The two case reports by Cataneo et al. have the great interest to
complete the
knowledge upon yawning. Our purpose is to give another view of the
meaning of excessive yawning observed during brainstem stroke. Among
mammals, there are three types of morphologically identical yawns
occurring
in three distinct situations: situations relative to circadian rest-
activity
rhythms, situations relative to f...
The two case reports by Cataneo et al. have the great interest to
complete the
knowledge upon yawning. Our purpose is to give another view of the
meaning of excessive yawning observed during brainstem stroke. Among
mammals, there are three types of morphologically identical yawns
occurring
in three distinct situations: situations relative to circadian rest-
activity
rhythms, situations relative to feeding, situations relative to sexuality
or
social interactions.[1] Until now, no specific cerebral structure has
been
identified as a yawning centre.
A good number of clinical and pharmacological arguments indicate that
yawning involves the hypothalamus (particularly the paraventricular
nucleus),
the bulbus and pontic regions, with frontal region connections in primates
and to the cervical medulla.[2] During the few hours of life of
anencephalous
babies, it has been noted that they yawn and stretch, a sign of the
mammalian syndrome of awakening activity or “Rekel Syndrom”.[3]
Patients
afflicted with the locked-in syndrome, still yawn, despite being paralysed.[4,5,6,7] This shows that yawning originates in the brain’s archaic
structures
common to all vertebrates. The central nervous system is based on a common
overall organisational plan and reveals, from the most ancient to the most
recent vertebrates, a gradual increase in complexity corresponding to life
levels that are increasingly independent and functionally developed.
Yawning
helps understand the phylogenesis of the encephalon by inferring a
functional organisational pattern of the nervous system similar to that
advanced by Paul MacLean[8] with the superposition of: (a) an ancestral
“reptilian” brain (brain stem and diencephalon), where yawning originates;
(b)
a “paleomammalian” brain (limbic system) common to all mammifers,
functioning as a synaptic and humoral interface, in fact the seat of the
monkeys’ emotivity yawn; (c) a “neomammalian” brain characterised by
human’s cortical development, particularly the frontal lobes, seat of the
“contagious” yawn.
The phylogenetic appearance of sleep proposes that the nocturnal rest of
poikilotherms most probably becomes in mammals a form of the rapid eye
movement sleep (REM sleep) or paradoxical sleep which is characterized by
peripheral muscular atonia originating in the dorsal part of the
brainstem,
rostral to the pons.[9] The ultrasound investigation specifies is
ontogenesis
precociousness between 12 and 15 weeks of gestation. Based on numerous
studies of fetuses and infants in a variety of mammalian species, it is
widely
believed that the earliest form of sleep is properly characterized as
active
sleep, that is an immature form of REM sleep and preponderant at birth.
Accordingly, it is thought that quiet sleep, an immature form of slow-wave
sleep (SWS), emerges as REM sleep’s predominance diminishes during
ontogeny. Behavioural pattern continuity from prenatal to postnatal life
shows
a strict parallelism between the ontogeny of REM sleep and yawning.
Basically, REM sleep in the human declines from 50% of total sleep time (8 hours)
and a frequency of 30 to 50 yawns per day, in the fetus and newborn, to
15%
of total sleep time (1 hour) and less than 20 yawns per day, in the adult.
This
decrease takes place mainly between birth and the end of puberty. As a
flip-
flop switch, the reciprocal interactions between sleep and wake promoting
brain regions allow the emergence of distinct states of arousal. By its
ontogenical links with REM sleep, yawning appears as a behaviour which
procures an arousal reinforcement through the powerful stretch and the
neuromuscular rewiring induced. The powerful muscular contraction caused
by yawning releases arousal by activation of the reticular-formation
(locus
coeruleus) to which the cranial nerves send retro-projections. At becoming
aware, the yawning and stretching reverse the muscular atonia which
characterize REM-sleep.[10]
Face-scratching, nose-face rubbing movements, yawning, sighs have
been
reported as automatisms before or after typical absence seizures or
minimal
epileptic seizures arising from sleep and they evoke temporal lobe
seizures.[11] These behaviours are also seen as a characteristic behavioural pattern
of
the arousal from sleep in healthy subjects. Velocity and repetition of the
movements change in a different physiological (sleep arousal) or
pathological
(epileptic seizure, brainstem stroke) context. These behaviours can be
related
to the activation of brainstem and diencephalic circuitries, where the
'central
pattern generators' of these behaviours are located, when cortex appears
as
deconnected by the epileptic discharge or stroke. The networks
controlling
awaking must be tonically reinforced and yawning appears as a behaviour
testifying arousal reinforcement.
References
1. Walusinski O, Deputte B. The phylogeny, ethology and nosology of
yawning. Rev Neurol (Paris). 2004 Nov;160(11):1011-21. Review. French.
2. Baenninger R. On yawning and its functions. Psychonomic Bul Rev.
1997;4.(2)198-207.
3. Gamper E. Bau und Leistungen eines menschlichen Mittelhirnwesens
(Arhiencephalie mit Encephalocele). Zeitschr.f.d.ges.Neurol.u.Psychiat.
1926;104:49-120.
4. Gschwend J. Yawning in a case with transsecting glioma of the pons
Fortschr. Neurol. Psychiat.1977;45:652-655.
5. Bauer G, Gerstenbrand F, Hengl W. Involuntary motor phenomena in the
locked-in syndrome. J. Neurol. 1980;223:191-198.
6. Ghika J, Vingerhoets F, Bogousslavsky J. Dissociated preservation of
automatic-voluntary jaw movements in a patient with biopercular and
unilateral pontine infarcts. Eur Neurol. 2003;50(3):185-8
7. Krasnianski M, Gaul C, Neudecker S, Behrmann C, Schluter A,
Winterholler
M. Yawning despite trismus in a patient with locked-in syndrome caused by
a
thrombosed megadolichobasilar artery. Clin Neurol Neurosurg. 2003 Dec;106
(1):44-6.
8. MacLean P. Evolutionary psychiatry and the triune brain. Psychol Med.
1985;15:219-221.
9. Nicolau MC, Akaarir M, Gamundi A, Gonzalez J, Rial RV. Why we sleep:
the
evolutionary pathway to the mammalian sleep. Prog Neurobiol. 2000 Nov;62
(4):379-406.
10. Walusinski O, Kurjak A, Andonotopo W, Azumendi G. Fetal yawning
assessed by 3D and 4D sonography. The ultrasound Rev Obst Gynecol. 2005;
in press.
11. Meletti S, Cantalupo G, Stanzani-Maserati M, Rubboli G, Tassinari A.
The
expression of interictal, preictal, and postictal facial-wiping behavior
in
temporal lobe epilepsy: a neuro-ethological analysis and interpretation.
Epilepsy Behav. 2003;4(6):635-643.
I read with interest the article looking at headache as an isloated
symptom of venous thrombosis.
As a radiologist, I was interested in the assertion that a "normal CT
scan" necessitated a MRI/MRV scan. In my experience if the symptomatology
is atypical, performing a CT venogram, particularly on the multislice CT
scanner can give an accurate result in a large proportion of cases.
We perform CT venog...
I read with interest the article looking at headache as an isloated
symptom of venous thrombosis.
As a radiologist, I was interested in the assertion that a "normal CT
scan" necessitated a MRI/MRV scan. In my experience if the symptomatology
is atypical, performing a CT venogram, particularly on the multislice CT
scanner can give an accurate result in a large proportion of cases.
We perform CT venography on a 16 slice scanner and the multiplanar
reconstructions of the 1.25mm images in sagittal and coronal reformats
enables visualisation of the venous sinuses adequately.
Secondly, what technique was used for MRV studies? A difference can
be seen if phase contrast technique (more accurate) is used in preference
to time of flight protocol. Also, 3-D MR venography is often superior to
2D MR venography in the delineation of major cerebral venous structures in
children, because artifactual loss of signal is seen with the use of 2D MR
venography in nondominant transverse sinuses.
Thirdly, mention should be made of cases which can present on
unenhanced CT with areas of infarction secondary to venous thrombosis and
further imaging may be directed accordingly in these cases.
References
1. Leach JL, Jones BV, Tomsick TA, Stewart CA, Balko MG. Normal
appearance of arachnoid granulations on contrast-enhanced CT
and MR of the brain: differentiation from dural sinus disease. Am J
Neuoradiol 1996; 17:1523-32.
2. Casey SO, Alberico RA, Patel M, Jimenez JM, Ozsvath RR, Maguire
WM, et al. Cerebral CT venography. Radiology 1996; 198:163-70.
3. Ayanzen RH, Bird CR, Keller PJ, McCully FJ, Theobald MR,
Heiserman JE. Cerebral MR venography: normal anatomy and
potential diagnostic pitfalls. Am J Neuoradiol 2000; 21:74-8.
4. Huisman TA, Holzmann D, Martin E, Willi UV. Cerebral venous
thrombosis in childhood. Eur Radiol 2001; 11:1760-5.
5. Rollins N, Ison C, Reyes T, Chia J.- Cerebral MR venography in
children: comparison of 2D time-of-flight and gadolinium-enhanced 3D
gradient-echo techniques- Radiology. 2005 Jun;235(3):1011-7. Epub 2005 Apr
28.
We read with great interest the paper by Dr. Lavrijsen and colleagues
on”Prevalence and characteristics of patients in a vegetative state (VS)
in Dutch nursing homes”.[1] They point out that –there is a difference
between the prevalence in Vienna and Netherlands (Vienna 19/1 000 000;
Netherlands 2/1 000 000).[2] Because of this considerable difference
between these two results we would like to figure o...
We read with great interest the paper by Dr. Lavrijsen and colleagues
on”Prevalence and characteristics of patients in a vegetative state (VS)
in Dutch nursing homes”.[1] They point out that –there is a difference
between the prevalence in Vienna and Netherlands (Vienna 19/1 000 000;
Netherlands 2/1 000 000).[2] Because of this considerable difference
between these two results we would like to figure out possible reasons.
First reason seems to be population-related. Lavrijsen and his colleagues
recorded only patients with VS in Dutch nursing homes. In our study acute
wards as well as nursing homes were included. If we excluded all patients
with VS , treated in acute wards, from our data the prevalence of VS for
nursing homes in Vienna would be 11/1 000 000. So even after splitting the
groups of patients the results differ sizeably. Another difference is that
one investigation was in the capitol city of Austria, Vienna (1.620 000
inhabitants) and on the other hand the whole Netherlands (16.200 000). So
one survey deals only with an urban population while the other reflects on
a mix from urban and rural populations.
The second possible reasons from our point of view are the different
methods in investigation. Lavrijsen et al. recorded the data from all
patients with VS during one month. In Vienna data were recorded within
three days, and all patients were assessed by one examiner. In the work of
Lavrijsen et al. only in those instances where there were doubts about the
diagnosis, one of three examiners assessed the patients.
Before comparing such complex data, the differences in health care in
patients with VS, beginning from the acute impact to nursing facilities,
have to be evaluated. If there is great variability it has to be accounted
on in analysis.
Lavrijsen results differ not only from our study but also from others,
like Higashi
(25/1 000 000) and Ashwal (24/1 000 000).[3,4] Therefore it would be very
interesting to discuss these differences of results with the authors.
References
1. Lavrijsen JCM, vd Bosch JSG, Koopmans RTCM, et al. Prevalence and
characteristics of patients in a vegetative state in Durch nursing homes.
J Neurol Neurosurg Psychiatry 2005;76:1420-1424.
2. Stepan Ch, Haidinger G, Binder H. Prevalence of Vegetative State/
Apallic Syndrome in Vienna. Eur J Neurol 2004; 11(7):461-6.
3. Higashi K, Sakata Y, Hatano M, et al. Epidemiological studies on
patients with a persistent vegetative state. J Neurol Neurosurg Psychiatry
1977:40;876-885.
4. Ashwel S, Eyman RK, Call TL. Life expectancy of children in a
persistant vegetative state. Pediatr Neurol 1994; 10:27-33.
We are concerned that the recent article by Rosenberg et al.[1]
contains numerous inaccuracies and methodological errors
rendering their conclusion that “it is unlikely that chronic peripheral
neuropathy… is associated with coeliac disease” unsound.
The essence of their own contribution to the field is the screening
of 16 patients with idiopathic neuropathy one of whom had positive
antiglia...
We are concerned that the recent article by Rosenberg et al.[1]
contains numerous inaccuracies and methodological errors
rendering their conclusion that “it is unlikely that chronic peripheral
neuropathy… is associated with coeliac disease” unsound.
The essence of their own contribution to the field is the screening
of 16 patients with idiopathic neuropathy one of whom had positive
antigliadin antibodies but no evidence of coeliac disease (CD) on
duodenal biopsy. In the abstract of their article they state: “In 425 of
the 478 patients, a cause other than coeliac disease was
established. In the patients with no determined cause for
neuropathy, one had abnormally increase IgA antigliadin
antibodies but duodenal biopsy was normal.” The abstract is
misleading, giving the impression that they have screened 53 (478
minus 425) patients with idiopathic neuropathy when in reality they
have screened only 16 patients (as indicated in the text). This
issue is important as the small number renders the study
underpowered, making any sound conclusion on the prevalence
of CD in patients with idiopathic neuropathy impossible.
The issue of small numbers screened may well be what prompted
the authors to perform a systematic review of the literature. We
have concerns about a number of issues relating to this review:
1. Study selection for systematic review
For this systematic review they considered studies to be eligible if
they included original data and excluded publications with “results
presented in an editorial without details”. They included 10 studies
that apparently fulfilled these criteria, claiming that the study
design was described in them all. The authors should therefore
explain the inclusion of an editorial (2) and a book chapter (3),
both by the same authors. The study design and methodology are
stated in neither of these publications and the data presented are
apparently anecdotal. Furthermore both of these publications refer
to the same study population, something that the authors
acknowledge, yet still proceed to include this population twice,
rendering their statistical calculation invalid.
2. Assessment for the presence of neuropathy
In 3 out of 4 of the studies that contribute to Group B (patients
with
CD investigated for polyneuropathy) the extent of neurological
and/or neurophysiological investigation for a neuropathy of the
whole cohort of patients with CD is not mentioned. Two of these
studies[2,3] should not have been included for the reasons
highlighted in point 1 above. Only in one of these studies[4] were
systematic neurological and neurophysiological assessments
performed in all of their patients with CD, giving the true
prevalence of polyneuropathy in patients with CD of 23%. This is
in marked contrast to the figure of 0.9% derived from wrongly
combining all 4 studies.
3. Exclusion of patients with CD
Throughout their systematic review Rosenberg et al exclude all
patients with CD who also have an additional autoimmune
disease that may be aetiologically linked to a neuropathy. It is well
known that patients with CD have a higher prevalence of other
autoimmune diseases. This however does not mean that the
aetiology of the neuropathy is more likely to be due to the
additional autoimmune disease anymore than it is due to CD.
Furthermore they also exclude all patients where the diagnosis of
CD preceded the diagnosis of neuropathy. Just because CD
preceded the neuropathy does not mean that CD should not be
considered aetiologically linked to the neuropathy. By excluding
such patients they greatly underestimate the prevalence of CD in
patients with polyneuropathy.
4. Inaccurate representation of data
One of the studies[5] featured in Group A (patients in whom
polyneuropathy preceded duodenal biopsy) has as its subject the
neurological manifestations in a cohort of 144 patients with CD.
Rosenberg et al do not include these data in their review but use
the anecdotal report in the discussion section of 3 out of 204
patients with idiopathic neuropathy who were found to have CD.
This is despite a clear statement by the authors of this paper that “it
is probable that these calculations underestimate the frequency of
CD because screening for CD in this group was not systematic”.
Further problems arise with the interpretation of the third study[6] where Rosenberg et al make the assumption that the 400 patients
screened all had idiopathic neuropathy.
Yours sincerely,
Marios Hadjivassiliou
Richard Grünewald
References
1. Rosenberg NR, Vermeulen M. Should coeliac disease be
considered in the work up of patients with chronic peripheral
neuropathy? J Neurol Neurosurg Psychiatry 2005;76:1415-1419.
2. Pengiran Tangah DS, Wills AJ, Holmes GK. Neurological
complications of coeliac disease. Postgrad Med J 2002;78:893-8.
3. Holmes GK. Neurological and psychiatric complications in
coeliac disease. In:Epilepsy and other neurological disorders in
coeliac disease. London:John Libbey 1997:251-64.
4. Luostarinen L, Hinamen SL, Luostarinen M, Collin P, Pirttila T.
Neuromuscular and sensory disturbances in patients with well
treated coeliac disease. J Neurol Neurosurg Psychiatry
2003;74:490-494.
5. Luostarinen L, Pirttila T, Collin P. Coeliac disease presenting
with neurological disorders. Eur Neurol 1999;42:132-135.
6. Chin RL, Sander HW, Brannagan TH, Green PHR, Hays AP,
Alaedini A, Latov N. Celiac neuropathy. Neurology 2003.
I enjoyed reading Sun et al.’s (2004) article regarding effects of
the tongue acupuncture (invasive treatment) on children with cerebral
palsy. But I note that some important issues were not covered in the
article.
The authors reported "the treatment group received 40 sessions of TAC
(tongue acupuncture) in a daily basis" and "Sterile gauze was used to pick
and station the tongue with the ac...
I enjoyed reading Sun et al.’s (2004) article regarding effects of
the tongue acupuncture (invasive treatment) on children with cerebral
palsy. But I note that some important issues were not covered in the
article.
The authors reported "the treatment group received 40 sessions of TAC
(tongue acupuncture) in a daily basis" and "Sterile gauze was used to pick
and station the tongue with the acupuncturist's left hand and quick and
accurate insertion into the acupoints was performed with the right".
1) Since the subjects are children, their tongues are tiny and soft,
and nine of them with mental retardation. How did the authors measure the
accuracy and repeatability of the needle insertion, in terms of angle,
depth and location, by naked eyes? Particularly the tongues were being
grabbed and deformed.
2) The sensitive tongues being stabbed daily for 8 weeks, any local
inflammation or nerve damage was resulted? Especially the authors claimed
they could accurately stab the same acupoints daily. Were all the children
able to express their possible discomfort, e.g. numbness?
Regardless of my comments, the authors have presented an interesting
study. I admire their attempt at establishing an evidence-based
alternative therapy and would not hesitate to recommend their article to
anyone who is interested in the field of neurology or Chinese medicine.
Michael Wong
Hong Kong
Reference
1. Sun JG, Ko CH, Wong V, Sun XR. Randomised control trial of tongue
acupuncture versus sham acupuncture in improving functional outcome in
cerebral palsy. J Neurol Neurosurg Psychiatry 2004; 75: 1054-1057.
The effectiveness of rt-PA in the elderly is an important and as yet
an incompletely resolved topic. The authors provide convincing data that
patients older than 80 years that receive rt-PA are less likely to achieve
a favourable outcome than their younger counterparts.[1] This is in
keeping with our own data showing that 5/24 (21%) patients treated with rt
-PA aged 80 years or older were independent (...
The effectiveness of rt-PA in the elderly is an important and as yet
an incompletely resolved topic. The authors provide convincing data that
patients older than 80 years that receive rt-PA are less likely to achieve
a favourable outcome than their younger counterparts.[1] This is in
keeping with our own data showing that 5/24 (21%) patients treated with rt
-PA aged 80 years or older were independent (mRS 0-2) after three months
compared to 39/77 (51%) patients younger than 80 years.
However, their and our data provide no indication that rt-PA is less
effective in the elderly. The chance of a favourable outcome of a stroke
declines with advancing age.[2] To show that effectiveness of rt-PA
decreases with age, the authors would need to have demonstrated that the
worse outcome in the very elderly with rt-PA is more pronounced than in
the group without rt-PA. This of course can only be achieved, ideally, in
randomised studies or otherwise by comparison to age matched cohorts that
have not received rt-PA.
An example of a similar situation is the following. It is well
established that the outcome of treatment with rt-PA is worse in severe
strokes than in those with less severe stroke.[3] This does not mean that
the effectiveness of rt-PA is any less in more severe strokes. In a
reanalysis of the NINDS trial, the prognosis of patients with a National
Institute of Health Stroke Scale (NIHSS) score of >20 was much worse
than that in patients with a NIHSS score of 6-10. Nonetheless, the odds
ratios for effectiveness of rt-PA were equally high (2.6) in the two
groups.[4]
We agree that the treatment of the very elderly with rt-PA needs to
be closely monitored and further studies are required. However, the
conclusion that “older patients are much less likely to benefit from iv rt
-PA” and the title suggesting that actual effectiveness is compared in
this study are misleading and may unjustly lead physicians to withhold rt-
PA in the very elderly.
We declare that we have no conflict of interest.
References
[1]. Mouradian MS, Senthilselvan A, Jickling G, McCombe JA, Emery DJ,
Dean N, Shuaib A. Intravenous rt-PA for acute stroke: comparing its
effectiveness in younger and older patients. J Neurol Neurosurg Psychiatry
2005; 76(9):1234-1237.
[2]. Chambers BR. Prognosis of acute stroke. Neurology 1987;
37(2):221-225.
[3]. Hacke W, Donnan G, Fieschi C, Kaste M, von Kummer R, Broderick
JP, Brott T, Frankel M, Grotta JC, Haley EC, Jr., Kwiatkowski T, Levine
SR, Lewandowski C, Lu M, Lyden P, Marler JR, Patel S, Tilley BC, Albers G,
Bluhmki E, Wilhelm M, Hamilton S. Association of outcome with early stroke
treatment: pooled analysis of ATLANTIS, ECASS, and NINDS rt-PA stroke
trials. Lancet 2004; 363(9411):768-774.
[4]. Ingall TJ, O'Fallon WM, Asplund K, Goldfrank LR, Hertzberg VS,
Louis TA, Christianson TJH. Findings from the reanalysis of the NINDS
tissue plasminogen activator for acute ischemic stroke treatment trial.
Stroke 2004; 35(10):2418-2424.
I am looking for others with stroke ataxia -
this movement disorder has been with me since I had
an aneurysm burst in my cerebellum 14 years ago.
Although I have found ways of compensating for the deficits
I feel there must be research information available which I
hope to find.
Please contact me if your ataxia is not of genetic origin.
I belong to Internaf, where the medical informatio...
I am looking for others with stroke ataxia -
this movement disorder has been with me since I had
an aneurysm burst in my cerebellum 14 years ago.
Although I have found ways of compensating for the deficits
I feel there must be research information available which I
hope to find.
Please contact me if your ataxia is not of genetic origin.
I belong to Internaf, where the medical information is
excellent - but the primary focus is the genetic ataxias.
I have reviewed your study which is a small size study of only 15 patients.
Your result showed that disease aggravation was unlikely during study period, but you have not mentioned about duration and type of sun exposure during this period which is very important factor in this study as well as in other studies.
Is there any role of calcitriol during relapse, as you ha...
I have reviewed your study which is a small size study of only 15 patients.
Your result showed that disease aggravation was unlikely during study period, but you have not mentioned about duration and type of sun exposure during this period which is very important factor in this study as well as in other studies.
Is there any role of calcitriol during relapse, as you have mentioned only use of corticosteroids during this period?
In your study there is no measurment of serum parathyroid hormone level at any time?
Is there any relation between serum level of parathyroid hormone, calcitriol and calcium with Relapsing-remitting multiple sclerosis?
Dr. Rameshwar Nath Chaurasia
Senior Resident,Department of Neurology
Institute of Medical Sciences Banaras Hindu University
Varanasi-221005, India
We were very interested in the clinical experience of Eerola and
colleagues in applying Beta-CIT SPECT to aid movement disorder diagnosis.
However, in posing the question: “How Beta-CIT SPECT differentiates
idiopathic Parkinson’s disease from other conditions” they have tested the
ability of the technique to differentiate patients with Parkinson’s
disease (PD) from those with Dementia with Lewy Bodies...
We were very interested in the clinical experience of Eerola and
colleagues in applying Beta-CIT SPECT to aid movement disorder diagnosis.
However, in posing the question: “How Beta-CIT SPECT differentiates
idiopathic Parkinson’s disease from other conditions” they have tested the
ability of the technique to differentiate patients with Parkinson’s
disease (PD) from those with Dementia with Lewy Bodies (DLB), Parkinson’s
plus (P+) disorders, vascular parkinsonism, essential tremor, psychogenic
parkinsonism, drug-induced parkinsonism or dystonia, and found a low
specificity for the technique. Since presynaptic dopaminergic SPECT cannot
accurately differentiate PD from DLB or P+ disorders, a higher specificity
has been shown when the more clinically meaningful question: “Does this
patient have degenerative parkinsonism or non-degenerative parkinsonism?”
was asked.[1-3] The higher incidence of P+ and DLB in older patients
(reflected in the mean age over 65 years exceeding that of their other
diagnostic groups) compounded the issue, leading to the conclusion that
the technique is less useful in older patients. Another report concludes
the opposite, namely that FP-CIT SPECT dopamine transporter imaging is
probably more helpful in the older patient.[4]
As a separate point, we would welcome information regarding their
gold-standard clinical diagnosis at follow-up; was the assessor blinded to
clinical progression, treatment and SPECT results? Increasing congruence
over time between baseline imaging and clinical diagnosis from blinded
video review at up to 4 years reinforces the validity of the SPECT
technique (Marek K, International Congress on Parkinson’s Disease and
Related Disorders, Berlin, 2005).
References
1. Benamer HT, Oertel WH, Patterson J, Hadley DM, Pogarell O,
Hoffken H, Gerstner A, Grosset DG. Prospective study of presynaptic
dopaminergic imaging in patients with mild parkinsonism and tremor
disorders: part 1. Baseline and 3-month observations. Mov Disord.
2003;18:977-84.
2. Catafau AM, Tolosa E, DaTSCAN Clinically Uncertain Parkinsonian
Syndromes Study Group. Impact of dopamine transporter SPECT using 123I-
Ioflupane on diagnosis and management of patients with clinically
uncertain Parkinsonian syndromes. Mov Disord. 2004;19:1175-82.
3. Parkinson Study Group. A multicentre assessment of dopamine
transporter imaging with DOPASCAN/SPECT in parkinsonism. Neurology
2000;55:1540-7.
4. Seenan, P., MacPhee, G., Stewart, D, and Patterson, J.
Retrospective analysis of the utility of FP-CIT SPECT scanning in the
diagnosis of movement disorders in old age. Parkinsonism and Related
Disorders 11(Supp 2), 152 [PT013-12]. 2005.
DG has received consultancy fees from GE Healthcare
I've read with interest the recent 5-page JNNP editorial directive by Thompson et al. for “Management of Spasticity.” This paper is not only remarkable for its authoritative vigour; the authors frankly confess, “There is no agreed evidence-based model available for the management of spasticity…A key component of management is the education of all involved.”[1]
I've read with interest the recent 5-page JNNP editorial directive by Thompson et al. for “Management of Spasticity.” This paper is not only remarkable for its authoritative vigour; the authors frankly confess, “There is no agreed evidence-based model available for the management of spasticity…A key component of management is the education of all involved.”[1]
But their educational argument is unfortunately afflicted with imprecise definitions, lack of clinical data base, and consequent conceptual perversion. “Stretch reflexes in healthy subjects are complex.…Spasticity is seen after an upper motor neuron (UMN) lesion, the relative importance of descending pathways remains unclear….Lack of descending control over spinal cord interneuronal circuits results in a decrease in the effectiveness of spinal inhibitory circuits such as those mediating reciprocal, presynaptic, and recurrent inhibition….The paucity of inhibitory spinal cord control means that this activity could, once triggered, continue relatively unabated…. Spasms or sudden involuntary, often painful, movements are often included under the umbrella term of spasticity. However, physiologically these appear to be an independent entity….Spasticity and spasms are, however, only two of the symptoms of the UMN syndrome. Other symptoms such as muscle weakness, decreased postural responses, and reduced dexterity all have an impact on an individual’s function. These features may be independent of each other, but it is often difficult to assess the relative contribution each has to reduction in function.” (The editorial’s Reference [1], “Pathophysiology of spasticity,” is a misprinted citation to next century volume 238 of JNNP.) Not cited is James Lance’s non-complex, now classical definition, “Spasticity is a motor disorder characterized by a velocity-dependent increase in tonic stretch reflexes (muscle tone) with exaggerated tendon jerks, resulting from hyperexcitability of the stretch reflex, as one component of the UMN syndrome.”[2]
This confusion is more than an issue of academic semantics; the product is their all-inclusive causal indictment: “Spasticity can cause discomfort and stiffness, while spasms can be annoying and painful and may interfere with function. Physical activities such as walking, transferring, picking up objects, washing, dressing, and sexual activity can all be affected. Likewise the ongoing presence of spasticity and spasms can have an emotional impact on, for example, mood, self image, and motivation. Poorly managed spasticity can also be responsible for muscle shortening and the development of tendon and soft tissue contractures, which together with spasms can lead to compromised safety in lying and sitting.” Secondary indictments from contractures include “difficulties with personal hygiene or dressing, positioning, and at times the inability to sit, which may lead to restricted community mobility and social isolation…development of pressure sores…in children...failure of normal muscle growth…torsion of long bones…joint instability and degeneration.” Thus they attribute all of the disabilities of upper motor neuron impairment (UMNI) to spasticity.
Joint and muscle contracture are the consequence of every variety of chronically restricted joint excursion, whether due to muscular dystrophy, arthritis, local pain, trauma, or orthopaedic fixation. Blaming the reflexes rather than the primary disuse hallmark of UMNI is justified neither by Occam’s razor nor the practical facts.
“Symptom” is the subjective verbalization by the patient of what isn’t functioning properly. The negative symptom language of a patient with UMNI includes words like “weak, clumsy, numb, paralyzed, stiff, tired.” Among these concepts, either patient or physician may play verbal games like attributing “weakness” to “stiffness,” or the reverse; empirical evidence of such relationships does not exist. Nor is there evidence that subjective “stiffness” in task performance is a valid measure of “spasticity.” “Spasticity” is a technical doctor word, not a patient’s symptom complaint. It specifies a complex observation by the physician, inferred to be the result of brain/spinal cord dysfunction or lesion, not a cause. The central concept is increased reactivity, not steady state. Spastic muscles at rest are flaccid. The negative symptoms of UMNI, disturbed voluntary (Jackson’s term) coordination, dexterity, and maintenance of force are attributed to functional or structural disconnection of the spinal final common path from finely tuned integrated brain control. Cerebral cortex Brodmann area 4 (M-1), its corticomotoneuronal projection fibres, and the much broader hemispheral source of the pyramidal tract are only the major central output components. The essential working machinery includes thalamus, basal ganglia, cerebellum, and brain stem. A variety of physiological approaches have consistently failed to show that spasticity phenomena contribute significantly to the negative symptoms of UMNI.[2]
Recent study of a large series of hemiplegic strokes showed that “Spasticity was present in only 19% three months after stroke. Severe disabilities were seen in almost the same number of non-spastic as spastic patients. These findings indicate that the focus on spasticity in stroke rehabilitation is out of step with its clinical importance.”[3] I know of no evidence that the Ashworth scale of spasticity has reliable correlation with the functional performance that patients seek to restore. A much needed recent review of oral antispastic drugs found that none improved motor function significantly, with the exception of some flexor spasm relief by baclofen.[4]
The claim that local injection of botulinum toxin is efficacious is specious.[5] Regarding lifelong spinal infusion of baclofen for the most seriously afflicted patients, I share reservations about the perpetual technical tie-up, economic cost, risk of infection, and arachnoiditis. Since sphincter function is already seriously impaired in most such patients, I concur that the alternative concept of intrathecal phenol deserves more careful study.
The authors’ recommendation of individualized “seamless and multidisciplinary” long-term management of UMNI in order to sustain maximal patient autonomy is not controversial. The critical lack of any controlled, much less Cochrane standard data base for both medications and procedures is apparent. Our patients’ management merits more than a model map.
2. Landau WM. Muscle tone: hypertonus, spasticity, rigidity. Elsevier’s Encyclopedia of Neuroscience, Third Edition: 1-5, 2001.
3. Sommerfeld DK, Eek EU-B, Svensson A-K, Holmqvist LW, von Arbin MH. Spasticity after stroke. Its occurrence and association with motor impairments and activity limitations. Stroke 2004; 35:134-140. Landau WM. Letter to the editor: Spasticity after stroke: Why bother? Stroke 2005; 35:1787-1788.
4. Montané E, Vallano A, Laporte JR. Oral antispastic drugs in nonprogressive neurologic diseases. a systematic review: Neurology 2004; 63:1357-1363. Landau WM. Letter to the editor. Neurology 2005; 64:1989-90.
5. Landau WM. Letter to the editor: Botulinum toxin for spasticity after stroke. New Engl J Med 2003; 348-258.
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Dear Editor,
I've read with interest the recent 5-page JNNP editorial directive by Thompson et al. for “Management of Spasticity.” This paper is not only remarkable for its authoritative vigour; the authors frankly confess, “There is no agreed evidence-based model available for the management of spasticity…A key component of management is the education of all involved.”[1]
But their educational argument is unfor...
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