, Aguilar JL, Palacios Martin R. Electron
microscopic analysis of particles from surgical gloves and their possible
introduction into the epidural space during epidural anesthesia. Rev Esp
Anestesiol Reanim 1999; 46: 60-6.
(7). López A, Reina MA, Machés F, De Leon Casasola O, De Andrés JA,
García Trapero J. Electrón microscopy in quality control of equipment used
in regional anesthesia. Tech Reg Anesth Pain Management 2002; 6: 172-179.
(8). Reina MA, Dittmann M, Lopez Garcia A, van Zundert A. New
perspectives in the microscopic structure of human dura mater in the
dorsolumbar region. Reg Anesth 1997; 22: 161-6.
(9). Reina MA, Lopez-Garcia A, Dittmann M, de Andres JA. Structural
analysis of the thickness of human dura mater with scanning electron
microscopy. Rev Esp Anestesiol Reanim 1996; 43: 135-7.
(10). Reina MA, Lopez-Garcia A, Dittmann M, de Andres JA. Analysis of
the external and internal surface of human dura mater with scanning
electron microscopy. Rev Esp Anestesiol Reanim 1996; 43: 130-4.
(11). Reina MA, Lopez A, Benito-Leon J, Pulido P, Maria F. Intracranial
and spinal subdural hematoma: a rare complication of epidural and
subarachnoid anestesia. Rev Esp Anestesiol Reanim 2004; 51: 28-39.
(12). Reina MA, De Leon Casasola O, Lopez A, De Andres JA, Mora M,
Fernandez A. The origin of the spinal subdural space: ultrastructure
findings. Anesth Analg 2002; 94: 991-5.
(13). Reina MA, Lopez A, De Andres JA. Origin of spinal subdural
hematomas: a postmortem anatomical study. Rev Esp Anestesiol Reanim 2004;
51: 240-6.
(14). Reina MA, Alvarez-Linera J, Lopez A, Benito-Leon J, De Andres JA,
Sola RG. Magnetic resonance in dural post-puncture headache in patient
with cerebrospinal fluid hypotension. Rev Esp Anestesiol Reanim 2002; 49:
89-100.
(15). Chen CC, Luo CL, Wang SJ, Chen CM, Fuh JL, Lin SH. Colour Doppler
imaging for diagnosis of intracranial hypotension. Lancet 1999; 354: 826-
829.
We read with great interest the article of Shaw et al [1] reporting
on risk factors for the development of a schizophrenia-like psychotic
disorder following temporal lobectomy, and would like to offer one
additional demographic risk factor not attended by the authors: the
seasonality of births.
In schizophrenia, a consistent 5-8% winter-spring
(i.e. December - June) excess of births...
We read with great interest the article of Shaw et al [1] reporting
on risk factors for the development of a schizophrenia-like psychotic
disorder following temporal lobectomy, and would like to offer one
additional demographic risk factor not attended by the authors: the
seasonality of births.
In schizophrenia, a consistent 5-8% winter-spring
(i.e. December - June) excess of births for individuals who develop the
condition has been established in numerous studies including a total of
more than 400,000 patients [2]. In temporal lobe epilepsy, birth
seasonality has not been established thus far. Here we present a similar
seasonal birth excess in two Northern Hemisphere collectives of patients
with temporal lobe epilepsy.
Figure 1
Top:Zürich series 1975 - 1999: Seasonality of births in 408 patients
with temporal lobe epilepsy undergoing amygdalohippocampectomy (grey
bars, scale on the right). Data are corrected for birth seasonality of
the normal population by using 194 patients with extratemporal
epilepsy (black bars, scale on the left). Middle: Toronto series 1997 - 2004: Seasonality of births in
175 patients with temporal lobe epilepsy (grey bars, scale on the
right). Data are corrected for birth seasonality of the normal
population by using 707 patients from a neuroradiological database
(black bars, scale on the left). Bottom: Grouping of both series. Comparison between
winter-spring and autumn-summer months; numbers on y-axis correspond
to percentage of patients per month (Mann-Whitney-U 19.0, p<_0.01. _="_" font="font"/>
We feel that an account of
schizophrenia-like psychosis in patients with temporal lobe epilepsy would
be incomplete without allusion to these neuroastrological constraints.
References
(1). P Shaw, J Mellers, M Henderson, et al. Schizophrenia-like
psychosis arising de novo following a temporal lobectomy: timing and risk
factors. J Neurol Neurosurg Psychiatry 2004;75:1003–1008
(2). Torrey EF, Miller J, Rawlings R, et al. Seasonality of births in
schizophrenia and bipolar disorder: a review of the literature. Schizophr
Res 1997;28:1-38
The relationship of migraine and platelets is a very interesting
issue. The “platelet theory” of migraine by Deschmuck and Meyer, the
“migraine as a platelet disorder” by Hannington and more recent papers
discharging the importance of platelet aggregation in this kind of head
pain.
However, the migranous infarct, as described in the HIS
Classification and also in the clinical practice, was...
The relationship of migraine and platelets is a very interesting
issue. The “platelet theory” of migraine by Deschmuck and Meyer, the
“migraine as a platelet disorder” by Hannington and more recent papers
discharging the importance of platelet aggregation in this kind of head
pain.
However, the migranous infarct, as described in the HIS
Classification and also in the clinical practice, was a matter of
discussion. Spreading depression Olyguemia Excitatory amminoacids.
Even
after huge clinical and laboratorial investigation of a young person with
a typical picture of migraine with aura, for example, who develops an
infarct, various neurologists offer resistance to point as the cause of
the stroke the migraine.
This paper from Kiel is a very important step to the understanding of
migranous strokes. The platelet-leucocyte is a very important and verified
finding, linking the conventional strokes to the migraine ones.
After all, the platelets continue to be important in migraine, even
in a different approach.
We appreciate Dr. Deogaonkar's interest in our article. We also
appreciate his pointing out the feasibility of thecoperitoneal shunting in
treating syringomyelia associated with adhesive arachnoiditis (SAA).
However, our opinion on this subject is somewhat different from his
remarks. We have done simulation of thecoperitoneal shunting using our
model of SAA; it showed that, if performed wit...
We appreciate Dr. Deogaonkar's interest in our article. We also
appreciate his pointing out the feasibility of thecoperitoneal shunting in
treating syringomyelia associated with adhesive arachnoiditis (SAA).
However, our opinion on this subject is somewhat different from his
remarks. We have done simulation of thecoperitoneal shunting using our
model of SAA; it showed that, if performed without myelotomy,
thecoperitoneal shunting rather worsened the pressure gradient between
inside and outside the syrinx cavity. We can intuitively understand this
result: shunting the subarachnoid space reduces the pressure outside the
spinal cord, thereby increasing the pressure gradient across the syrinx
cavity. We should be cautious, however, in interpretig this result,
because shunting itself may reduce the overall CSF pressure, which may
have a larger effect on the syrinx generation.
In this respect, we are cautious about promoting thecoperitoneal
shunting as a standard measure to treat SAA. Although this procedure has
been present since 1980's, we don't think that it has yet become the
standard surgical procedure for SAA. The sizes of the reported series are
relatively small; some of them had an associated procedure of myelotomy.
In our own experience of two cases of SAA treated with thecoperitoneal
shunting, we had mixed results: one patient had enlargement of the syrinx
after thecoperitoneal shunting, the other patient had improvement after
surgery, but we also had performed partial dissection of the adhesion at
the same time, which might have been the main cause of the improvement.
Thus, we are still suspicious whether this procedure is truly effective on
SAA or not. However, our clinical experience of thecoperitoneal shunting
is limited; so we would appreciate it if one would convince us of its
effect with a relatively large series. SAA is a very difficult disease to
treat; we look forward to a new development of its effective treatment.
We note the report of an unusual organophosphorus (OP) pesticide
poisoning published in your journal [1]. However, from the data presented, we
are not convinced that the patient’s death can be attributed to OP
poisoning. Furthermore, we do not believe that this report can be used to
expand the spectrum of syndromes seen following OP poisoning.
There was no history of ingestion of an OP. In a...
We note the report of an unusual organophosphorus (OP) pesticide
poisoning published in your journal [1]. However, from the data presented, we
are not convinced that the patient’s death can be attributed to OP
poisoning. Furthermore, we do not believe that this report can be used to
expand the spectrum of syndromes seen following OP poisoning.
There was no history of ingestion of an OP. In addition, no
quantitative data was presented on the amount of thiometon that was
detected in blood or urine, so it is not possible to decide whether it
reflected environmental exposure or acute self-poisoning. No mention is
made of the presence of pesticide solvents in the stomach. The
butyrylcholinesterase (pseudo-cholinesterase) levels are not particularly
low – even mildly symptomatic poisoning with chlorpyrifos, for example,
results in values around zero. The mild reduction seen here could have
resulted from a variety of non-toxicological acute illnesses [2].
The patient’s clinical features do not suggest OP poisoning [3]. The
authors report that their “patient did not show the well defined
neurological syndromes”, including the “acute cholinergic crisis”.
However, later in the discussion, they write that “Another clue for
organophosphate intoxication of the patient was typical reversible
cholinergic signs with atropine administration such as improving
bradycardia.”
The normal blood pressure and a heart rate of 62 in a 31-yr-old man
means little – heart rates can be low, normal, or high in significant OP
poisoning [3]. The only muscarinic features reported are tracheal secretion
and miosis, with no mention of other common signs such as bronchospasm,
bronchorrhoea, incontinence, and sweating [3[. The raised temperature on
admission is unexpected – hypothermia is usual.
Clinical features of acute OP poisoning are not focal, typically
involving widespread involvement of autonomic ganglia, CNS and
neuromuscular junction [3]. This patient had a focal feature (deviation of
the left eye) that is consistent with a brain stem lesion seen on MRI.
Bilateral positive Babinski signs and increased deep tendon reflexes are
uncommon in OP poisoning [3]. Only T2 MRI imaging sequences are reported. The
wedge-shaped T2 hyperintensities in the cerebellar grey and white matter
are more suggestive of a stroke than poisoning. Further information could
be gained from reporting other MRI sequences or the results of a CT head.
Other diagnoses need to be excluded before a diagnosis of OP
poisoning with atypical neurology can be accepted. An allergy history is
important since people with bee allergy can have severe reactions to Royal
Bee Jelly [4]. The raised temperature and white cell count, and focal
neurological signs are consistent with infective or inflammatory processes
in the CNS. The T2 hyperintensity in the central midbrain /pontine region
is compatible with infarction, pontine myelinolysis, or haemorrhage.
Fundamentally, it is difficult to exclude any of these pathologies without
the results of a post-mortem.
We agree with Teke et al that OP pesticide poisoning is a
major problem in rural areas of the developing world. However, in few
places is it responsible for “nearly half” of acute poisoning admissions.5
The case fatality also varies widely,5 being dependent on the locally
common OPs, the level of ICU facilities available for treatment, and the
number of patients who survive to hospital admission. It is not possible
to report a case fatality that is accurate for all parts of the world
where OP pesticide poisoning is a problem.
References
(1). Teke E, Sungurtekin H, Sahiner T, Atalay H, Gur S.
Organophosphate poisoning case with atypical clinical survey and magnetic
resonance imaging findings. J Neurol Neurosurg Psych 2004;75:936-7.
(2). Karalliedde L, Edwards P, Marrs TC. Variables influencing the
toxic response to organophosphates in humans. Food Chem Toxicol 2003;41:1-
13.
(3). Ballantyne B, Marrs TC. Overview of the biological and clinical
aspects of organophosphates and carbamates. In: Clinical and experimental
toxicology of organophosphates and carbamates, 0 edn. Oxford, Butterworth
heinemann, 1992:3-14.
(4). Thien FC. Asthma and anaphylaxis induced by royal jelly. Clin Exp
Allergy 1996;26:216-22.
(5). Eddleston M. Patterns and problems of deliberate self-poisoning
in the developing world. Q J Med 2000;93:715-31.
Hyndman and Ashburn [1] find that those who stopped walking when
talking were significantly more disabled (p<_0.001 _-="_-" that="that" is="is" they="they" were="were" more="more" dependent="dependent" in="in" activities="activities" of="of" daily="daily" living="living" had="had" worse="worse" gross="gross" function="function" as="as" well="well" upper="upper" and="and" lower="lower" limb="limb" depression="depression" p="p"/>
Neurobiological features are suggested by reports linking harm avoidance
and dysregulation of mood with dopamine (DA) abnormalities lateralised to
the right hemisphere. This hypothesis is supported by optimum response
organisation and working memory at intermediate DA tone in a
mediofrontostriatal activation system[2,3]which may optimise multi-task
performance[4].
The fact that speech pause time is a behavioural correlate of
mood[2]prompts evaluating differences in speech patterns between stoppers
and nonstoppers[4] by analysing speech hesitation pauses (SHPs) on a time-
base[2]. Such examination of the elements of speech itself and their
effects on gait patterns [4] is supported by the association of the
reduction of blood pressure with longer, less recurrent SHPs of
approximately two seconds. These responses are linked with the feeling of
rhythmical and prefrontal cortical modulation of DA during the delayed
alternation task [2].
Therefore, opportunities for motoric neurorehabilitation[4] may
include auditory training of asymmetrical changes in cortical neuronal
activity [2]. This method is supported by a study demonstrating that the
brains of people who stutter also react differently when they are
listening to words, not reading them. When the situation was less clear-
cut, the stutterers used different parts of the brain-especially the right
side-and arrived at an answer more slowly [5].
References
(1). Hyndman D, Ashburn A. "Stops walking when talking" as a predictory of
falls in people with stroke living in the community. J Neurol Neurosurg
Psychiatry 2004;75:994-7.
(2). Friedman EH. Music and neuroscience (Letter). New York Academy of
Sciences Magazine Update April/May 2004, Page 1.
(3). Tomer R, Aharon-Peretz J. Novelty seeking and harm avoidance in
Parkinson's disease: effects of asymmetric dopamine deficiency. J Neurol
Neurosurg Psychiatry 2004; 75:972-5.
Dr Grueger raises an interesting and relevant management point about
the usefulness or not of testing patients with suspected paraneoplastic
neurological disease for the presence of anti-neuronal antibodies.
I do
not agree however that this test has no benefit. These antibodies are
highly specific for an underlying tumour e.g. anti-Hu for small cell lung
cancer and anti-Yo for breast and gy...
Dr Grueger raises an interesting and relevant management point about
the usefulness or not of testing patients with suspected paraneoplastic
neurological disease for the presence of anti-neuronal antibodies.
I do
not agree however that this test has no benefit. These antibodies are
highly specific for an underlying tumour e.g. anti-Hu for small cell lung
cancer and anti-Yo for breast and gynaecological malignancy. Every test
has false positives and false negatives but the majority of patients with
positive anti-neuronal antibodies will have an underlying and potentially
treatable cancer. For example in the classic paper by Peterson et al, 52
out of 55 patients with cerebellar degeneration and anti-Yo antibodies had
an underlying malignancy.
Furthermore in 34 of these 52 patients the
neurological syndrome predated the diagnosis of cancer. It may be that Dr
Grueger has the facilities to do body scans on all his patients with
suspected paraneoplastic disease but this is not the case in all centres
and a low index of suspicion would not normally be sufficient to justify a
large dose of radiation.
I agree that a negative test may be falsely
reassuring but a positive test is highly informative and, even where no
tumour is found, allows a useful discussion with the patient about
diagnosis and prognosis.
Reference
(1). Peterson K, Rosenblum MK, Kotanides H, Posner JB.
Paraneoplastic cerebellar degeneration. I. A clinical analysis of 55 anti-
Yo antibody-positive patients.
Neurology. 1992 Oct;42(10):1931-7.
Zeller et al showed platelet adhesion to leukocytes during the
headache-free interval and a higher baseline of platelet activation in
migraine patients without aura; the authors suggest a link between
migraine and stroke at the cellular level [1]. Also, they believe that
enhanced platelet activation in migraine patients is a marker of the
inflammatory process in the trigeminovascular system.
Zeller et al showed platelet adhesion to leukocytes during the
headache-free interval and a higher baseline of platelet activation in
migraine patients without aura; the authors suggest a link between
migraine and stroke at the cellular level [1]. Also, they believe that
enhanced platelet activation in migraine patients is a marker of the
inflammatory process in the trigeminovascular system.
Several lines of evidence challenge the presumed pathogenetic link
between platelets and migraine as well as the conclusions of the authors.
(i) The specificity of the findings to migraine pathophysiology is
debatable. Platelet hyperaggregability has been noted in a range of other
medical conditions and is found with high levels of stress.
Use of
unstressed controls in this study is an important confounding factor.
(ii) Propranolol, an established migraine prophylactic agent, enhances
platelet aggregability [2]. In this study, 45 of 72 (62.5%) migraine
patients were receiving propranolol, one constituting another confounding
factor. (iii) Logically, the dissociation of results of baseline platelet
activation between migraine without aura and migraine with aura patients
cannot be reconciled.
We do not know why patients of migraine with aura
should not have enhanced platelet activation; a laboratory artifact or
epiphenomenon might be involved. (iii) Plasma methionine-enkephalin levels
remain frequently elevated in migraine patients between headache attacks [3].
Migraine patients with frequent headache may never return to the
“baseline” neuroendocrine function; a headache-free interval of 24 h, as
used in this study, is probably not reflective of the “trait” baseline in
such patients. (iv) Contrary to the assertion, one evidence for migraine
prophylactic value of aspirin is poor [4]. (v) A negative correlation exists
between migraine and antibodies to phospholipids (the membrane-binding
moiety increasing platelet aggregability), suggesting a degree of
protection against development of migraine [5]. (vi)
Migraine headache has
been reported in patients with thrombocytopenia [6]. (vii) Although platelet
aggregation and adhesion are commonly increased in diabetes mellitus, it
is hypogylcaemia rather than hyperglycaemia that precipitates migraine [7].
(viii) Menstrual migraine typically improves with pregnancy [8]. but
estrogens increase epinephrine induced platelet aggregation [9]. (ix)
Migraine-like headache is a sequela of cocaine use, [10]. but cocaine inhibits
platelet aggregation and dissociates preformed platelet aggregates [11].
Zeller et al extend the postulated parallel between the platelet and
the neuron by suggesting that platelet activation mirrors
trigeminovascular system inflammation. Believing that platelet function
tells us anything about brain neuronal function involves complete
suspension of scientific disbelief [12]. No systemic influence, including
platelet dysfunction, can rationalize the characteristic lateralization
(unilateral, bilateral or side-shift) of migraine headache [13].
Third,
whereas atherothrombotic disease and incidence of ischaemic stroke
generally advances with age, migraine remits in advancing years in
American populations [14].
Finally, in contrast to atherothrombotic stroke,
ischaemic stroke is a rarity in younger migraine subjects [15]. The posterior
cerebral artery is anatomically particularly labile at its origin; rare
occurrence of posterior cerebral circulation infarcts in the migraine
patient likely reflects the outcome of an idiosyncratic critical reduction
of perfusion in an anatomically vulnerable region [16]. rather than the
outcome of a cellular level interaction mediated by platelets between
migraine and stroke.
References
(1). Zeller JA, Frahm K, Baron R, et al. Platelet-leukocyte interaction
and platelet activation in migraine: a link to ischemic stroke? J Neurol
Neurosurg Psychiatry 2004;75:984-7.
(2). Steiner TJ, Joseph R, Clifford Rose, F. Migraine is not a platelet
disorder. Headache 1985;25:434-40.
(3). Mosnaim AD, Diamond S, Wolf ME, et al. Endogenous opioid-
like peptides in headache. An overview. Headache 1989; 29:368-72.
(4). Grotemeyer K-H, Scharafinski H-W, Schlake HP, et al.
Acetylsalicylic acid vs. metoprolol in migraine prophylaxis – a double-
blind cross-over study.
Headache 1990;30:639-41.
(5). Markus HS, Hopkinson N. Migraine and headache in systemic lupus
erythematosus and their relationship with antibodies against
phospholipids. J Neurol 1992;239:39-42.
(6). Appenzeller O. Pathogenesis of migraine. Med Clin North Am
1991;75:763-89.
(7). Blau JN, Thavapalan M. Preventing migraine: a study of
precipitating factors. Headache 1988;28:481-3.
(8). Silberstein SD, Merriam GR. Estrogens, progestins, and headache.
Neurology 1991;41:786-93.
(9). Altura BM, Altura BT. Some physiological factors in vascular
reactivity. V. Influences of sex hormones, oral contraceptives and
pregnancy on vascular muscle and its reactivity. In: Carrier O and Shibata
S. (eds) Factors influencing vascular reactivity. Tokyo: Igaku-Shoin Ltd.,
1977.
(11). Jennings LK, White MM, Sauer CM, et al. Cocaine-induced platelet
defects. Stroke 1993;24:1352-9.
(12). Wessely S. Britain on the cough: treating a low serotonin
society. BMJ 1998;316:83.
(13). Gupta VK. Migraine following haemorrhage in brain stem cavernous
angioma: pathophysiological considerations. J Neurol Neurosurg Psychiatry
Online, 23 June 2003. Published electronic response to: Afridi S, Goadsby
PJ. New onset migraine with a brain stem cavernous angioma. J Neurol
Neurosurg Psychiatry 2003; 74:680-1. Available at:
http://jnnp.bmjjournals.com/cgi/eletters/74/5/680
(14). Ziegler DK. Headache. Public health problem. Neurol Clin
1990;8:781-91.
(15). Broderick JP, Swanson JW. Migraine-related strokes. Clinical
profile and prognosis in 20 patients. Arch Neurol 1987;44:868-71.
(16). Gupta VK. Regional cerebral blood flow patterns in migraine: what
is the contribution to insight into disease mechanisms? Eur J Neurol
1995;2:586-7.
In the Letter to the Editor (Wennberg R. Short term benefit of
battery depletion in vagus nerve stimulation for epilepsy. J Neurol
Neurosurg Psychiatry 2004;75:939), the author stated that 58% of subjects
improved after battery depletion.
The information provided in the VNS
Therapy Physician's Manual states that the information provided was
referenced to BASELINE, not to the time just befor...
In the Letter to the Editor (Wennberg R. Short term benefit of
battery depletion in vagus nerve stimulation for epilepsy. J Neurol
Neurosurg Psychiatry 2004;75:939), the author stated that 58% of subjects
improved after battery depletion.
The information provided in the VNS
Therapy Physician's Manual states that the information provided was
referenced to BASELINE, not to the time just before battery depletion [1].
The data therefore indicates that 58% of subjects had not yet returned to
their baseline seizure rates within 4 weeks after VNS Therapy battery
depletion. As such, Wennberg's conclusion is incorrect.
Ristanovic et al
previously presented these data in an abstract that described a loss of
benefit within 4 weeks after battery depletion.
References
(1). Physician's manual for the VNS therapy pulse model 102 generator.
Houston, TX: Cyberonics, Inc., 2002.
(2). Ristanovic RK, Bergen D. The Vagus Nerve Stimulation Group. Withdrawal
seizures do not accompany vagus nerve stimulation's battery depletion--
long-term follow-up. Epilepsia 1999;40:92 (Abstract).
The authors [1]. usefully describe a large series of patients and compare
the occurrence of non-epileptic seizures arising whilst apparently asleep.
This clinical differentiation remains problematic and the rule appears to
be emerging that there are no rules. However, to my knowledge there is
only one study [2]. (quoted by Duncan et al) with video-EEG-recording,
maintaining that patients can...
The authors [1]. usefully describe a large series of patients and compare
the occurrence of non-epileptic seizures arising whilst apparently asleep.
This clinical differentiation remains problematic and the rule appears to
be emerging that there are no rules. However, to my knowledge there is
only one study [2]. (quoted by Duncan et al) with video-EEG-recording,
maintaining that patients can have a non-epileptic seizure, without prior
arousal, documented on EEG. If true, this would revolutionise views on
non-epileptic attacks and clearly it needs verification.
In every other
documented case, the patient wakes up before the attack and to say they are
in “pseudosleep” is obfuscation by jargon – they are awake. Arousal from
sleep before the attack is often brief; anyone who has woken in a sweat
the night after a tricky exam knows this.
The problem as always in
epilepsy diagnosis, is that until the attack is recorded in the telemetry
laboratory, the evidence on which the diagnosis is based is from the
history, which is simply wrong. It is widely held that epilepsy is a
clinical diagnosis; this too is wrong.
Epilepsy is due to pathological
electrical discharges, but unfortunately usually we can’t record them
because they are too infrequent. Consequently, we diagnose epilepsy by a
clinical educated guess, but a guess is not a diagnosis, it is just the
best we can manage and it usually works OK. This needs to be remembered in
all studies looking at seizure histories.
The authors also state that they include patients with any episodes
apparently arising in sleep in their study, no matter how infrequent. The
numbers here are important. The patient who has a sudden onset of
refractory seizures as a young adult with the occasional one in the night
probably has non-epileptic seizures and is very different from the one who
has 80% of their attacks at night and wakes with a bitten tongue. I would
be interested to know these data.
Finally, the authors hold up my article for the educational supplement for
JNNP [3]. as an example of a modern paper with an out-dated view that misleads
clinicians. In fact this article states: “attacks arising from sleep are
organic (though not always epileptic) though it may take an EEG to prove
that the patient is asleep at the onset”.
In my view, with the proviso of
Orbach’s study, this remains entirely accurate and Duncan et al’s final
sentence merely paraphrases it. To have been misrepresented in this way is
highly regrettable and I take this opportunity to set the record straight.
References
(1). Duncan R, Oto M, Russell, AJC, Conway P. Pseudosleep events in
patients with psychogenic non-epileptic seizures: prevalence and
associations. JNNP 2004;75:1009-1012.
(2). Orbach D, Ritaccio A, Devinsky O. Psychogenic non-epileptic
seizures associated with EEG-verified sleep. Epilepsia 2003;44:64-68.
(3). Manford M. Assessment and investigation of possible epileptic
seizures. JNNP 2001;70(suppl.2)3-8
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