With interest we read the recent review by Donnellan et al.[1] on coping strategies after stroke. The review highlights the existing literature on coping strategies in stroke patients, in part with the aim to identify coping strategies that are typical for this patient group. In
addition, the review investigates methodological issues in terms of definition and measurement of coping. The review makes i...
With interest we read the recent review by Donnellan et al.[1] on coping strategies after stroke. The review highlights the existing literature on coping strategies in stroke patients, in part with the aim to identify coping strategies that are typical for this patient group. In
addition, the review investigates methodological issues in terms of definition and measurement of coping. The review makes it abundantly clear that this area is in need of significant improvement, especially in stroke research.
The authors also show that with the current data it is difficult to pinpoint certain coping strategies that are used either immediately after the stroke, or in the long term. However, we feel that the main question concerning the existence of specific coping strategies that are used by stroke patients, is perhaps less relevant than examining which coping strategies are related to important outcomes. The review mentions a limited number of studies that have related coping strategies to the outcome measure depression. Several coping strategies such as avoidance
coping, decreased behavioural action, and apathy were related to depression.[1]
While the relation between depression and coping is an important finding, depression as an outcome measure is somewhat one-sided because it does not cover multiple aspects of well-being. Quality of life (QoL) in
recent years has received a lot of attention in healthcare research, as it attempts to measure the multiple aspects of well-being. Indeed research in stroke patients has shown that QoL of stroke patients is impaired.[2][3]
We recently conducted a longitudinal study on coping strategies in stroke patients, all of which were discharged to go home, and related coping strategies to the patient’s QoL. The coping strategies were derived from
the Dual Process Model of coping by Brandtstädter and Renner,[4] who describe coping in terms of adjusting or pursuing goals that existed before the stroke occurred. The study consisted of four measurement moments up to 9-12 months after discharge. Our results showed that while
taking the level of physical functioning into account both coping strategies at baseline were positively and independently associated with QoL, at least 5 months after discharge.[5] These are significant findings of an exploratory study of relatively fortunate patients in terms of impaired physical functioning.
Unlike traits such as neuroticism, which in fact tends to also be a strong determinant of outcome measures such as QoL, coping strategies are dependent on context and therefore in part modifiable. Patients who present with a poor perceived QoL relative to their physical impairment
may benefit from an intervention designed to improve the way these patients cope with their impaired physical functioning. The challenge for the near future is in our view to further explore the relationship between
coping and QoL of both patient and proxy. ‘Therapeutic’ approaches that may help stroke survivors to improve their coping behaviour should be developed and evaluated. Such studies should not only be directed to coping strategies in general (e.g. problem-focussed, emotion-focussed and
adjusting/pursuing goals), but also to coping strategies in specific daily life situations (e.g. work, family and friends, leisure activities). Whether such approaches will be effective from a clinical and economical point of view should be evaluated as rigorously as in medical intervention research.
Anne-Sophie E.Darlington
References
1. Donnellan C, Hevey D, Hickey A et al. Defining and quantifying coping strategies after stroke: a review. J Neurol Neurosurg Psychiatry 2006;77:1208-1218.
2. Sturm JW, Donnan GA, Dewey HM et al. Quality of life after stroke. The North East Melbourne Stroke Incidence Study (NEMESIS). Stroke 2004;35:2340-2345.
3. Paul SL, Sturm JW, Dewey HM, et al. Long-term outcome in the North East Melbourne Stroke Incidence Study: predictors of quality of life at 5 years after stroke. Stroke 2005;36:2082-2086.
4. Brandtstädter J, Renner G. Tenacious goal pursuit and flexible goal adjustment: explication and age-related analysis of assimilative and accommodative strategies of coping. Psychol Aging 1990;5:58-67.
5. Darlington ASE, Dippel DWJ, Ribbers GM, et al. Coping strategies as determinants of quality of life in stroke patients: A longitudinal study. Cerebrovasc Dis, in press.
We read with great interest the article by Park et al1 concerning the frequency and associations of hypoplastic vertebral artery (HVA) with posterior circulation stroke. In this study, 529 patients with ischemic stroke were classified according to their stroke location (anterior or
posterior circulation strokes). The investigators found that among all patients 35.2% (185 patients) had HVA, and more im...
We read with great interest the article by Park et al1 concerning the frequency and associations of hypoplastic vertebral artery (HVA) with posterior circulation stroke. In this study, 529 patients with ischemic stroke were classified according to their stroke location (anterior or
posterior circulation strokes). The investigators found that among all patients 35.2% (185 patients) had HVA, and more importantly that patients with posterior circulation strokes showed a significantly higher rate of HVA than those with anterior circulation strokes. Similar results were reported in 2 other very recent studies.2,3 In addition, our mini-series suggested that a HVA in association with at least 2 other risk factors for
stroke may contribute to an ischemic posterior circulation event even in young population.
On the other hand, variations in anatomy of the vertebral arteries are relatively frequent, as in 4-15% of the healthy population one vertebral artery is atretic with minimal contribution to vertebrobasilar blood flow, while lesser degrees of asymmetry are more frequent. The two
vertebral arteries are of similar size in 25%, while the left is the dominant artery in 50% of the population. The absence of vertebrobasilar insufficiency symptoms in all these cases without other stroke risk factors led to the impression that even a pronounced vertebral artery
asymmetry was innocent and should be regarded as normal variant. The discrepancy between these studies may be due to the fact that other stroke risk factors were not taken into account. Thus, HVA may be asymptomatic if there are no other risk factors, but it may contribute to posterior
circulation stroke in some patients, if other risk factors are present.
It is obvious that the clinical significance of HVA is not yet clearly defined and that larger perspective studies are needed to characterize the role of HVA in posterior circulation stroke.
Sotirios Giannopoulos, Maria Kosmidou, Sygliti-Henrietta Pelidou, Athanassios P. Kyritis
References
1. Park JH, Kim JM, Roh JK. Hypoplastic vertebral artery; Frequency and associations with ischemic Stroke territory. J Neurol Neurosurg Psychiatry. 2006 Nov 10; [Epub ahead of print]
2. Perren F, Poglia D, Landis T, Sztajzel R. Vertebral artery hypoplasia: a predisposing factor for posterior circulation stroke? Neurology. 2007 Jan 2;68(1):65-67.
3. Chuang YM, Huang YC, Hu HH, Yang CY. Toward a further elucidation: Role of vertebral artery hypoplasia in acute ischemic stoke. Eur Neurol 2006;55:193-197.
4. Giannopoulos S, Markoula S, Kosmidou M, Pelidou H-S, Kyritsis AP. Lateral medullary ischemic events in young adults with hypoplastic vertebral artery. J Neurol Neurosurg Psych (In press).
5. Trattnig S, Schwaighofer B, Hubsch P, Schwarz M, Kainberger F. Color-coded Doppler sonography of vertebral arteries. J Ultrasound Med. 1991 Apr;10(4):221-6.
Dr Hintzen and Dr van den Born describe a patient with acute zonal occult outer retinopathy (AZOOR) who also fulfilled the criteria of clinically definite multiple sclerosis. AZOOR is a rare, newly recognized retinal disorder occurring predominantly in young Caucasian females. [1] The aetiology remains unknown, but an inflammatory origin is suspected. [1][2] As reported by Gass et al. [1], the inflamma...
Dr Hintzen and Dr van den Born describe a patient with acute zonal occult outer retinopathy (AZOOR) who also fulfilled the criteria of clinically definite multiple sclerosis. AZOOR is a rare, newly recognized retinal disorder occurring predominantly in young Caucasian females. [1] The aetiology remains unknown, but an inflammatory origin is suspected. [1][2] As reported by Gass et al. [1], the inflammatory signs typically develop within several weeks following the onset of AZOOR, and probably result from an inflammatory response to the dead retinal receptor cells.
Occasionally, weeks or months later, narrowing of the retinal vessels, particularly the retinal arteries, perivascular sheathing and reactive changes in the RPE occur, including hypopigmentation and migration of RPE
into the overlying retina similar to that occurring in RP in the zones of receptor cell loss.
Given this background, in our opinion, while on the one hand, the authors fulfilled the criteria of clinically definite multiple sclerosis, on the other hand the ophthalmic examination didn’t fulfil the clinical criteria
of AZOOR. In fact, given that funduscopy showed areas with depigmentation of retinal pigment epithelium and scattered intraretinal pigmentation (bone spicule pigmentation), narrowed retinal vessels and a pale optic nerve in both eyes, the patient could be either diagnosed with retinitis
pigmentosa, associated with multiple sclerosis, either with late AZOOR. In addition, visual field analysis of the right eye revealed a concentric scotoma, typical of retinitis pigmentosa (RP); the field of the left eye was severely constricted, typical, again, of RP.
AZOOR is currently a diagnosis made entirely on clinical grounds and is frequently a diagnosis of exclusion. Given that several reports [3–5] have appeared to confirm Gass’s initial suspicion that there is considerable coincidence between AZOOR and the so called ‘‘white dot’’ syndromes, such as MEWDS (multiple evanescent white dots syndrome) and AIBSE (acute idiopathic blind spot enlargement syndrome), we believe that one should look for the inflammatory signs typical of these diseases, in case of
suspected early AZOOR.
Here we report the case of a 30-year-old women who was diagnosed with early AZOOR, following a complete ophthalmological examination including visual field analysis, electroretinography, fluorescein angiography,
indocyanine green angiography. This young women also fulfilled the criteria of clinically definite multiple sclerosis.
Showing some clinical features of early AZOOR associated with multiple sclerosis from our patient (figure), we want to highlights the need for an early correct approach of such cases. Given that AZOOR is frequently a diagnosis of exclusion, we believe that only following an early complete ophthalmological and neurological examination showing the early inflammatory signs one should make the definitive diagnosis of AZOOR associated with multiple sclerosis.
Giuseppe Querques
Department of ophthalmology, University of Foggia
Figure 1
Colour fundus photography showing some inflammatory signs such as little white dots and mild optic disk edema (top left panel, A). Indocyanine green angiography late frame showing late hypofluorescent lesions scattered at the
posterior pole and in mid periphery (bottom left panel, B). MRI frame showing white matter abnormalities (right panel, C).
References
1. Gass JD, Agarwal A, Scott IU. Acute zonal occult outer retinopathy: A long-term Follow-up Study. Am J Ophthalmol 2002;134:329-339.
2. Jampol LM, Becker KG. White spot syndromes of the retina: a hypothesis based on the common genetic hypothesis of the autoimmune/inflammatory disease. Am J Ophthalmol 2003;135:376-379.
3. Jacobson S, Morales D, Sun X, et al. Pattern of retinal dysfunction in acute zonal occult outer retinopathy. Ophthalmology 1995;102:1187–96.
4. Volpe N, Rizzo J, Lessell S. Acute idiopathic blind spot enlargement syndrome. Arch Ophthalmol 2001;119:59–63.
5. Holz F, Kim R, Schwartz S, et al. Acute zonal occult outer retinopathy (AZOOR) associated with multifocal choroidopathy. Eye 1994;8:77–83.
The conundrums, depicted in Dr. Pavao Martins’ well documented report, 1 have recently been resolved.
The author described five patients who became aphasic during repeated episodes of complicated migraine affecting the right cranium, followed by complete recovery. Based on the fact that they were all (behaviorally, see below) right handed, the author engaged in speculative assumptio...
The conundrums, depicted in Dr. Pavao Martins’ well documented report, 1 have recently been resolved.
The author described five patients who became aphasic during repeated episodes of complicated migraine affecting the right cranium, followed by complete recovery. Based on the fact that they were all (behaviorally, see below) right handed, the author engaged in speculative assumptions related to possible transfer of “speech center” from left to right hemisphere; ignoring recent documentations that speech is merely a convenient marker
of the hemisphere of action where all commands are initiated regardless of the laterality of the effector addressed by that command (i.e. the command center or the major hemisphere). Thus, it has been shown that commands
destined for those effectors ipsilateral to the command center arrive at their destination late, by an amount equal to transcallosal interhemispheric transfer time (IHTT).2-5 In vast majority of behavioral right handers the command center lies on the left, whereas it lies on the right side in about 50 % of those who avow left handedness. 6 The twin fact that the ratio of right to left handedness in the congenitally blind mirrors that of the same in general public and that of the existence of an eight fold increase in the incidence of left handedness among the families of a sighted left hander point to the role of volition in adopting a favorite hand different from that designated by nature (i. e. neural handedness).
In the past, this disparity of the two modes of laterality had caused chaos in the classical literature which was satisfied by cataloguing these instances as “crossed” aphasias or “crossed” nonaphasias (as the case may
be).
Thus, it is the proximity to the command center that underpins the laterality of the dominant side of the body; with other side being further away from the command by a callosum-width. This differential is manifested by an increased reaction time of the nondominant side of the body by an amount equal to the IHTT.
The following observation provides an example, while corroborating Pavao-Martin’s findings:
DW is a 50 years old right handed woman with history of migraine since childhood. These headaches are usually right sided although on occasion they may start as frontal headaches affecting both sides. She describes three “strokes” associated with migraines, all affecting the left side of the body, with the last one involving her left leg (lasting two hours, without a sequel). She has difficulty with orientation to place and time with some of her headaches. In other occasions she cannot express
herself and has difficulty understanding what she hears. These speech episodes typically lasted minutes to an hour or more. The latest attack was associated with “tremor” of the left arm. This headache which was associated with nausea, vomiting and blurred vision, did not respond to
Imitrex (6 mg, subcutaneously). There was no history of epilepsy or head trauma. Her MRI of brain was unremarkable. In the absence of headaches, neurological examination in the areas of visual fields, cranial nerves,
motor and sensory examination and equilibrium has been unremarkable.
Method and Results:
DW underwent a reaction time study, using proprietary software prepared for such purpose. The latter allowed determination of time (in milliseconds) taken from the appearance of a GO signal (after a GET READY warning) in the center of the computer screen to the pushing of a
designated button (in this case the buttons for letters “a” and ‘l,’ for the blocks using the left and right hand (respectively). Each block consisted of 39 trials. Results of two consecutive trials are depicted
below:
Average response delays (reaction time)
(a) left hand 240 ms, (l) right hand 263 ms.
a 281, 1 329
a 266 , l 250
a 281 , l 187
a 250 , l 219
a 281 , l 250
a 266 , l 265
a 265 , l 250
a 235 , l 235
a 218 , l 234
a 235 , l 203
a 172 , l 235
a 203 , l 218
a 250 , l 250
a 234 , l 266
a 250 , l 266
a 219 , l 250
a 234 , l 218
a 188 , l 219
a 187 , l 406
a 250 , l 438
a 219 ,l 297
a 250 , l 250
a 344 , l 250
a 250 , l 219
a 218 , l 234
a 203 , l 359
a 266 , l 219
a 250 , l 313
a 313 , l 281
a 235 , l 219
a 281 , l 265
a 234 , l 235
a 313 , l 296
a 265 , l 250
a 235 , l 235
a 218 , l 265
a 219 , l 250
a 234 , l 250
a 219 , l 266
Conclusion: As demonstrated above, there is a delay of 23 ms for performing a simple reaction time with the ostensibly dominant hand in DW, making her a neurally left handed subject. 2-5,9 The relationship of avowed handedness to that underpinned by the abovementioned circuitry is statistical (not biological).
Iraj Derakhshan
References:
1. Pavao Martins I. Crossed aphasia during migraine aura.
Transcallosal spreading depression? J Neurol Neurosurg Psychiatry. 2006; 1-3.
2. Derakhshan I. Laterality of seizure onset and the simple reaction time: revamping the Poffenberger's paradigm for seizure surgery. Neurol Res. 2006; 28:777-784.
3. Derakhshan I. Nonconvulsive status epilepticus with an unusual EEG: a fresh look at lateralities of motor control and awareness. Epilepsy Behav. 2006; 9:204-210.
4. Derakhshan I. Crossed-uncrossed difference (CUD) in a new light: anatomy of the negative CUD in Poffenberger's paradigm. Acta Neurol Scand. 2006; 113:203-208.
5. Derakhshan I. How do the eyes move together? New understandings help explain eye deviations in patients with stroke. CMAJ. 2005; 172:171-173.
6. Goodglass H, Quadfasel FA. Language laterality in left-handed aphasics. Brain. 1954; 77:521-548.
7. Kutas M, McCarthy G, Donchin E. Differences between sinistrals' and dextrals' ability to infer a whole from its parts: a failure to replicate. Neuropsychologia. 1975; 13:455-464.
8. Oishi M, Suzuki K, Sasaki O, Nakazato S, Kitazawa K, Takao T, Koike T. Crossed aphasia elicited by direct cortical stimulation. Neurology. 2006; 67:1306-1307.
9. Derakhshan I. Crossed aphasia elicited by direct cortical stimulation. Correspondence, accepted for publication in Neurology (copy attached and available online).
I have read all the three articles (1), (2), (3), published in Vol .77, 2006, and found them to be very good studies. It also gives a new nsight to Parkinson’s disease and seems to be very useful in our day to day practice. In this connection I would like to add a few things.
Camptocormia was first described by Brodie, in 1918. Reichel G et al, (4) proposed for new classification for cam...
I have read all the three articles (1), (2), (3), published in Vol .77, 2006, and found them to be very good studies. It also gives a new nsight to Parkinson’s disease and seems to be very useful in our day to day practice. In this connection I would like to add a few things.
Camptocormia was first described by Brodie, in 1918. Reichel G et al, (4) proposed for new classification for camptocormia , as -(a)Primary form, which is a segmental dystonia of abdominal muscles, (b) Secondary forms, where Parkinson’s disease is one of the causes.
Azher S.N. et al ,( 5) also proposed camptocormia to be a
heterogeneous disorder having multiple etiologies and needs etiological classification,which also responds poorly to levodopa therapy. D Jaldetti R et al, (6) considered camptocormia to be either a rare form of
dystonia or an extreme form of rigidity. In his study the response to levodopa was variable, even in some cases camptocormia was aggravated. Slawek J et al, (7) concluded in his study that camptocormia is probably not a form of dystonia of trunk, but may be dysfunction in other non
dopaminergic nigrostrital projection. Since then many theories have been suggested, but the exact pathogenesis of this is not yet clear. F Blotch, et al (1) have tried to link the hypothesis of focal dystonia as primary
cause,and focal myopathy as a secondary event. It seems more or less justifiable. Now if dystonia is the primary cause in camptocormia then it is worth trying botulinum toxin as a form of treatment for these camptocormia, but the exact dose, the muscles to be injected needs further
studies. Melamed et al, (8) reported that occasional patients may benefit from intramuscular botulinum toxin injection or from deep brain stimulation. However it needs further studies to explore the real pathogenetic mechanism of camptocormia in Parkinson’s disease so as to find the correct mode of treatment.
Micheli F et al, (9) in a patient of camptocormia with Parkinson’s disease reported that camptocormia improved with bilateral pallidal stimulation. Yamada K et al, (10) reported a striking alleviation of camptocormia after chronic bilateral sub-thalamic stimulation, Boulos Paul Bijjenni et al, (11), also reported that bilateral timulation of sub thalamus improves the axial symptoms of Parkinson’s disease. There is also a synergistic effect obtained when levodopa was used in conjunction
with bilateral stimulation of sub thalamic nucleus stimulation. So a comparative trial is needed to find out the best form of therapy.
Keeping these in view, patients presenting with camptocormia, should be thoroughly investigated for the presence of Parkinson’s disease. If they are found to
have Parkinsons disease, then which modes of treatment is the best for the patient on an individual basis, is the question. Whether the combination of deep brain stimulation of sub-thalamic nucleus and levodpa therapy, or only deep brain stimulation, or levodopa in
conjunction with botulinum toxin injection is better, for alleviating the axial dystonia as well as other features of Parkinson’s disease needs a controlled trial.
References
1. F Blotch, J L Houteo, S Tenzenas du Montcel, F Bonneville, F Etchepare, M L Weter, S Rivaud-Pechoux, V Hahn Barma, T Maisonobe, C Behar, J Y Lazennec, E KURYS, I Arnuf, A M Bonnet, Y Agid. Parkinson’s disease with camptocormia. J Neurol Neurosurg Pschiatry, 2006,77,1223-1228
2. A-C Lepoutre, D Devos, A Blanchard, Dauphin, V Pardessus, C A Maurage, D Ferriby, J F Hurtevent, A Cotton, A destee, L Defebvre. A specific patteren of camptocormia in Parkinson’s Disease. J Neurol Neurosurg Psychiatric,2006,77,1229-1234.
3. R Djaldetti,E Melamed. Camptocormia in Parkinson’s disease: new insights. J Neurol Neurosurg Pschiatry, 2006, 77, 1205.
4. Reichel G, Kirchhofer U, Stenner A. Camptocormia-segmental dystonia. Proposal of a new defination for an old disease. Nervenarzt 2001,April,72,(4):281-285. Abstract.
5. Azher S N,Jancovic J. Camptocormia: pathogenesis, classification, and response to therapy. Neurology, 2005, Aug 9,65,(3):355-359.
6. Djaldetti R, Mosberg-Galili R,Soroka H, Merims D, Melamed E. Camptocormia(bent spine) in patients with Parkinson’s disease-charecterization and possible pathogenesis of an unusual phenomena. Mov Disord, 1999, May, 14(3):443-447.
7. Slawek J, Derejko M, Camptocormia,a rare form of motor system disorders in Parkinson’s disease. Neurol Neurochir Pol. 2001 35(6): 1133-40 Abstract.
8. Melamed E, Djaldetti R. Cam,ptocormia in Parkinson’s disease. J Neurol.Dec,253 Suppl7,vii14-vii16.
9 .Micheli F, Cersosimo M G, Piedimonte F. Camptocormia in a patient with Parkinson’s disease: beneficial effects of pallidal deep brain stimulation. Case report, JNeurosurg.2005, Dec, 103, 6):1081-1083.
10. Yamada K, Goto S, Matsuzaki K, TamuraT, MuraseN, ShimazuH, Nagahiro S,Kuratsu J,Kaji R. Alleviation of camptocormia by bilateral subthalamic nucleus
stimulation in a patient with Parkinson’s disease. Parkinsonism Relat Disorder 2006, 12,(6):372-5,Epub2006 May 30.Abstract.
11. Boulos-Paul Bejjani,David Gervais,Isbelle Arnulf Savas
Papadopoulos,Sophie Demeret,Anne Marie Bonnet,Philippe
Cornu,PhilippeDamier,Yves Agid. Axial Parkinsonian symptoma can be improved:the role of levodopa and bilateral subthalmic stimulation. J Neurol Neurosurg Psychiatric, 2000, 68,595-600.
Leach et al (“Which electroencephalography (EEG) for epilepsy? The relative usefulness of different EEG protocols in patients with possible
epilepsy.” Journal of Neurology, Neurosurgery & Psychiatry.
2006;77:1040-2) compared the yield of 3 types of EEGs in 85 patients with epilepsy, diagnosed after two or more generalized tonic clonic seizures (GTCs). The median age of the patients was 17.9 years...
Leach et al (“Which electroencephalography (EEG) for epilepsy? The relative usefulness of different EEG protocols in patients with possible
epilepsy.” Journal of Neurology, Neurosurgery & Psychiatry.
2006;77:1040-2) compared the yield of 3 types of EEGs in 85 patients with epilepsy, diagnosed after two or more generalized tonic clonic seizures (GTCs). The median age of the patients was 17.9 years and maximum age 35
years (interquartile range 15.7 – 22.1 years).
In the study, each patient received 3 EEGs in random order, separated by at least 7 days, prior to initiation of treatment. EEGs were read blind to protocol by a single reader. The authors report more epileptiform
abnormalities occurred in sleep deprived (SD) EEGs and conclude that SD-EEGs should be considered as a preferred protocol for “young patients presenting with epilepsy.”
This is an important study, and its emphasis on identifying a cost-effective protocol is much appreciated, but it is worth emphasizing a few points with regard to its conclusions.
First, the results of this study should not be generalized to “young patients” who are children. In two separate pediatric studies we have published of 820 EEGs performed as routine, partially sleep deprived, and fully sleep-deprived protocols, and of 2500 EEGs performed either sleep-deprived or routine protocols, we found no evidence that SD-EEGs had a higher yield.[1][2]
Second, the authors’ use of the term “Sensitivity” is not consistent with standard usage. The test haracteristic “Sensitivity,” also known as “Positive Predictive Value,” refers to the proportion of individuals “with-the-disease” who have a positive test result. The presence of the disease, the denominator of this proportion, is determined by a separate
“Gold Standard” for diagnosis. In contrast, the authors’ criteria for disease is not a based on any separate gold standard but is the sum total of individuals with epileptiform discharges on any of 3 EEGs they performed. This is post hoc. More importantly, this fails to acknowledge two forms of diagnostic misclassification: patients with epilepsies with normal EEGs and patients for whom an EEG may be “over-read” or inaccurately interpreted. The distinction between the standard definition and the authors’ definition affects (probably increases) their calculated proportions, and leads to an inflated impression of the EEG “Sensitivity.”
Rather than taking an established test characteristic and changing the definition, the authors should have used “yield” rather than “sensitivity”
in column 2, table 2.
Third, estimates should have confidence intervals, and the failure to report confidence intervals in table 2 is disappointing. In addition, the authors failed to consider or acknowledge an additional source of imprecision in any estimate of yield for EEGs, problems of inter-observer
inconsistency between EEG interpreters.[3][4][5] Thus, a good feature of this study is that there is a single reader, but the absolute yield from this reader may not apply to other EEG readers, and the study design does
not allow for assessment of the important trade-off between sensitivity and specificity in EEG.[3]
Finally, when differences are reported, an estimate is needed of the probability that a difference this large could have been observed if in fact the null hypothesis (no difference) were true. The authors’ choice of
a Chi Square Test for this purpose is questionable because the subsamples for each Chi Square test are selected on the basis of the results of the EEGs (the independent variable), not a priori. Therefore, the number of
individuals in the dependent variable columns is dependent on the numbers of subjects in the other independent variable rows. This appears to violate the requirement for Chi Square Tests that measured variables are independent. Moreover, since the population is selected on the basis of a single reader’s interpretations, the p value estimates may only apply to future studies of patients whose EEGs were read as positive by that reader(JPL).
Despite these problems, this study provides some evidence that, in young adults with clinically diagnosed, recent-onset epilepsy, SD-EEGs are somewhat more likely to show generalized or partial discharges, serving as a guide for medical decision making.
References
1. Gilbert DL, DeRoos S, Bare MA. Does sleep or sleep deprivation increase epileptiform discharges in pediatric electroencephalograms? Pediatrics. 2004;114:658-62.
2. Gilbert DL, Gartside P. Factors affecting the yield of pediatric EEGs in clinical practice. Clin Pediatr (Phila). 2002;41:25-32.
3. Gilbert DL, Sethuraman G, Kotagal U, et al. Meta-analysis of EEG test performance shows wide variation among studies. Neurology. 2003;60:564-70.
4. van Donselaar CA, Schimsheimer RJ, Geerts AT, et al. Value of the electroencephalogram in adult patients with untreated idiopathic first seizures. Archives of Neurology. 1992;49:231-37.
5. Williams GW, Luders HO, Brickner A, et al. Interobserver variability in EEG interpretation. Neurology. 1985;35:1714-19.
Transient global amnesia (TGA) is a clinical syndrome
characterized by a sudden onset of anterograde and
retrograde amnesia in the absence of other neurological
signs and symptoms, which is resolved within 24 hours.
Although the etiology of TGA remains unknown, recently
Lewis 1) suggested that a Valsalva-like action appears to
be a common triggering event among patients with TGA.
Although TGA follow...
Transient global amnesia (TGA) is a clinical syndrome
characterized by a sudden onset of anterograde and
retrograde amnesia in the absence of other neurological
signs and symptoms, which is resolved within 24 hours.
Although the etiology of TGA remains unknown, recently
Lewis 1) suggested that a Valsalva-like action appears to
be a common triggering event among patients with TGA.
Although TGA following medical procedures has not been
established, Hiraga and Matsunaga 2) reported encountering
three patients who developed TGA after upper
gastrointestinal endoscopy (UGI). However, they did not
perform single photon emission CT (SPECT). We dealt with a
case of TGA occurring immediately after UGI and performed
SPECT test during the TGA attack.
Case report. A middle aged right-handed patient underwent UGI by a veteran endoscopist. The UGI was administered under lidocaine spray anesthesia without further premedication. There was no history of migraine, epilepsy, or cerebrovascular disease. When the endoscope was being removed, the patient held their breath and strained as in the Valsalva maneuver, but no cardiac arrhythmia was noted during electrocardiographic monitoring. Just after the examination, the patient suddenly developed complete anterograde amnesia and retorograde amnesia of the recent past five or six years. Neurological examination results were normal except for severe memory impairment. Magnetic resonance imaging (MRI) of the brain, including diffusion-weighed imaging (DWI) of the brain performed during the attack, three hours after onset, showed no abnormalities. Cervical artery color duplex sonography and electroencephalography (EEG) findings were normal during the attack. The first Tc-
99m ECD SPECT study was performed during the attack, four
hours after onset, and showed hyperperfusion in the right
thalamus.
Figure 1a-b(A) First SPECT study during the transient global amnesia (TGA) attack discloses a focus of increased activity uptake in the right thalamus (arrow).
(B) Second SPECT study one month after TGA discloses decreased activity uptake in the same region as that of the previously demonstrated increased uptake.
Both hematological and hemocoagulation screening test results were normal. Twelve hours after onset, the patient had recovered completely but a memory gap for a part of the previous day remained. In the second SPECT study, conducted 1 month later, no asymmetry was detected either visually or through quantification.
Findings for the second brain MRI, also conducted 1 month
later, were normal, too.
Discussion.
Our patient met all the proposed criteria for TGA. The
amnesia of our patient was not produced by anesthesia,
because the patient did not receive any sedation or premedication except for lidocaine spray. Furthermore DWI MRI of our patient did not show hyperintensity, thus making an ischemic origin unlikely. Although the occurrence of TGA after UGI is rare, two other reports of TGA following UGI 3-4) have been published, and both cases were from Japan as in the study by Hiraga and Matsunaga 2). These cases did not receive any sedation, because UGI is usually administered without sedation in Japan. TGA may be overlooked in some cases in Western countries because the transient nature of the event and concomitant sedation may obscure TGA occurrence. Hiraga and Matsunaga 2) proposed that autonomic dysfunction or emotional stress might be a possible cause of TGA. In addition, Valsalva-like action without sedation may also have been a triggering factor in our case as suggested by Lewis.
While none of the previously reported cases were
examined by SPECT after UGI, our SPECT findings support the notion that TGA can occur after UGI. SPECT performed during TGA of our patient showed increased activity uptake in the right thalamus. Spontaneous temporal lobe seizures are unlikely to have occurred because EEG during the episode was normal and no epileptic seizures were observed.�@Although SPECT findings have shown hypoperfusion in memory relevant brain structures in almost all patients with TGA, some studies reported transient hyperperfusion in the left medial temporal lobe during TGA attack 5).
Although TGA is a rare complication of medical procedures, physicians should be aware of its potential occurence.
References
1. Lewis SL. Aetiology of transient global amnesia. Lancet
1998;352:397-99.
2. Hiraga A, Matsunaga T. Trasient global amnesia after
gastroscopy. J Neurol Neurosurg Psychiatry 2006;77:995-996.
3. Joshita Y, Mineo E, Kihira K, Sato K, Kasano T, Yoshida
Y, Ido K, Kimura K, Yoshida M. Rare hazard of gastrointestinal endoscopy. A case of transient global
amnesia. Gastroenterol. Endosc 1990;32:589-92. (in
Japanese)
4. Sawada Y, Kamihira M, Hirakawa R, Yoshida Y, Imawari M.
A case of transient global amnesia precipitated by
gastrointestinal endoscopy. Progress of Digestive endoscopy 2002;60:44-46. (in Japanese)
5. Matsuda H, Higashi S, Tsuji S, Sumiya H, Miyauchi T,
Hisada K, Yamashita J. High resolution Tc-99m HMPAO SPECT
in a patient with transient global amnesia. Clin Nucl Med
1993;18: 46-49.
I have read your article(1) with interest ,which is also a very good study .However, in this connection I would like to mention that ,in your study the mean time of recording the EEG is almost double in sleep deprivation EEG than that of routine EEG. Whether this long duration of recording in sleep deprived cases has given much more abnormal EEG than that of others and whether sleep deprived EEG should b...
I have read your article(1) with interest ,which is also a very good study .However, in this connection I would like to mention that ,in your study the mean time of recording the EEG is almost double in sleep deprivation EEG than that of routine EEG. Whether this long duration of recording in sleep deprived cases has given much more abnormal EEG than that of others and whether sleep deprived EEG should be taken for longer duration in all cases, to get a higher yield is the question. Also whether sleep deprived EEG should be a routine procedure in young adults with newly diagnosed epilepsy?
Although many studies have shown that the yield of abnormal EEG is profound in patients suspected of having epilepsy after a sleep deprived EEG, but it is to be noted that all night sleep deprivation prior to EEG recording causes much inconvenience to the patient, as well as to the family members especially in pediatric cases. Degen R et al (2) in a study of EEG of 190 patients reported the activation rate of epileptic activity in 52.6% (without sleep deprivation) and 53.2%(with sleep deprivation) and
also noted no real differences between the two methods in classifying the epileptic discharges. Kubicki S et al (3) reported electroencephalographic activity indicative of seizure disorder in 53.6%in patients suspected to have epilepsy, when a short term sleep EEG recorded following a partial sleep deprivation during the previous night. Evangeline et al(4) have found melatonin induced sleep EEG was as informative as sleep deprived EEG in pediatric groups. Melatonin also do not alter the microstructure of
sleep. Milstein et al (5) reported melatonin induced sleep recording to be safe and reliable in adults.
Considering all these factors, I think it is better to carry out a study in adult patients to prove that partial sleep deprivation during previous night followed by a melatonin induced sleep recording can yield the same information as that of a total sleep deprivation recording. It is then that a protocol for EEG recording with total sleep deprivation in newly diagnosed epileptic patients is to be considered.
REFERENCES
1 JP Leach, LJ Stephen, C Salveta, M J Brodie--Which
electroencephalography(EEG)for Epilepsy? The relative usefulness of different EEG protocols in patients with possible epilepsy.J Neurol Neurosurg Psychiatry, 2006, 77, 1040-1042.
2 Degen R, DegenH E, Reker M---Sleep EEG or without sleep deprivation? Does sleep deprivation activate more epileptic activity in patients suffering from different types of epilepsy? Eur Neurol.1987, 26(1):51-9 Abstract PubMed.
3 Kubicki S, Scheuler W,Wittenbecher H---Short term sleep EEG recordings after partial sleep deprivation as a phenomena: an evaluation of 719 EEG recordings.Epilepsy Res Suppl. 1991,2:217-30.Abstract PubMed
4 Evangeline Wassmer,Paul F B Carter, Gina Welsh, Stefano Seri, William P Whitehouse--Melatonin is useful for recording sleep EEG a prospective audit of outcome,--Developmental Medicine&Child Neurology,2001,43,735-738
In response to our article, Spengos et al. suggested that we should evaluate the circadian variation of stroke onset separately for the aetiologically different subtypes of ischaemic stroke. Stroke diagnostic criteria of the registry in our study are based essentially on MONICA
manual version 1.1, which classifies cerebral infarction (CIF) into that due to cerebral thrombosis (TMB), embolic brain infarction...
In response to our article, Spengos et al. suggested that we should evaluate the circadian variation of stroke onset separately for the aetiologically different subtypes of ischaemic stroke. Stroke diagnostic criteria of the registry in our study are based essentially on MONICA
manual version 1.1, which classifies cerebral infarction (CIF) into that due to cerebral thrombosis (TMB), embolic brain infarction (EMB) and other or unknown aetiology.[1][2] Unfortunately, it was impossible to separate lacunar stroke (LACS) and atherosclerotic stroke, and both were
categorised as TMB in the registry.
The registry categorises CIF into TMB, which accounted for 47.3% of CIF cases (3,582/7,575), EMB which accounted for 15.6% (1,181/7,575) and other or unknown aetiology, which accounted for 37.1% (2,812/7,575).
The percentages of cases of CIF in which stroke onset occurred while the patient was asleep were 16.5%, 13.5% and 11.7%, respectively. The percentage of cases occurring while sleeping was lower among patients with EMB than among those with TMB (P<0.05). The percentages of cases
occurring during sleep in both TMB and EMB were greater than those of intracerebral haemorrhage (ICH) and subarachnoidal haemorrhage (SAH) (P<0.005 and <0.001, respectively). The time-specific onset for
twelve 2-h periods for separated CIF categories were calculated in the same way as in our article.[2] The cases in which TMB occurred during sleep showed a higher single peak than other categorised CIF during the period from 06:00 to 07:59.
The cases in which EMB occurred during sleep showed a single but lower peak than that of TMB.
Cases of other or unknown aetiology showed a single peak, which was higher than that of EMB but lower than that of TMB.
The cases of TMB, EMB and other in which onset occurred in the waking state showed two similar peaks; a higher peak in the morning and a lower peak in the afternoon. TMB, which accounted for 47.3% of cases of CIF, showed a marked influence on circadian rhythm of whole CIF onset. Spengos et al.
reported that onset of LACS was associated with stroke during sleep (SDS).[3] LACS may have accounted for the high percentage of TMB in our study, and influenced circadian variation of onset of the whole CIF, especially onset during sleep or status in sleep.
Spengos et al. expressed doubt about the relation between stroke onset of CIF and variation in blood pressure (BP) according to lack of information of BP on admission. Our study not only suggested that BP dropped during sleep, but also that various changes during sleep, such as the drop in BP, respiratory disorders during sleep and haemostatic
functions, are risk factors and triggers for onset of CIF.[2]
The results of our study suggested that sleep or status in sleep was a risk factor for CIF but not for ICH or SAH, because all cases of stroke onset during sleep and with unknown situation occurred equally between midnight and 06:00, and circadian rhythm lost its nadir during the night in CIF, but not in ICH or SAH.[2] Spengos et al. also expressed doubt about our assumption of an equal distribution of SDS between midnight and 06:00. The purpose of this method, which was intentionally biased for
circadian variation in all onset situations from midnight to early morning, was not to evaluate circadian variation, but to evaluate the relation between sleep or status in sleep and the risk of occurrence of stroke in each subtype.
In the registry, SDS of CIF in which onset time was registered between midnight and early morning accounted for most cases, and the number of SDS cases of CIF in the other time zone was markedly lower. Many of the cases
of SDS in which onset occurred during the daytime or was unspecified were supposed to be unconscious and to have been found to have had a stroke late as the patients lived alone or due to the absence of housemates.
However, these cases were also exposed to a risk of SDS. We feel that it is appropriate to redistribute SDS during sleeping hours for evaluation of the risk of SDS in our study.
In their recent study, Spengos et al. suggested that there is a relation between bimodal variation of stroke onset and siesta.[3] Bimodal variation of stroke onset has been reported in the UK and Japan, both countries in which siesta is uncommon.[2][4] Therefore, factors other than
siesta may be involved. We supposed that BP variation, which showed bimodal variation, is responsible for the bimodal circadian rhythm.[2][5] In our study, we showed that the evening peak from 18:00 to 19:59 is higher than the morning peak of 08:00 to 09:59 among patients with ICH and SAH in which stroke onset occurred during waking hours, whereas CIF showed a higher morning peak.[2] In addition, the reasons for these differences in peak height between ischaemic and hemorrhagic stroke were discussed
with regard to haemostatic functions. The reader�fs suggestion that we did not underline these results is mistaken.
As noted by Spengos et al., it is very important to evaluate circadian variation of CIF onset and risk factors and triggers by subtype for aetiological differences. Such studies will provide important information regarding risk factors and triggers of stroke onset.
References
1. World Health Organization MONICA Project. Event Registration Data Component, MONICA Manual Version 1.1. Document for meeting of MONICA Principal Investigators, 1986.
2. Omama S, Yoshida Y,Ogawa A, et al. Differences in circadian variation of cerebral infarction, intracerebral haemorrhage and subarachnoid haemorrhage by situation at onset. J Neurol Neurosurg Psychiatry published 17 August 2006, 10.1136/jnnp.2006.090373
3. Spengos K, Vemmos K, Tsivgoulis G, et al. Two-peak circadian distribution of stroke onset in Greek patients. A hospital based study. Cerebrovasc Dis 2003; 15: 70-77.
4. Wroe SJ, Sandercock P, Bamford J, et al. Diurnal variation in incidence of stroke: Oxfordshire community stroke project. BMJ 1992;18:155-157.
5. Stergiou GS, Vermmos KN, Pliarchopoulou KM, et al. Parallel morning and evening surge in stroke onset, blood pressure, and physical activity. Stroke 2002;33:1480-1486.
Samarasekera et al. reported four patients with non-
paraneoplastic acute limbic encephalitis (ALE), who had negative testing for voltage-gated potassium channel auto-antibodies[1]. We wish to report a patient with a previously unreported association of ALE with
hemophagocytic syndrome (HPS) and discuss the possible pathophysiology.
A 9-year-old boy, the second child of healthy non-consanguin...
Samarasekera et al. reported four patients with non-
paraneoplastic acute limbic encephalitis (ALE), who had negative testing for voltage-gated potassium channel auto-antibodies[1]. We wish to report a patient with a previously unreported association of ALE with
hemophagocytic syndrome (HPS) and discuss the possible pathophysiology.
A 9-year-old boy, the second child of healthy non-consanguineous parents, was well until he showed fever (day 0 of illness). On day 3, he had leukopenia; white blood cells (WBC) count 1,400/micro l, and a mild
consciousness disturbance. On day 4, the leukopenia had worsened; WBC count 900/micro l, and thrombocytopenia appeared; platelet count 79,000/micro l. The blood chemistry showed some abnormalities; aminotransferase 75 IU/l, ferritin 1,320 ng/ml and soluble interleukin
(IL)-2 receptor 1,930 (reference range 124-466) U/ml. Polymerase chain reaction, for cytomegalovirus, Epstein-Barr virus, herpes simplex virus, human herpes virus 6, 7 and varicella-zoster virus, using peripheral blood or cerebro-spinal fluid (CSF), were all negative. Bone marrow aspiration revealed hemophagocytosis but no malignancy. On day 6, he had a transient loss of consciousness, and he had convulsions afterwards. Then, brain computed tomography and magnetic resonance imaging (MRI) did not detect any abnormalities. Methylprednisolone pulse (30 mg/kg/day for 3 days) and gamma globulin (400 mg/kg/day for 3 days) therapies were started on that
day. To control seizures, midazolam and phenobarbital were administered. On day 11, awake EEG showed no occipital theta or alpha activity with high
voltage slow wave. On day 12, peripheral blood natural killer (NK) cell activity was 7 (reference range 18-40)%. Consciousness disturbance was slowly improving and midazolam and phenobarbital were gradually replaced
by carbamazepine. On day 17, brain MRI showed bilateral claustral lesions. Perforin expressions in cytotoxic T and NK cells were not reduced. On day 24, brain MRI showed the widened lesions, involving bilateral claustrum and hippocampi. On day 26, the hematology and blood
chemistry showed normal results, including ferritin. Cytokines, including IL-2, 4, 6, 10, interferon-gamma and tumor necrosis factor-alpha, were examined with serum and CSF, all resulted within normal limits. On day
30, soluble IL-2 receptor and NK cell activity were 674 U/ml and 44 %, respectively. On day 33, forward and backward digit span length were 4 and 2, respectively. On day 34, brain MRI showed that bilateral claustral
lesions were reduced. On day 44, Wechsler Intelligence Scale for Children Third Edition showed borderline mentality, verbal IQ=81, performance IQ=75 and full-Scale IQ=76. Follow up brain MRI on day 124, showed no lesions.
The examinations with auto-antibodies against the glutamate receptors (GluR) delta 2 and epsilon 2 were prompted, using CSF on day 26, serum on day 26 and 124. Their results were non-specific, anti-GluR epsilon 2 IgG
was weakly positive in CSF on day26 and anti-GluR epsilon 2 IgM was positive in serum on day 124.
Our case is compatible with HPS, except ALE[2]. Although HPS often accompanies CNS involvement, ALE associated with HPS has not been reported. We hypothesize two possible pathological mechanisms, that seem to be polar opposites. One plausible explanation is immunological augmentation, which could result in an auto-antibody production. And the other is immunological compromise, which could result in viral infection. The increased soluble IL-2 receptor could result from T-cell activation, which seems to comprise the former possibility. On the other hand,
reduced NK cell activity seems to comprise the latter. The data from our patient are inconclusive. Further work is required to establish the immunological basis for ALE.
References
[1]Samarasekera SR, Vincent A, Welch JL, Jackson M, Nichols P, Griffiths TD. The course and outcome of acute limbic encephalitis with negative voltage-gated potassium channel antibodies. J Neurol Neurosurg Psychiatry (in print).
[2]Imashuku S, Hyakuna N, Funabiki T, Ikuta K, Sako M, Iwai A, et al.Low natural killer activity and central nervous system disease as a high-risk prognostic indicator in young patients with hemophagocytic lymphohistiocytosis. Cancer 2002;94:3023~31.
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With interest we read the recent review by Donnellan et al.[1] on coping strategies after stroke. The review highlights the existing literature on coping strategies in stroke patients, in part with the aim to identify coping strategies that are typical for this patient group. In addition, the review investigates methodological issues in terms of definition and measurement of coping. The review makes i...
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We read with great interest the article by Park et al1 concerning the frequency and associations of hypoplastic vertebral artery (HVA) with posterior circulation stroke. In this study, 529 patients with ischemic stroke were classified according to their stroke location (anterior or posterior circulation strokes). The investigators found that among all patients 35.2% (185 patients) had HVA, and more im...
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Dr Hintzen and Dr van den Born describe a patient with acute zonal occult outer retinopathy (AZOOR) who also fulfilled the criteria of clinically definite multiple sclerosis. AZOOR is a rare, newly recognized retinal disorder occurring predominantly in young Caucasian females. [1] The aetiology remains unknown, but an inflammatory origin is suspected. [1][2] As reported by Gass et al. [1], the inflamma...
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The conundrums, depicted in Dr. Pavao Martins’ well documented report, 1 have recently been resolved. The author described five patients who became aphasic during repeated episodes of complicated migraine affecting the right cranium, followed by complete recovery. Based on the fact that they were all (behaviorally, see below) right handed, the author engaged in speculative assumptio...
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Dear Editor,
Leach et al (“Which electroencephalography (EEG) for epilepsy? The relative usefulness of different EEG protocols in patients with possible epilepsy.” Journal of Neurology, Neurosurgery & Psychiatry. 2006;77:1040-2) compared the yield of 3 types of EEGs in 85 patients with epilepsy, diagnosed after two or more generalized tonic clonic seizures (GTCs). The median age of the patients was 17.9 years...
Dear Editor,
Transient global amnesia (TGA) is a clinical syndrome characterized by a sudden onset of anterograde and retrograde amnesia in the absence of other neurological signs and symptoms, which is resolved within 24 hours. Although the etiology of TGA remains unknown, recently Lewis 1) suggested that a Valsalva-like action appears to be a common triggering event among patients with TGA. Although TGA follow...
Dear Editor,
I have read your article(1) with interest ,which is also a very good study .However, in this connection I would like to mention that ,in your study the mean time of recording the EEG is almost double in sleep deprivation EEG than that of routine EEG. Whether this long duration of recording in sleep deprived cases has given much more abnormal EEG than that of others and whether sleep deprived EEG should b...
Dear editor
In response to our article, Spengos et al. suggested that we should evaluate the circadian variation of stroke onset separately for the aetiologically different subtypes of ischaemic stroke. Stroke diagnostic criteria of the registry in our study are based essentially on MONICA manual version 1.1, which classifies cerebral infarction (CIF) into that due to cerebral thrombosis (TMB), embolic brain infarction...
Dear Editor,
Samarasekera et al. reported four patients with non- paraneoplastic acute limbic encephalitis (ALE), who had negative testing for voltage-gated potassium channel auto-antibodies[1]. We wish to report a patient with a previously unreported association of ALE with hemophagocytic syndrome (HPS) and discuss the possible pathophysiology.
A 9-year-old boy, the second child of healthy non-consanguin...
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