Leão discovered the spreading negative slow voltage variations in response to either direct current electrical stimulation or bilateral occlusion of the internal carotid artery in 1947. Both neurones and astrocytes depolarise during a spreading negative slow voltage variation,
thereby inducing transmembraneous ionic shifts and intracellular oedema [1]. Under anoxia or severe ischaemia, this spreading...
Leão discovered the spreading negative slow voltage variations in response to either direct current electrical stimulation or bilateral occlusion of the internal carotid artery in 1947. Both neurones and astrocytes depolarise during a spreading negative slow voltage variation,
thereby inducing transmembraneous ionic shifts and intracellular oedema [1]. Under anoxia or severe ischaemia, this spreading depolarisation is permanent and referred to as anoxic depolarisation (AD) whereas, under normal conditions, it is transient and referred to as spreading depression(SD). AD and SD share similar, dramatic intra- and extracellular ionic changes and propagate similarly in the tissue [1]. However, in contrast to SD, AD initiates the cascades of neuronal death and is insensitive to N-methyl-D-aspartate receptor (NMDAR) antagonists [1]. The insensitivity of AD to NMDAR antagonists is possibly related to the recruitment of
additional cation channels. Energy depletion is not a ‘conditio sine qua non’ to induce AD and the subsequent neuronal necrosis but inhibition of the Na,K-ATPase with persistent breakdown of the double Donnan equilibrium
is sufficient for this purpose.
Leão coined the fundamental concept in 1947 that SD and AD in the cerebral cortex are of the same principal nature and represent the two extremes of a continuous spectrum of spreading depolarisations dependent on the energy status. In short, he based this concept on his observations
that SD becomes what was later called AD if the circulation is interrupted during SD and, vice versa, AD becomes SD if the circulation is restored during AD.
The full spectrum of spreading depolarisations is observed in focal ischaemia since gradients of perfusion, oxygen, and glucose exist between the core ischaemic region and the normal tissue. Thus, the spreading negative slow voltage variation starts in the ischaemic core as persistent AD, becomes an intermediate depolarisation as it spreads through the metabolically compromised penumbra, and traverses the surrounding healthy tissue as SD. This process is repetitive. While recurrent spreading
depolarisations arise, each event causes the lesion to grow in a stepwise fashion since it increases the ATP consumption and simultaneously constricts the cortical arterioles. As a consequence, the periods of spreading depression of the high-frequency electrocorticographic activity become increasingly prolonged during the cluster of spreading depolarisations, evolving to a state of persistent electrocorticographic depression. In patients with subarachnoid haemorrhage, these characteristic electrocorticographic features have now been unequivocally
recorded using subdural electrode strips during the development of delayed ischaemic stroke in the recording area[2].
That spreading depolarisations recruit tissue at risk into necrosis has been conclusively shown in a number of experimental studies in which artificially triggered spreading depolarisations invaded a mildly ischaemic zone from the outside. E.g., this was demonstrated in a rat
cranial window model using brain topical application of the vasoconstrictor endothelin-1 (ET-1). At an ET-1 concentration of 1µM underhalothane, at which only 50% of animals generated spreading depolarisations, a microarea with selective neuronal death was found only in those animals showing spreading depolarisations. In selected animals, which had not developed spreading depolarisations in response to ET-1, one spreading depolarisation was triggered at a second cranial window by KCl and propagated from there to the window exposed to ET-1. This treatment
also resulted in a microarea of neuronal damage. In contrast, spreading depolarisations invading from outside did not induce neuronal damage in the absence of ET-1 or in the presence of ET-1 if ET-1 was coapplied with
an ETA receptor antagonist [3].
Our clinical case is interesting since it is consistent with the pathophysiological basis and we speculated whether spreading depolarisations arose in our patient from the ischaemic zones of the left internal carotid artery territory and then propagated as normal SDs to
healthy cortical regions supplied by the posterior circulation. There they gave rise to the recurrent hallucinations of visual migraine auras. In fact it has been studied extensively that spreading depolarisations
typically cross the vascular boundary zones. Conclusively, they can also be elicited in animal and human brain slices that are devoid of the circulation [1].
The patient clearly and repetitively stated that the scintillation scotoma always affected his right visual hemifield. This can hardly be explained by a retinal spreading depression since there is no anatomical
or functional border in the midline of the retina. A retinal spreading depression usually spreads concentrically in the whole retina and, therefore, would have affected both right and left visual fields. In 1941,
Lashley has written a brillant paper why the pathophysiological correlate of migraine aura in a visual hemifield likely occurs in the contralateral visual cortex but not in the retina. SPECT and functional MRI during the
aura phase in migraineurs have strongly supported Lashley’s suggestion [1].
It is controversial whether SD is the cause of headache in
migraineurs. There seem to be two opposing hypotheses: Weiller and colleagues [4] have suggested that migraine headache is generated in the brainstem independently of SD using pooled PET data from migraineurs without aura. However, Sanchez del Rio and colleagues [5] were not able to reproduce these observations of a brainstem generator in individual patients using perfusion weighted MRI. They suggested that migraine headache is caused by a sterile inflammation in the dura mater in response to SD. Migraine headache is certainly an interesting issue but why some of
the SD opponents believe that the existence or non-existence of a relation between SD and migraine headache is of any major importance for the unequivally established relation of spreading depolarisations with stroke and traumatic brain injury remains enigmatic.
In conclusion, strong experimental evidence suggests that spreading depolarisations are not an epiphenomenon but a causal component of acute neuronal damage. Furthermore, spreading depolarisations have now been recorded abundantly in patients with traumatic brain injury, intracerebral haematoma, subarachnoid haemorrhage, delayed ischaemic stroke and malignant ischaemic stroke (compare www.cosbid.org) [2]. Therefore, it would be unethical if this field does not become a focus of clinical research in stroke and traumatic brain injury. It would be as absurd not to study this extensively as it would be absurd not to study epileptic electrocorticographic activity because some think that epileptic electrocorticographic activity is an epiphenomenon of epilepsy.
Jens P Dreier
References
1. Somjen GG. Ions in the brain. Normal function, seizures, and stroke. New York: Oxford University Press, 2004.
2. Dreier JP, Woitzik J, Fabricius M, et al. Delayed ischaemic neurological deficits after subarachnoid haemorrhage are associated with clusters of spreading depolarizations. Brain 2006;129: 3224-37.
3. Dreier JP, Kleeberg J, Alam M, et al. Endothelin-1-induced spreading depression in rats is associated with a microarea of selective neuronal necrosis. Exp Biol Med 2007; 232: 204-13.
4. Weiller C, May A, Limmroth V, et al. Brain stem activation in spontaneous human migraine attacks. Nat Med 1995; 1: 658-60.
5. Sanchez del Rio M, Bakker D, Wu O, et al. Perfusion weighted imaging during migraine: spontaneous visual aura and headache. Cephalalgia 1999; 19: 701-7.
Your paper is very interesting. However we consider hyperacusis symptom a possible disorder of stapedius muscle in your patients: have you evaluated this possibility? Assessement of stapedius function with
impedancemetry and measurement of its reflex should be useful in neuromuscular disease including myasthenia gravis and facial nerve paralysis. Actually the stapedius reflex consists of a contractio...
Your paper is very interesting. However we consider hyperacusis symptom a possible disorder of stapedius muscle in your patients: have you evaluated this possibility? Assessement of stapedius function with
impedancemetry and measurement of its reflex should be useful in neuromuscular disease including myasthenia gravis and facial nerve paralysis. Actually the stapedius reflex consists of a contraction of the stapedius muscle in response to a loud noise. The stapedius reflex arc
involves the spiral ganglion neurons, the auditory nerve, the cochlear nucleus, the superior olive, the facial nerve nucleus, the facial nerve, and the stapedius muscle. In the brainstem, commisures connect to the other side so an ipsilateral sound can generate a contralateral response.
It can be abnormal in a variety of situations that may not necessarily impair hearing and abnormalities have been reported in several neurological disorders.
In complex regional pain sindrome hyperacusis could be related to dystonia and consequently to stapedius dysfunction because of irregular contraction of the muscle or brainstem involvement.
The excellent review shows the limits of the descriptive epidemiology in the understanding of the pathogenesis of the amyotrophic lateral sclerosis. The destruction of neurons in its classical form takes place primarily in the motor tracts which would suggest a synaptic neuron to
neuron transfer of the harmful factor thus saving initially other networks.
The excellent review shows the limits of the descriptive epidemiology in the understanding of the pathogenesis of the amyotrophic lateral sclerosis. The destruction of neurons in its classical form takes place primarily in the motor tracts which would suggest a synaptic neuron to
neuron transfer of the harmful factor thus saving initially other networks.
The hypothetical effect could be related to a special protein species found in the myelin fraction isolated from brain of an ALS patient (1). Similar protein species have also been found in two further patients.
Investigation post mortem of the brain with modern neuroscientific methods could thus advance the understanding in the causation and progress of the disease.
Professor Heikki Savolainen
References
1. Palo J, Savolainen H, Kivalo E. Comparison between the proteins of human brain myelin in subacute sclerosing panencephalitis, amyotrophic lateral sclerosis and malignant diseases. J neurol Sci 1973; 18: 175-181
In our recent letter entitled “Pisa syndrome after unilateral pallidotomy in Parkinson’s disease: an unrecognised, delayed adverse event?” (J Neurol Neurosurg Psychiatr 2007;78:329-330), we described three
Parkinson’s disease (PD) patients who developed a lean to the opposite side several years after a unilateral pallidotomy. We wondered whether this was purely disease-related or perhaps a delayed cons...
In our recent letter entitled “Pisa syndrome after unilateral pallidotomy in Parkinson’s disease: an unrecognised, delayed adverse event?” (J Neurol Neurosurg Psychiatr 2007;78:329-330), we described three
Parkinson’s disease (PD) patients who developed a lean to the opposite side several years after a unilateral pallidotomy. We wondered whether this was purely disease-related or perhaps a delayed consequence of the
pallidotomy.
We would like to correct the statement that “… postoperative imaging in these three patients confirmed that the lesions were confined to the medial pallidum (…)”. Upon further subsequent expert review of the
postoperative MRI scans, it became apparent that although the medial pallidum was indeed successfully lesioned in all three patients, in each of them the lesion was in fact more extensive. In patient 1, the surgical lesion extended into the external globus pallidus and putamen; in patient
2 into the internal capsule; and in patient 3 into the external globus pallidus, with lesions further rostrally into the area of the sella media. Nevertheless, the key issue of whether the Pisa syndrome in these patients
was related solely to their advanced stage PD or to the surgical lesion in the medial pallidum (and beyond) remains unsettled. Therefore, our invitation to report on the very long-term follow-up of pallidotomy patients in relation to the localisation of the surgical lesion still
stands.
We apologise to the readership for this unfortunate and unintended error.
Bart PC van de Warrenburg, MD, PhD
Department of Neurology, Radboud University Nijmegen Medical Centre, Nijmegen, The Netherlands.
Kailash P. Bhatia, MD & Niall P. Quinn, MD
Sobell Department of Motor Neuroscience and Movement Disorders, Institute
of Neurology, London, United Kingdom
In a patient with high-grade internal carotid artery (ICA) stenosis and frequent migraine aura-like symptoms, Dreier et al [1] demonstrated widely scattered focal laminar cortical infarcts and resolution of visual symptoms following corrective surgery. These authors carry forward the speculation that brain ischemia-related cortical spreading depression (CSD) underlies the associated visual phenomena....
In a patient with high-grade internal carotid artery (ICA) stenosis and frequent migraine aura-like symptoms, Dreier et al [1] demonstrated widely scattered focal laminar cortical infarcts and resolution of visual symptoms following corrective surgery. These authors carry forward the speculation that brain ischemia-related cortical spreading depression (CSD) underlies the associated visual phenomena.
Key areas of concern include: (i) Dissociation between headache and visual phenomenon. While CSD has been assumed as the brain aberration that underlies migraine, the factual basis for an etiological role in scintillating scotoma sine headache is even more uncertain [2,3]. (ii)
The importance of precise delineation between binocular and monocular as well as between displaceable and non-displaceable visual phenomena cannot be overemphasized [2, 3]. In the index case, scintillating scotoma in the
“right visual field” [1] cannot be translated to a monocular or uniocular, a binocular, or a homonymous defect. The clinical opportunity to test for such key ophthalmological features presents only uncommonly and must be fully explored in future. Even in patients with background neuro-ophthalmologic knowledge, unless the laterality and the displaceability of scintillating scotomata are formally determined, we will get no closer to the truth [2]. (iii) There is a distinct need to conceptually segregate the visual and non-visual neurological phenomena in this case. While the lateralizing negative neurological features (right sided-facial paresis and global aphasia) can be acceptably linked to left cortical brain ischemia, the “right-sided” scintillating scotoma merits further analysis.
(iv) Rarity of lateralizing visual scintillating phenomenon in the relatively much more common aberration of cerebral ischemia is another red flag. (v) High-frequency scintillating scotomatous attacks in this patient
(up to 10 attacks/day) [1] in the absence of associated lateralizing negative neurological deficits (possibly barring the first episode) make an ischemic etiology further unlikely. If cerebral ischemia did provoke
recurrent CSDs, why should associated negative neurological features not also be manifest? (vi) High-frequency occurrence of CSD in humans with complete recovery of neuronal function on each occasion in an ischemic field is another assumption that creeps into the equation. (vii) The fundamental nature of CSD in cerebral ischemia – adaptive or pathogenetic – has not yet been resolved [2,3]. Recording of CSD in human brain [4]
does not prove the biological nature of the phenomenon. (viii) Prevention of migraine and aborting of migraine aura with drugs that do not cross the blood-brain barrier or significantly influence cortical neuronal function
is a pharmacotherapeutic absolute that rallies against CSD-based pathophysiological algorithms [2, 3]. (ix) Occurrence of scintillating scotomata in some patients with migraine with aura after onset of headache is a clinical absolute that also challenges currently prevalent theories. (x) Contrary to the assertion in the discussion [1], lateralizing laminar cortical infarcts relevant to the scintillating scotomata have not been seen in this patient. (xi) The possibility of aggravation of pre-existing energy depletion in the cortex [1], while theoretically intriguing, is unlikely in the absence of a lateralizing lesion as well the repetitive nature of the scintillating scotoma. With 95% left ICA stenosis, each wave of CSD would further lower the available cortical energy with little likelihood of repletion sufficient to initiate the next phase/flurry of scintillating scotomata. (xii) Propagation of CSD across cerebrovascular arterial territories [1] has no experimental or theoretical basis and is a highly speculative proposal. Overall, there is a real possibility of perpetuating circular arguments and the only definitive way forward is a careful clinical neuro-ophthalmological assessment as and when such
opportunity presents. Neuro-imaging, howsoever sophisticated, will not settle such key pathophysiological issues in migraine-related phenomenology [5].
Spreading depression is known to involve the retina [2, 3] and has been suggested as a possible mechanism for scintillating scotoma related to ICA dissection [6]. Following 95% left ICA stenosis, augmented flow in
the right ICA is distinctly possible and might have set the stage for ophthalmic artery flow-related spreading depression in the right eye in this patient.
As a possible disease mechanism, the concept of CSD has guided our thinking as a default pathophysiological process over the last five decades. As scientists, however, we are obliged to dispassionately search
for gaps in our comprehension.
Vinod K Gupta
References
1. Klingebiel R, Friedman A, Shelef I, Dreier JP. Clearance of a status aurae migraenalis in response to thrombendarterectomy in a patient with high grade internal carotid artery stenosis. J Neurol Neurosurg Psychiatry 2008;79:89-90.
2. Gupta VK. Monocular and "binocular" scintillating scotomata in migraine: a semantic and theoretical paradox. CMAJ (23 November 2006). Available at: http://www.cmaj.ca/cgi/eletters/173/12/1441#6490.
3. Gupta VK. Migrainous scintillating scotoma and headache is ocular in origin: a new hypothesis. Med Hypotheses 2006;66: 454-460.
4. Dreier JP, Woitzik J, Fabricius M, et al. Delayed ischaemic neurological deficits after subarachnoid haemorrhage are associated with clusters of spreading depolarizations. Brain 2006;129: 3224–37.
This is an interesting issue about post-traumatic epilepsy (PTE) in brain injured (TBI) patients (1). The authors use spectral electroencephalography (EEG), and brain Magnetic Resonance Image study (bMRI) with contrast (Gadolinium -DTPA) using semi-quantitative technique to define the abnormal signals, and found that MRI but not EEG is more
useful to reveal the abnormal cortical signals and can predi...
This is an interesting issue about post-traumatic epilepsy (PTE) in brain injured (TBI) patients (1). The authors use spectral electroencephalography (EEG), and brain Magnetic Resonance Image study (bMRI) with contrast (Gadolinium -DTPA) using semi-quantitative technique to define the abnormal signals, and found that MRI but not EEG is more
useful to reveal the abnormal cortical signals and can predict the occurrences of PTE with statistical difference (P=0.02). Authors conclude the disruption of blood-brain barrier (BBB) plays an important role in the happening of brain swelling (increasing cortex volume), no matter in focal or generalized lesion (2).
We know the probability of seizure attacks in TBI, but usually hard to predict who will occur or who should use medications from clinical practice (3). Although the practical parameter indicated that antiepileptic drugs (AEDs) for preventive therapy in TBI is evidence-based
(4), the strategy in using preventive AEDs is different from neurologists and neurosurgeons in many countries. In Taiwan, the AEDs are given depending on the timing of TBI. If imaging study did not reveal abnormal findings (subdural hematoma, subarachnoid hemorrhage, gyri effacement, brain swelling, etc), or if PTE occurred within 2 wks even EEG revealed slow waves or cortical instability, no lasting AEDs are advised by neurologists. However, the initial preventive therapy is still advocated
by neurosurgeons in many considerations including paramedical argument.
This dilemma in using AEDs based on clinical symptoms and EEG findings are frequently debating in the combined conferences.
Another issue about the BBB permeability in TBI is high in PTE (76.9%) than in non-PTE (33.3%) patients. The presumed explanation about the disruption of BBB in this study merely based on the increasing cerebral cortex volume and slow waves activity seemed too simple (5).
Since BBB played a role in controlling certain substances into the brain tissues, its damage in TBI can be reflected by the dysregulation of cerebral blood flow (CBF)(6). The mean velocity and resistance revealed the compliance of CBF throughout the conducting arteries can partly
reflect the integrity of BBB (7). By the role of vasodilatation-vasoconstriction cascade, if BBB is intact, the constant CBF and regulatory vasoconstriction will make intra-cerebral blood volume decrease(may decrease swollen cortex volume), and also lower intracranial pressure
(ICP) effectively in using mannitol infusion (8). If BBB was breakdown, poor vascular compliance would occur by virtue of rising CBF, inconstant cerebral flow pattern, and poor effect in lowering ICP. These viewpoints
have been verified by Muzzilaar et al, in experimental and empirical studies (9).
This simple study emphasize that, in empirical view, neither conventional EEG nor clinical symptom and history taking is enough to determine the occurrence of PTE and the usage of AEDs. An additional MRI can be helpful to decide the leakage of BBB and the lasting use of medication for controlling PTE with varied presentations of seizures, headache, or cognitive impairment. The perspectives including economic burden, severity of TBI, CBF, and ICP are warranted to make this creative finding of speculated mechanism more clear in the future.
Kao-Chang Lin, Jinn-Rung Guo
References
1. Annegers JF, Hauser WA, Coan SP, et al. A population-based study of seizures after traumatic brain injuries. N Engl J Med. 1998; 338:20-24.
2. Tomkins O, Shelef I, Kaizerman I, et al. Blood-Brain Barrier Disruption in Post-Traumatic Epilepsy. JNNP. 2007. (Ahead online published).
3. Garga N and Lowenstein DH. Posttraumatic epilepsy: a major problem in desperate need of major advances. Epilepsy Curr. 2006; 6:1-5.
4. Bernard S, Chang and Daniel H, Lowenstein. Practice parameter: Antiepileptic drug prophylaxis in severe traumatic brain injury: Report of the Quality Standards Subcommittee of the American Academy of Neurology. Neurology 2003; 60:10-16.
5. Rosner MJ, Coley IT: Cerebral perfusion pressure: A hemodynamic mechanism of mannitol and the postmannitol hemogram. Neurosurgery 1987; 21: 147-156.
6. Visocchi M, Chiaretti A, Cabezas D, et al. Hypoflow and hyperflow in diffuse axonal injury. Prognostic and therapeutic Implications of transcranial doppler sonography evaluation. Journal of Neurosurgical
sciences 2002; 46: 10-17.
7. Newell DW, Aaslid R, Stoos R, et al. The relationship of blood flow velocity fluctuations to intracranial pressure B waves. J Neurosurgery1992; 76: 415-421.
8. Bradley J. Phillips, Tisha K. et al. Traumatic Brain Injury: A Review. The Internet Journal of Surgery. 2005. Volume 6.
9. Muizelaar JP, Lutz HA III, Becker DP. Effect of mannitol on ICP and CBF and correlation with pressure auto-regulation in severely head-injured patients. J Neurosurgery 1984; 61: 700-706.
We write in response to the eLetter by Philip L Clatworthy on our systematic review ‘the effect of visual training for patients with visual field defects due to brain damage’ (1).
The focus of the study was to contribute to the development of appropriate methods for patients with visual field defects. During the literature search we were amazed that there were only few methodological
sound tr...
We write in response to the eLetter by Philip L Clatworthy on our systematic review ‘the effect of visual training for patients with visual field defects due to brain damage’ (1).
The focus of the study was to contribute to the development of appropriate methods for patients with visual field defects. During the literature search we were amazed that there were only few methodological
sound treatments. It became obvious that an important factor appeared to be the difficulty to create sufficient large groups due to the heterogeneity of the patients. Therefore, the RMD studies formed the majority of the selection and the only RCT study of Kasten (2) was part of
the overall criticism to the effect of VRT and poor fixation control in the discussion section.
However, after careful consideration we agree that our judgement of the methodological quality of the RCT of Kasten's study (2) might have been suboptimal on blinding and comparability of groups. Therefore, we thank our colleagues for their precise comments on the methodological quality of the of Kasten’s RCT (2).
Yours sincerely,
Lies Bouwmeester, Joost Heutink and Cees Lucas
References
1.Lies Bouwmeester MSc, Joost Heutink MSc, Cees Lucas PhD. The effect of visual training for patients with visual field defects due to brain damage. J Neurol Neurosurg Psychiatry 2007 Jun;78(6):555-64. Epub 2006 Nov 29.
2. Kasten E, Wust S, Behrens-Baumann W, Sabel BA. Computer-based training for the treatment of partial blindness. Nat Med 1998;4(9):1083-1087.
JJ Kuhn and colleagues (2007) report a remarkable change in abuse and dependence behavior using DBS neurosurgery.(1)
First, before DBS could become a potential therapeutic option in alcohol dependence, several factors should likely be considered as suggested by the authors. A key consideration in extending DBS to alcohol dependent patients would be the fact that many patients seeking treatmen...
JJ Kuhn and colleagues (2007) report a remarkable change in abuse and dependence behavior using DBS neurosurgery.(1)
First, before DBS could become a potential therapeutic option in alcohol dependence, several factors should likely be considered as suggested by the authors. A key consideration in extending DBS to alcohol dependent patients would be the fact that many patients seeking treatment for alcohol dependence have comorbid psychiatric disorders (which is also the case in the current study).(2)In this difficult to treat population best success is obtained by treating both the psychiatric and substance
use disorders concurrently, especially because alcohol dependent patients with comorbid anxiety disorder at alcoholism treatment onset are at a significantly greater risk for relapse to drinking.(3) Unfortunately, the
authors in this study did not observe a significant reduction in either anxiety or depressive symptoms. If indeed DBS has the potential to treat addiction but does not successfully address an underlying psychiatric
comorbidity than patients may still be at a greater risk of relapse, while being subjected to invasive neurosurgery.
Second, additional challenges could surface in the selection of patients for DBS in an alcohol dependent population. Presumably, only refractory patients would be considered for such a therapeutic option, and therefore a definition of treatment resistance in alcohol dependence would have to be established. Indeed, this definition may be difficult to establish if patients also suffer from psychiatric disorders or by the fact that patients do not always adhere to alcohol management programs.(4)
Since DBS requires postoperative procedures for device set-up as well as follow up across the lifespan, a thorough examination of the patient’s past compliance with treatment may be expected to demonstrate commitment
to a DBS program. The observation of a positive outcome due to DBS in one patient with alcohol dependence is an interesting result. The ethical aspects of performing DBS surgery in alcohol dependence and other behavioral and mental disorders need to be identified and addressed
thoroughly in parallel with such advances.
Emily C Bell and Eric Racine
References:
1. Kuhn J, Lenartz D, Huff W et al. Remission of alcohol dependency following deep brain stimulation of the nucleus accumbens : valuable therapeutic implications? J Neurol Neurosurg Psychiatry 2007; 78: 1152-53.
2. Schneider U, Altmann A, Baumann M et al. Comorbid anxiety and affective disorder in alcohol-dependent patients seeking treatment : the first Multicentre Study in Germany. Alcohol Alcohol 2001; 36:219-23.
3. Kushner M G, Abrams K, Thuras K L, et al. Follow-up study of anxiety disorder and alcohol dependence in comorbid alcoholism treatment patients. Alcohol Clin Exp Res 2005; 29: 1432-43.
4. Swift R. Emerging approaches to managing alcohol dependence. Am J Health-Syst Pharm 2007; 64:S12-22.
We read with interest ‘Hydrocephalus induced chorea’ by Voermans, Schutte, and Bloem (J Neurol Neurosurg Psychiatry 2007; 78: 1284-1285).
They discuss the causal relation between white matter lesions in the basal ganglia and chorea. Pontine lesions however are not mentioned. We found in this journal two previous cases of pontine myelinolysis and extrapontine
myelinolysis and extrapiramidal symptoms.1...
We read with interest ‘Hydrocephalus induced chorea’ by Voermans, Schutte, and Bloem (J Neurol Neurosurg Psychiatry 2007; 78: 1284-1285).
They discuss the causal relation between white matter lesions in the basal ganglia and chorea. Pontine lesions however are not mentioned. We found in this journal two previous cases of pontine myelinolysis and extrapontine
myelinolysis and extrapiramidal symptoms.1 Isolated central pontine myelinolysis was also reported in this journal inducing loss of deep sensitivity and pseudochoreoathetosis.2
Another, older report of central pontine myelinolysis also describes an isolated small pontine lesion without striatal myelinolysis in a case with dystonia and choreoathetosis.3
We present another case of chorea and vascular ischemic pathology of the midbrain.
A man in his eighties was referred to the neurological ward because of acute hemichorea/hemiballism. The complaints started several weeks after coronary artery bypass graft surgery. The man suffered from dysarthria and
dysphagia. Brainstem auditory evoked potentials showed prolonged peak latencies of the brainstem (wave III) and cortical (wave V) responses.
Magnetic resonance imaging of the brain showed areas of hyperintens signal in the brainstem (T2 and flair). The heterogenous hyperintens signals in the pons suggested chronic ischemia of the brainstem. Tiapride, also used
in Huntington’s disease, was successfully given at a dosage of 100 mg tid with regression of the complaints. Unfortunately, the patient died a couple of months later because of cardiac failure.
This is another case showing that not only lesions in the basal ganglia, but also isolated pontine lesions ( of different origin) can induce chorea.
Harald De Cauwer
Klina Regional Hospital
References
1. Seiser A, Schwarz S, Aichinger-Steiner MM, Funk G, Schnider P, Brainin M. Parkinsonism and dystonia in central pontine and extrapontine myelinolysis. J Neurol Neurosurg Psychiatry 1998; 65: 119-121.
2. Federlein J, Postert T, Przuntek H, Müller T. Central pontine myelinolysis causes bilateral loss of deep sensitivity and pseudochoreoathetosis. J Neurol Neurosurg Psychiatry 1998; 65: 607-609.
3. Tison FX, Ferrer X, Julien J. Delayed onset movement disorders as a complication of central pontine myelinolysis. Mov Disord 1991; 6: 171-173.
We read with great interest the submitted neurological picture of Jeon et Kang.(1) Together with two recent case reports in the neuroscience field,(2,3) it might have failed to spot the grossly underestimated differential diagnosis of retrograde cerebral venous air embolism
secondary to central venous access.(4) In contrast to the well studied and reported paradoxical cerebral arterial air embolism in...
We read with great interest the submitted neurological picture of Jeon et Kang.(1) Together with two recent case reports in the neuroscience field,(2,3) it might have failed to spot the grossly underestimated differential diagnosis of retrograde cerebral venous air embolism
secondary to central venous access.(4) In contrast to the well studied and reported paradoxical cerebral arterial air embolism in literature, recent papers on possible retrograde cerebral venous air embolism would strongly
suggest that awareness needs still to be raised to this dangerous clinical adverse event but apparently new research field of brain pathology.(5-11)
To our knowledge, current neuroscience literature still has not defined retrograde cerebral venous air embolism and its morphologic sequelae in the brain. Research should be emphasised on this topic. Emergency treatment to retrograde cerebral venous air embolism, that was suggested using the Trendelenburg (head down) position to induce air bubbles to leave the cerebral veins and return to central venous circulation,(12) as well as treatment of already fixed cerebral venous air embolism like
hyperbaric oxygenation would need evaluation.
Christoph J Schlimp
References
1. Jeon SB, Kang DW. Neurological picture. Cerebral air emboli on T2-weighted gradient-echo magnetic resonance imaging. J Neurol Neurosurg Psychiatry 2007;78:871.
2. Laguillo-Sala G, Canete-Abajo N, Castano-Duque CH, Guardia-Mas E, de Juan-Delago M, Ruscalleda-Nadal J. Cerebral gas embolism secondary to withdrawal of a central venous line. Rev Neurol 2007;44:92-4.
3. Caulfield AF, Lansberg MG, Marks MP, Albers GW, Wijman CA. MRI characteristics of cerebral air embolism from a venous source. Neurology 2006;66:945-6.
4. Schlimp CJ, Loimer T, Rieger M, Lederer W, Schmidts MB.The potential of venous air embolism ascending retrograde to the brain. J Forensic Sci 2005;50:906-9.
5. Brouns R, De Surgeloose D, Neetens I, De Deyn PP. Fatal venous cerebral air embolism secondary to a disconnected central venous catheter.Cerebrovasc Dis 2006;21:212-4.
6. Ferry T, Argaud L, Delafosse B, Robert D. Inactive tuberculosis cavity responsible for fatal cerebral air embolism. Intensive Care Med 2006;32:622-3.
7. Botez SA. Headache and cerebral venous air embolism. Neurology 2007;68:19.
8. Sowell MW, Lovelady CL, Brogdon BG, Wecht CH. Infant death due to air embolism from peripheral venous infusion. J Forensic Sci 2007;52:183-8.
9. Nedelmann M, Pittermann P, Gast KK, Mueller-Forell W, Dieterich M.Involvement of jugular valve insufficiency in cerebral venous air embolism. J Neuroimaging 2007;17:258-60.
10. Mendenhall ML, Spain DA. Venous air embolism and pressure infusion devices. J Trauma 2007;63:246.
11. Menendez-Gonzalez M, Oliva-Nacarino P, Alvarez-Cofino A. Cerebral gas embolism caused by pleural fibrinolytic treatment. Stroke 2007;38:2602-4.
12. Schlimp CJ, Loimer T, Rieger M, Schmidts MB, Lederer W. Pathophysiological mechanism and immediate treatment of retrograde cerebral venous air embolism. Intensive Care Med 2006;32:945.
Dear Editor
Leão discovered the spreading negative slow voltage variations in response to either direct current electrical stimulation or bilateral occlusion of the internal carotid artery in 1947. Both neurones and astrocytes depolarise during a spreading negative slow voltage variation, thereby inducing transmembraneous ionic shifts and intracellular oedema [1]. Under anoxia or severe ischaemia, this spreading...
Dear Editor
Your paper is very interesting. However we consider hyperacusis symptom a possible disorder of stapedius muscle in your patients: have you evaluated this possibility? Assessement of stapedius function with impedancemetry and measurement of its reflex should be useful in neuromuscular disease including myasthenia gravis and facial nerve paralysis. Actually the stapedius reflex consists of a contractio...
Dear Editor
The excellent review shows the limits of the descriptive epidemiology in the understanding of the pathogenesis of the amyotrophic lateral sclerosis. The destruction of neurons in its classical form takes place primarily in the motor tracts which would suggest a synaptic neuron to neuron transfer of the harmful factor thus saving initially other networks.
The hypothetical effect could be relat...
Dear Editor
In our recent letter entitled “Pisa syndrome after unilateral pallidotomy in Parkinson’s disease: an unrecognised, delayed adverse event?” (J Neurol Neurosurg Psychiatr 2007;78:329-330), we described three Parkinson’s disease (PD) patients who developed a lean to the opposite side several years after a unilateral pallidotomy. We wondered whether this was purely disease-related or perhaps a delayed cons...
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In a patient with high-grade internal carotid artery (ICA) stenosis and frequent migraine aura-like symptoms, Dreier et al [1] demonstrated widely scattered focal laminar cortical infarcts and resolution of visual symptoms following corrective surgery. These authors carry forward the speculation that brain ischemia-related cortical spreading depression (CSD) underlies the associated visual phenomena....
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This is an interesting issue about post-traumatic epilepsy (PTE) in brain injured (TBI) patients (1). The authors use spectral electroencephalography (EEG), and brain Magnetic Resonance Image study (bMRI) with contrast (Gadolinium -DTPA) using semi-quantitative technique to define the abnormal signals, and found that MRI but not EEG is more useful to reveal the abnormal cortical signals and can predi...
Dear Editor,
We write in response to the eLetter by Philip L Clatworthy on our systematic review ‘the effect of visual training for patients with visual field defects due to brain damage’ (1).
The focus of the study was to contribute to the development of appropriate methods for patients with visual field defects. During the literature search we were amazed that there were only few methodological sound tr...
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JJ Kuhn and colleagues (2007) report a remarkable change in abuse and dependence behavior using DBS neurosurgery.(1)
First, before DBS could become a potential therapeutic option in alcohol dependence, several factors should likely be considered as suggested by the authors. A key consideration in extending DBS to alcohol dependent patients would be the fact that many patients seeking treatmen...
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We read with interest ‘Hydrocephalus induced chorea’ by Voermans, Schutte, and Bloem (J Neurol Neurosurg Psychiatry 2007; 78: 1284-1285). They discuss the causal relation between white matter lesions in the basal ganglia and chorea. Pontine lesions however are not mentioned. We found in this journal two previous cases of pontine myelinolysis and extrapontine myelinolysis and extrapiramidal symptoms.1...
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We read with great interest the submitted neurological picture of Jeon et Kang.(1) Together with two recent case reports in the neuroscience field,(2,3) it might have failed to spot the grossly underestimated differential diagnosis of retrograde cerebral venous air embolism secondary to central venous access.(4) In contrast to the well studied and reported paradoxical cerebral arterial air embolism in...
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