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
Jankovic reviews the expanding list of approved and off-label
indications for therapeutic use of botulinum toxin (BT). [1]. One of the
prominent off-label indications for use of BT is migraine, the advent of
which therapy was serendipitous.
Use of BT for migraine prevention is
gaining momentum through the results of randomized controlled trials (RCT)
– both completed and ongoing – and, in th...
Jankovic reviews the expanding list of approved and off-label
indications for therapeutic use of botulinum toxin (BT). [1]. One of the
prominent off-label indications for use of BT is migraine, the advent of
which therapy was serendipitous.
Use of BT for migraine prevention is
gaining momentum through the results of randomized controlled trials (RCT)
– both completed and ongoing – and, in the effort to evolve a broad
consensus, certain clinical reservations have been recently addressed [2].
In
this period of elucidation of anti-migraine mechanisms of BT that would
eventually lead towards formal approval of its use for clinical practice,
it is important to maintain an open, cautious, and critical approach to
the literature.
A direct skeletal muscle-spasmolysis independent prolonged analgesic
action is believed to underlie efficacy of BT in preventing migraine
attacks for three months or more [2-4]. The following facts do not sustain
this theoretical premise: (i) Three RCTs in human volunteers do not
support a direct or genuine analgesic action of BT [5-7]. (ii) Dose-dependent
modification of analgesia-related behaviour in rats lasts only for two
weeks with the higher (medium) dose tested [8]. (iii) In clinical trials in
migraine patients, neither a predictable nor a dose-dependent response has
been seen [9]. (iv) Peak responses to BT-A in migraine patients are seen at 8
-12 weeks2,3,4 whereas BT-A affected nerve endings in mice fully recover
function between 63-91 days [10]. (v) BT does not cross the blood-brain
barrier [8]. and cannot influence either meningeal pain receptors or dural
inflammation believed to underlie migraine headache [11]. or the aura [3].
While
BT cannot influence central sensitization, blocking of peripheral
sensitization through suppression of release of substance P does not
contribute to analgesia in humans [6]. and is limited to 15 days in cultured
embryonic rat dorsal root ganglia [12]. (vi) Donepezil – that exerts central
and peripheral cholinergic activity opposite to that of BT -- remits
migraine with aura or migraine without aura, an effect comparable to
propranolol in controlled conditions [13]. (vii)
The clinical utility of BT
in migraine has not been compared with other established prophylactic
agents. (vii) Approximately 1% of patients receiving BT-A injections
develop severe, debilitating headaches that may persist for 2-4 weeks [14].
The placebo effect cannot be reliably excluded in RCT, particularly
with soft end points that hamper migraine research; RCT with BT in off-
label indications such as migraine can misguide clinicians if undertaken
without sufficient conceptual clarity [15]. Without a defensible core
research vision to direct it, migraine remains a loosely-connected chain
of assumptions and is in its infancy; great care should be taken before
making further pathophysiological assumptions as well as therapeutic
recommendations [16].
References
(1). Jankovic J. Botulinum toxin in clinical practice. J Neurol
Neurosurg Psychiatry 2004;75:951-7.
(2). Silberstein SD, Aoki KR. Botulinum toxin type A: myths, facts, and
current research. Headache 2003;43(supplement 1): 1.
(3). Evans RW, Blumenfeld A. Botulinum toxin injections for headache.
Headache 2003;43:682-5.
(4). Dodick DW. Botulinum neurotoxin for the treatment of migraine and
other primary headache disorders: from bench to bedside. Headache 2003;
43: (supplement 1):25-33.
(5). Voller B, Sycha T, Gustorff B, Schmetterer L, Lehr S, Eichler HG,
Auff E, Schnider P. A randomized, double-blind, placebo controlled study
on analgesic effects of botulinum toxin A. Neurology 2003;61:940-4.
(6). Kramer HH, Angerer C, Erbguth F, Schmelz M, Birklein F. Botulinum
Toxin A reduces neurogenic flare but has almost no effect on pain and
hyperalgesia in human skin. J Neurol 2003;250:188-93.
(7). Blersch W, Schulte-Mattler WJ, Przywara S, May A, Bigalke H,
Wohlfarth K. Botulinum toxin A and the cutaneous nociception in humans: a
prospective, double-blind, placebo-controlled, randomized study. J Neurol
Sci 2002;205:59-63.
(8). Cui M, Khanijou S, Rubino J, Kei Roger Aoki KR. Subcutaneous
administration of botulinum toxin A reduces formalin-induced pain. Pain
2004;107:125-33.
(9). Silberstein S, Mathew N, Saper J, Jenkins S. Botulinum toxin type
A as a migraine preventive treatment. Headache 2000;40:445-50.
(10). de Paiva A, Meunier FA, Molgo J, et al. Functional repair of
motor endplates after botulinum toxin-A poisoning: bi-phasic switch of
synaptic activity
between nerve sprouts and their parent terminals. Proc Natl Acad Sci
(USA). 1999;96:3200-5.
(11). Silberstein SD. Neurotoxins in the neurobiology of pain. Headache
2003;43(suppl 1):2-8.
(12). Welch MJ, Purkiss JR, Foster KA. Sensitivity of embryonic rat
dorsal root ganglia neurons to Clostridium botulinum neurotoxins. Toxicon
2000;38:245-58.
(13). Nicolodi M, Galeotti N, Ghelardini C, Bartolini A, Sicuteri F.
Central cholinergic challenging of migraine by testing second-generation
anticholinesterase drugs. Headache 2002;42:596-602.
(14). Alam M, Arndt KA, Dover JS. Severe, intractable headache after
injection with botulinum A exotoxin: report of 5 cases. J Am Acad Dermatol
2002;46:62-5.
(15). Gupta VK. Randomized controlled trials: the hijacking of basic
sciences by mathematical logic. BMJ Online (6 July 2004). Available at:
http://bmj.bmjjournals.com/cgi/eletters/329/7456/2#65969
(16). Gupta VK. Bureaucratisation of migraine. Lancet Neurol
2004;3:396.
We appreciate the interesting comment on our paper [1]
and the important clinical observations by Teramoto et al.
In their recent
studies the authors have shown that the simple swallowing provocation test
(SPT) is able to identify patients being predisposed to aspiration
pneumonia.[2,3] Based on their experience, featuring a failure of the
SPT in 18 of 26 patients (70%), the authors are rig...
We appreciate the interesting comment on our paper [1]
and the important clinical observations by Teramoto et al.
In their recent
studies the authors have shown that the simple swallowing provocation test
(SPT) is able to identify patients being predisposed to aspiration
pneumonia.[2,3] Based on their experience, featuring a failure of the
SPT in 18 of 26 patients (70%), the authors are right in mentioning that
the swallowing reflex is not always easily provoked in patients having
suffered a severe stroke. Our own data are in apparent conflict with their
findings, since we observed a failure of the reflex placement of
nasogastric tubes in only 2 of 16 patients (12.5%). There are, however,
some differences between the studies in question that may easily account
for this discrepancy. First, the patient collective studied by Teramoto et
al. was older than ours (72.4 ± 4.1 years versus 67.9 ± 14.4 years). This
may be of importance as several studies have shown an age-dependent
increase in the delay of pharyngeal swallow.[4,5]
Second, Teramoto et
al. studied patients who had acquired aspiration pneumonia at that time
already. These patients are prone to suffer from pharyngeal pooling of
mobilised bronchial secretions, which they are unable to disgorge or to
swallow. As has been shown by Langmore et al., the presence of pharyngeal
secretion impedes the assessment of the swallowing reflex and may lead to
false negative findings.[6] Therefore the study of Teramoto et
al. may
indeed overrate the incidence of a disturbed swallowing reflex in their
patient collective. To avoid such problems we recommend to apply gentle
suctioning of the pharyngeal space prior to testing the swallowing reflex
and also prior to using the "reflex placement" method of nasogastric
tubes.
References
1. Dziewas R, Schilling M, Konrad C, Stögbauer F, Lüdemann P (2003)
Placing nasogastric tubes in stroke patients with dysphagia: efficiency
and tolerability of the reflex-placement. J Neurol Neurosurg Psychiatry
74:1429-1431.
2. Teramoto S, Fukuchi Y (2000) Detection of aspiration and swallowing
disorder in older stroke patiens: simple swallowing provovation test
versus water swallowing test. Arch Phys Med Rehabil 81:1517-1519.
3. Teramoto S, Matsuse T, Fukuchi Y (1999) Simple two-step swallowing
provocation test for elderly patients with aspiration pneumonia. Lancet
353:1243.
4. Tracy JF, Logemann JA, Kahrilas PJ, Jacob P, Kobara M, Krugler C (1989)
Preliminary observations on the effects of age on oropharyngeal
deglutition. Dysphagia 4:90-94.
5. Logemann JA, Pauloski BR, Rademaker AW, Colangelo LA, Kahrilas PJ,
Smith CH (2000) Temporal and biomechanical characteristics of
oropharyngeal swallow in younger and older men. J Speech Lang Hear Res
43:1264-1274.
6. Langmore SE, Aviv JE, Endoscopic procedures to evaluate oropharyngeal
swallowing, in Endoscopic evaluation and treatment of swallowing
disorders, Langmore SE, Editor. 2001, Thieme: New York, Stuttgart. p. 73-
100.
We read with interest the letter by Teke et al,[1] which described
a case of organophosphate (OP) poisoning with atypical features and also
the magnetic resonance imaging (MRI) findings.
The number of acute pesticide poisoning is estimated at three million a
year world wide, resulting in over 200,000 deaths.[2,3] In a survey of
deaths due to acute poisoning in the District of Kandy , Sri Lanka f...
We read with interest the letter by Teke et al,[1] which described
a case of organophosphate (OP) poisoning with atypical features and also
the magnetic resonance imaging (MRI) findings.
The number of acute pesticide poisoning is estimated at three million a
year world wide, resulting in over 200,000 deaths.[2,3] In a survey of
deaths due to acute poisoning in the District of Kandy , Sri Lanka from
1967 to 1987 , the agent in 77% of the instance was a pesticide mainly OP.[4]
Teke et al. described the triphasic effects of OP poisoning in humans as
acute cholinergic crisis, intermediate syndrome and delayed polyneuropathy.[1]
This is probably an over simplification of the neurological effects
of OP poisoning. Cranial nerve palsies in intermediate syndrome were well
described by Senanayake and Karalliadde in their original paper (8 patients among the original description of their ten patients with
intermediate syndrome) and all of these patients had flexor plantar
response.[5]
Three patients were described with bilateral recurrent laryngeal
palsies after successful treatment of OP poisoning.[6] The OP insecticide
which caused poisoning in these patients is known to cause delayed
neurological effects .It is postulated that the mechanism of recurrent
laryngeal palsy is same as organophosphate induced delayed polyneuropathy.
Case reports of opsoclonus, cerebellar ataxia, atypical ocular bobbing,
and choreo –athetosis, extra pyramidal manifestation has been described
secondary to OP poisoning.[7-12]
95% of the OP poisoning occurs in the developing world [3] where MRI is
not available in majority of the centres.
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 Psychiatry 2004;75:936-939
2.World Health Organization. Public health impact of pesticide use in
agriculture.Geneva;WHO,1990
3.Jeyaratnam J. Pesticide poisoning : major global health problem. World
Health Statistics Quarterly 1990;43:139-144
4.Senanayake N, Peiris H. Mortality due to poisoning in a developing
agricultural country; trends over 20 years. Human and Experimental
Toxicology 1995,14:808-811
5. Senanayake N, Karalliadde L. Neurotoxic effects of oraganophosphorus
insecticide: an intermediate syndrome. N Engl J Med 1987;316:761-3
6.de Silva HJ, Sanmuganathan PS, Senanayake N. Isolated bilateral
recurrent laryngeal paralysis : a delayed complication of organophosphorus
poisoning . Human and Experimental Toxicology 1994;13:171-173
7.Pullicina P, Aquillana J.Opsoclonus in organophosphate poisoning .
Archives of Neurology 1989;46:704-705
8.Michotte A, Van Dijck l,Maes V, D’Haenen H. Ataxia as the only delayed
neurotoxic manifestation of organophosphate poisoning. European Neurology
1989;29:23-26
9.Hata S, Bernstein E, Davis L. Atypical ocular bobbing in acute
organophosphorus poisoning. Archives of Neurology 1986;43:185-186
10. Joubert J.,Joubert PH, van der Spuy M, van Graan E. Acute
organophosphate poisoning presenting with choreo – athetosis. Clinical
Toxicology 1984;22:187-191
11. Senanayake N, Sanmuganathan PS. Extrapyramidal manifestations
complicating organophosphorus insecticide poisoning. Human and
Experimental Toxicology 1995;14:600-604
12.Davis KL, Yesavage JA, Berger PA. Possible organophosphate induced
parkinsonism. Journal of Nervous and Mental Disease 1978;166:222-225
How useful is antibody testing for paraneoplastic disease in a
patient without known tumour?
Dr Rees proposes to search for paraneuroplastic antibodies in
patients with possible paraneoplastic syndromes. At the same time he
points out that the incidence of specific disabling neurological
paraneoplastic syndromes is very low. No information on the sensitivity
and specifity of an antibody scre...
How useful is antibody testing for paraneoplastic disease in a
patient without known tumour?
Dr Rees proposes to search for paraneuroplastic antibodies in
patients with possible paraneoplastic syndromes. At the same time he
points out that the incidence of specific disabling neurological
paraneoplastic syndromes is very low. No information on the sensitivity
and specifity of an antibody screening is given. One might speculate that
- for example - in the comparatively large population of patients with
polyneuropathies without obvious cause positive antibody tests without
underlying tumour could outnumber true positive findings. In the study on
Anti-Hu positive Encephalomyelitis cited by Dr Rees,[1] 17% of the
patients never developed a tumour. I find it difficult to label them
paraneoplastic. Anyway, the treatment of a patient with or without
antibodies will probably not be
modified until the underlying tumour is found.
In conclusion, I fail to understand the benefit of the test for the
management of individual patients: in a patient with a possibly
paraneoplastic neurological syndrome the tumour must be searched anyway.
Negative antibodies will not exclude the presence of an identifiable
tumour nor will positive antibodies prove it. My personal experience is
that negative antibody screenings may lead to false reassurance and thus
sometimes delay the
diagnosis of an underlying malignancy. As emphasized during the PSA
discussion, false positive results may also be harmful.
Reference
1. Graus F, Keime-Guibert F, Rene R, et al. Anti-Hu-associated
paraneoplastic encephalomyelitis: analysis of 200 patients. Brain
2001;124:1138–48.
Dear Editor,
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...
Dear Editor,
Hyndman and Ashburn [1] find that those who stopped walking when talking were significantly more disabled (p...
Dear Editor
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...
Dear Editor
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.
...Dear Editor
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...
Dear Editor
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...
Dear Editor
Jankovic reviews the expanding list of approved and off-label indications for therapeutic use of botulinum toxin (BT). [1]. One of the prominent off-label indications for use of BT is migraine, the advent of which therapy was serendipitous.
Use of BT for migraine prevention is gaining momentum through the results of randomized controlled trials (RCT) – both completed and ongoing – and, in th...
Dear Editor
We appreciate the interesting comment on our paper [1] and the important clinical observations by Teramoto et al.
In their recent studies the authors have shown that the simple swallowing provocation test (SPT) is able to identify patients being predisposed to aspiration pneumonia.[2,3] Based on their experience, featuring a failure of the SPT in 18 of 26 patients (70%), the authors are rig...
Dear Editor
We read with interest the letter by Teke et al,[1] which described a case of organophosphate (OP) poisoning with atypical features and also the magnetic resonance imaging (MRI) findings. The number of acute pesticide poisoning is estimated at three million a year world wide, resulting in over 200,000 deaths.[2,3] In a survey of deaths due to acute poisoning in the District of Kandy , Sri Lanka f...
Dear Editor
How useful is antibody testing for paraneoplastic disease in a patient without known tumour?
Dr Rees proposes to search for paraneuroplastic antibodies in patients with possible paraneoplastic syndromes. At the same time he points out that the incidence of specific disabling neurological paraneoplastic syndromes is very low. No information on the sensitivity and specifity of an antibody scre...
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