I recently read the article by Satoh and colleagues (1) with great
interest and have the following question and comments for authors. Their
right handed violinist patient became unable to coordinate the movements
of bowing and fingering hands as a result of a callosal infarct affecting
the entire anterior aspect of the callosum per MRI. From what appears in
the figure, as published, the splenium per...
I recently read the article by Satoh and colleagues (1) with great
interest and have the following question and comments for authors. Their
right handed violinist patient became unable to coordinate the movements
of bowing and fingering hands as a result of a callosal infarct affecting
the entire anterior aspect of the callosum per MRI. From what appears in
the figure, as published, the splenium per se seems intact. This, however,
is a mute point in view of forthcoming observations.
Now, the question: Since the directionality of sensory callosal
traffic in a right hander is from the minor (right) to the major (left)
hemisphere (2), it is hard to understand the sensory defects detected on
the right side of the body as depicted in section "examination of callosal
functions." This may have been a typographical or clerical error and if so
it would be important to correct it for readers (or explain it).
Second, the authors statement, “left fingers require finer movements
than the right, as they press the violin strings,” displays unfamiliarity
with playing a string instrument and overlooks the critical role of the
right hand in allowing production of sounds by the fingering hand (i.e.
violin playing requires very fine tuning of movements by the bowing hand);
since movements of bowing hand must precede those the fingering (by an
interhemispheric transfer time, (IHTT)) to allow vibration of the strings
if sounds are be made by fingering the strings. This has been documented
in the past (2, 3).
According to the one-way callosal traffic circuitry underpinning the
lateralities of motor and sensory control (2, 4, 5), their patient’s “left
hemianopia for musical symbols,” displayed in tachistoscopic examinations,
was in fact due to patient’s difficulty in moving his eyes to the left in
the time allowed, as documented in patients with callosotomy (6, Fig. 7)
rather than to a role by the splenium of the corpus callosum in vision (4,
6).
References
1. Satoh M, Furukawa, Takeda K, Kuzuhara S. Left hemianopia of
musical symbols caused by callosal infarction.
J Neurol Neurosurg
Psychiatry 2006; 77: 705-706.
2. 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.
3. Baader AP, Kazennikov O, Wiesendanger M. Coordination of bowing
and fingering in violin playing.
Brain Res Cogn Brain Res. 2005; 23:436-
443.
4. Derakhshan I. Nature's shell game revealed: evidence for non-
Newtonian laterality of macular vision (Ocular integration in the human
visual cortex.
Can J Ophthalmol. 2007; 42:485-486.
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. Holtzman JD. Interactions between cortical and subcortical visual
areas: evidence from human commissurotomy patients.
Vision Res. 1984;
24:801-813.
We read with interest the excellent review by Ng and Kitchen regarding
neurosurgery and pregnancy(1). We would like to make two additional
remarks. In our opinion the authors failed to address the issue of the
pregnant patient with a spinal or dural arteriovenous malformation (sAVM).
Due to the absence of valves in the epidural venous plexus, the increased
intra-abdominal pressure, the additio...
We read with interest the excellent review by Ng and Kitchen regarding
neurosurgery and pregnancy(1). We would like to make two additional
remarks. In our opinion the authors failed to address the issue of the
pregnant patient with a spinal or dural arteriovenous malformation (sAVM).
Due to the absence of valves in the epidural venous plexus, the increased
intra-abdominal pressure, the additional stress on the venous circulation
during pregnancy and delivery, as well as hormonal changes and increased
vascular volume, symptoms of a sAVM may deteriorate severely(2;3).
Therefore women with a known sAVM should be informed that pregnancy may
worsen their neurological symptoms(3). In women with a myelopathy
presenting during pregnancy a sAVM should be ruled out.
Regarding intracranial AVMs the authors state that the risk of
haemorrhage is increased in the second trimester of pregnancy, when
cardiac output is at its greatest, however novel data demonstrate that
during pregnancy cardiac output is at its greatest in the third trimester
and the puerperium(4). Moreover other studies demonstrate an increased
incidence of intracranial AVM related haemorrhages in the third trimester
and during the puerperium(5).
References
1. Ng J, Kitchen N. Neurosurgery and pregnancy.
J Neurol Neurosurg
Psychiatry 2008;79:745-52.
2. Berenstein A, Lasjaunias P, TerBrugge KG. Spinal arteriovenous
malformations. In: Berenstein A, Lasjaunias P, TerBrugge KG, eds. Surgical
neuroangiography 2.2. Clinical and endovascular treatment aspects in
adults.
Berlin: Springer Verlag 2004: 737-847.
3. Shephard RH. Spinal Arteriovenous Malformations and Subarachnoid
Haemorrhage.
British Journal of Neurosurgery 1992;6:5-12.
4. Trivedi R, Kirkpatrick P. Arteriovenous malformations of the
cerebral circulation that rupture in pregnancy.
Journal of Obstetrics and
Gynaecology 2003;23:484-9.
5. Sadasivan B, Malik GM, Lee C, Ausman JI. Vascular malformations
and pregnancy.
Surgical Neurology 1990;33:305-13.
We did a similar study about perceived memory complaints and memory
function in polychlorinated biphenyls (PCBs) exposed elderly in Taiwan.
PCBs are lipid-soluble and known to affect central nervous functioning.
The previous report that developmental delay in children and memory
decline in the elderly are merit (1-4). We recruited subjects from Yu-
Cheng cohort and selected exposed and unexposed con...
We did a similar study about perceived memory complaints and memory
function in polychlorinated biphenyls (PCBs) exposed elderly in Taiwan.
PCBs are lipid-soluble and known to affect central nervous functioning.
The previous report that developmental delay in children and memory
decline in the elderly are merit (1-4). We recruited subjects from Yu-
Cheng cohort and selected exposed and unexposed controls of age¡Ù60 for
comparison. Several items including Mini-mental state examination (MMSE),
Digit symbol (DS), Visual Memory Span (VMS), Attention and Digit Span
(ADS), five trials of Verbal Memory Recalls (VMR), Learning Ability, a
Delay Recall in 30 minutes, and the Geriatric Depression Scale-Short Form
(GDS-S) etc, were tested. In total, 162 cases and 151 controls were
analyzed. Tests of memory modalities by adjusting confounders revealed
decline in ADS, VMS, Learning ability, VMR with statistical significance
(p<0.05), but a trend in delay recall in 30 minutes and MMSE, and non-
significant in executive motor and sensory function and DS were noted
(table). The subjective memory complaints (SMC) correlated to memory
decline was seen that male with SMC declined in VMR and female with SMC
declined in ADS after adjusted the depression scores.
However, the whole neuropsychological tests are difficult to
complete, as most researchers do. Therefore, selective purposeful test
items are mandatory important. For example, MMSE is useful for general
cognitive evaluation but not for specific memory purpose, as in this study
or in ours. The ADS is almost universally significant in memory function
survey, even in toxic-related studies (5). It implies that a highly
selective test is important to reveal a significant result. A poor
neuropsychological test battery will lead to a different outcome or even
with conflicting finding. From published papers, we can not find using the
same tests on studying neuropsychological evaluation with the same outcome
exactly. It is worthy to learn how to choose a suitable tool to disclose a
meaningful effect in cognitive assessments.
This study showed significant objective memory impairment and self-
perceived memory deficit in the elderly independent to age-, sex-, as well
as white matter changes in the brain. This result highlighted a similar
point that SMC can be a precursory self-perceived symptom to have memory
modalities decline after years later (6). It draws clinician attention
that even a trivial complaint from the elderly should be matters and alert
for developing a dementia in the future.
References
1. Chen YC, Guo YL, Hsu CC, et al. Cognitive development of Yu-Cheng ("oil
disease") children prenatally exposed to heat-degraded PCBs.
JAMA 1992a:
268:3213-8.
2. Guo YL, Lambert GH, Hsu CC, et al. Yucheng: Health effects of prenatal
exposure to polychlorinated biphenyls and dibenzofurans.
Int Arch Occup
Env Health 2004; 77:153-8.
3. Schantz SL, Gasior DM, Polverejan E, et al. Impairment of memory and
learning in older adults exposed to polychlorinated biphenyls via
consumption of Great Lake fish.
Environ Health Perspect 2001; 109:605-11.
4. Lin KC, Guo NW, Tsai PC, et al. Neurocognitive Changes Among Elderly
Exposed to PCBs/PCDFs in Taiwan.
Environ Health Perspect 2008; 116:184-
189.
5. Zhou W, Liang Y, Christiani DC. Utility of the WHO Neurobehavioral Core
Test Battery in Chinese workers¡X A meta-analysis.
Environ Res 2002; 88:94
-102.
6. Liu HC, Teng EL, Lin KN, et al. Performance on a dementia screen test
in relation to demographic variables: A study of 5,297 community residents
in Taiwan.
Arch Neurol 1994; 51:910-5.
We read with interest the review of Neurosurgery and
pregnancy by Ng and Kitchen.(1) Although reference is made to teamwork including, among others, a neuroanaesthetist, we wish to raise awareness of some specific obstetric anaesthetic issues that may not be familiar to
your readers, including some neuroanaesthetists.
First, general anaesthesia, recommended by Ng and Kitchen for cerebral aneury...
We read with interest the review of Neurosurgery and
pregnancy by Ng and Kitchen.(1) Although reference is made to teamwork including, among others, a neuroanaesthetist, we wish to raise awareness of some specific obstetric anaesthetic issues that may not be familiar to
your readers, including some neuroanaesthetists.
First, general anaesthesia, recommended by Ng and Kitchen for cerebral aneurysms and tumours, has particular risks during pregnancy. There is an approximately tenfold increased risk of difficult or failed tracheal intubation (the latter occurring in ~1:200-300 general anaesthetics),(2) and an increased risk of regurgitation of gastric
contents, which combine to make general anaesthesia a major cause of maternal death in past decades (3). Hence, obstetric anaesthetists usually prefer regional (spinal or epidural) anaesthesia whenever possible. Furthermore, the standard technique for reducing these risks during induction of general anaesthesia (the ‘rapid sequence induction’) classically avoids the use of adjuncts that might otherwise be used to reduce the sometimes marked hypertensive response to laryngoscopy and intubation, and the acute increase in intracranial pressure that
accompanies it. Although it may be possible to modify or reduce this response, this may risk excessive hypotension which is good for neither mother nor baby. Finally, the use of certain manoeuvres that might reduce intracranial pressure, such as hypoventilation, may be associated with
reduced blood flow to the uterus and placenta.
Conversely, both spinal anaesthesia (in which the dura is intentional punctured with a small (typically 25-27 G) needle) and accidental dural tap during epidural anaesthesia (in which a large (16-18 G) needle is
used) are associated with the potential for a CSF leak and post-dural puncture headache, the latter with an overall incidence in obstetric anaesthesia of about 0.5-1%.(4) In the presence of raised intracranial pressure, a CSF leak might lead to coning.(5) Meanwhile, epidural injections themselves may be associated with an increase in intracranial pressure, depending on the speed and volume of injection,(6, 7) and both techniques may be associated with hypotension, occasionally severe (especially spinal anaesthesia).
The above problems mean that the choice of anaesthetic and analgesic technique must be carefully made after weighing up the risks and benefits in each individual patient. A multi-specialty approach and good communication are of course vital. As obstetric anaesthetists, what we
would like to know from our neurological and neurosurgical colleagues are estimations of: (i) how harmful would a sudden large swing in blood pressure, both up and down, be in this patient? (ii) how harmful would an acute increase in intracranial pressure be? (iii) how harmful would a
dural puncture be? and (iv) which acute measures, if any, would you suggest if there was a sudden deterioration? This kind of information is crucially important in informing the choice of the obstetric anaesthetist
confronted by a patient with neurological disease.
Catherine Sheehan, SpR Anaesthetist
Steve Yentis, Consultant Anaesthetist
References
1. Ng J, Kitchen N. Neurosurgery and pregnancy. J Neurol Neurosurg Psychiatry 2008; 97: 745-52.
2. Rahman K, Jenkins JG. Failed tracheal intubation in obstetrics: no more frequent but still managed badly. Anaesthesia 2005; 60: 168-71.
3. Lewis, G (ed). The Confidential Enquiry into Maternal and Child Health (CEMACH). Saving Mothers’ Lives: reviewing maternal deaths to make motherhood safer 2003-2005. The Seventh Report on Confi dential Enquiries into Maternal Deaths in the United Kingdom. London, CEMACH:
2007.
4. Paech M, Banks S, Gurrin L. An audit of accidental dural puncture during epidural insertion of a Tuohy needle in obstetric patients. Int J Obstet Anaesth 2001; 10: 162-7.
5. Su, Thung-Ming; Lan, Chu-Mei MS et al. Brain tumour presenting with fatal herniation following delivery under epidural anaesthesia. Anaesthesiology 2002; 96: 5089.
6. Grocott H, Mutch W. Epidural anaesthesia and acutely raised ICP: Lumbar epidural space hydrodynamics in a porcine model. Anaesthesiology 1996; 85: 1086-91.
7. Hilt H, Gramm HJ, Link J. Changes in intracranial pressure associated with extradural anaesthesia. Br J Anaesth 1986; 58: 676-80.
First of all, we would like to congratulate Carpio et al., (2008) for their paper entitled “The effects of albendazole treatment on neurocysticercosis: a randomized controlled trial”. However, we are not in agreement with the authors urge for a new antihelminthic drug for the
treatment of neurocysticercosis (NCC). Therapy for NCC aims at clearance of cysts in the brain and reduced risk of seizure in futu...
First of all, we would like to congratulate Carpio et al., (2008) for their paper entitled “The effects of albendazole treatment on neurocysticercosis: a randomized controlled trial”. However, we are not in agreement with the authors urge for a new antihelminthic drug for the
treatment of neurocysticercosis (NCC). Therapy for NCC aims at clearance of cysts in the brain and reduced risk of seizure in future. The authors (Carpio et al., 2008) in the present study had found significant reduction
in the number of active cysts in treatment group compared to placebo group (37.7% vs. 20.0%; p=0.048) at the end of 12 months follow up; however the difference in the occurrence of symptoms was not significant. Earlier
studies from different parts of the world had also reported more or less same findings (Garcia et al, 2004). However these studies had over looked two most important questions: (1) why few cysts do not respond to
antihelminthic drug (AHD) treatment, and (2) whether the asymptomatic NCC cases be given AHD prophylactically.
It is evident from the population based studies, few cysts respond to anti-parasitic drug therapy (degenerate and may get clear on neuroimaging); while others do not respond. The penetrating power of albendazole (ABZ) in brain parenchyma may be considered as one of the
reason for different outcome, but this will stand true only for cysts at different locations; however few cysts do not respond to ABZ in close vicinity of responding cysts in same patient, or at the same locations in
different patients. That indicates that the reason might be different from the penetrating power of ABZ, and drag our attention towards the immunological environment of that non responding cyst and genetic make up
of host-parasite. The immunological changes associated with the natural course and following anti-parasitic treatment with and without steroid largely remain unknown. Very few immuno-histochemical studies have been
done due to limited specimen tissue (Flisser et al., 1990, Restrepo et al., 1998). It has been reported that genetic differences in cysticerci may affect their infectivity and pathogenicity, and may also contribute to the severity of the disease (Vega et al., 2003). Studies related to immune
interaction and genetic make up of host-parasite as risk for seizures may clarify the relation between NCC and epilepsy in future. It would be worthwhile to know what are the immunological parameters associated with
these non-responding cysts. Prospective study on large animal model of NCC(swine) to evaluate the immune profile following ABZ therapy with and without steroid and comparing the immune response with responder and non-
responder will help better understanding of the disease immunopathogenesis and to develop management strategy for patients suffering from NCC, instead of looking for newer AHD.
Many studies had shown, a large number of the people harboring different stages of NCC remain asymptomatic in the otherwise normal individuals (Prasad et al., 2008; Montano et al., 2005). We had earlier reported a large number of these asymptomatic individuals carry vesicular
cysts (22.6%; Prasad et al., 2008). The presence of degenerating NCC in the asymptomatic group questions the need of prophylactic treatment with anti-epileptic and anti-parasitic drugs for such individuals. The option
to follow up such individuals with imaging and to treat them only if they become symptomatic needs to be explored.
Competing interest: None
References:
1.Flisser A, Gnzalez D, Skhurovich M. Parziquantel treatment of porcine brain and muscle Taenia solium cysticercosis: radiological, physiological and histopathological studies. Parasitol Res 1990; 76: 263-269.
2.Restrepo BI, Liaguno P, Sandoval MA, Enciso JA, Teale JM. Analysis of immune lesions in neurocysticercosis patients: central nervous system response to helminth appears Th-1 like instead of Th-2. J. Neuroimmunol
1998; 89: 64-72
3.Montano SM, Villaran MV, Ylquimiche L et al. Neurocysticercosis: association between seizures, serology, and brain CT in rural Peru. Neurology 2005; 65: 229-33.
4.Prasad A, Gupta RK, Pradhan S et al. “What triggers seizures in neurocysticercosis?- A MRI based Study in Pig Farming Community from a District of North India”. Parasitol Int 2008; 55: 166-171.
5.Vega R, Pinero D, Ramanankandrasana B et al. Population genetic structure of Taenia solium from Madagascar and Mexico: implications for clinical profile diversity and immunological technology. Int. J Parasitol 2003; 33: 1479-85.
In a recent review about the prevalence and the natural history of pituitary dysfunction after traumatic brain injury(TBI),Behan et al(1) concluded that TBI is a major public health problem that exerts a high
cost for both the individual and society at large,and moreover,marked changes of the hypothalamo-pituitary axis have been documented in the acute phase of TBI such as: 1)gonadotrophin deficiency...
In a recent review about the prevalence and the natural history of pituitary dysfunction after traumatic brain injury(TBI),Behan et al(1) concluded that TBI is a major public health problem that exerts a high
cost for both the individual and society at large,and moreover,marked changes of the hypothalamo-pituitary axis have been documented in the acute phase of TBI such as: 1)gonadotrophin deficiency in 80% of patients, 2)growth
hormone deficiency in 18% ,3)corticotrophin deficiency in 16%, and 40% demonstrated vasopressin abnormalities leading to diabetes insipidus or the syndrome of inappropriate anti-diuresis. That is,there are a high
frequency of pituitary hormone deficiencies among the survivors of TBI.
In the manner of other authors (1,2),I believe that the post-traumatic hypopituitarism is due to microinfarcts located in one or several hypothalamic nuclei,as well as also in the infundibular stem, and later on, infarction in the pituitary gland. Because the TBI provoked by
motor vehicle accidents or during the boxing (3) can produce sudden shifting of the brainstem,especially of the midbrain and diencephalon(4,5). Thus.within the hypothalamus,the blood flow is reduced or absent,secondary to rupture by elongation of some branches of the anterior perforating arteries,but especilly of the superior
hypophyseal arteries(5 ).So therefore,magnocellular and parvocellular neuroendocrine cells of the hypothalamus are affected,and therefore,the synthesis and release of
hypothalamic releasing factors(hypophysiotropins )are reduced.According to Behan et al(1) seems that the producing hypothalamic nuclei of luteinizing
hormone-releasing hormone(LHRH) are the most injured.
In conclusion,based on the above-mentioned factors and surgical experiences with omental transplantation to the hypothalamic region and surrounding areas;I think that the revascularization of this brain zone by means of omentum can improve the function of residual neurons and/or axons
in the hypothalamus.Because the omentum is the best tissue for developing vascular connections with underlying and adjacent areas.
3-Tanriverdi F,Unluhizarci K,Kocyigit I, et al.Brief
communication:Pituitary volume and function in competing and retired male boxers. Ann Intern Med 2008;148:827-31.
4-Jellinger KA. Traumatic brain injury as a risk factor for Alzheimer`s disease.J Neurol Neurosurg Psychiatry 2004;75:511-2 (letter).
5.Rafael H.Rejuvenation after omental transplantation on the optic chiasma and carotid bifurcation. Case Rep Clin Pract Rev 2006;7:48-51. www.amjcaserep.com
The authors present a very interesting case of recurrent asystole in the acute phase of ischemic stroke. However, the pathophysiology of this rare event remains speculative. We agree that a Cushing reflex due to
intracranial hypertension is very unlikely to be the culprit as the asystole occurred well before the mass effect developed. An interruption of sympathetic cardiac tone as proposed by the aut...
The authors present a very interesting case of recurrent asystole in the acute phase of ischemic stroke. However, the pathophysiology of this rare event remains speculative. We agree that a Cushing reflex due to
intracranial hypertension is very unlikely to be the culprit as the asystole occurred well before the mass effect developed. An interruption of sympathetic cardiac tone as proposed by the authors is a possible mechanism, but the occurrence in the first 20 hours may also point towards focal seizures in the acute phase of stroke as underlying cause for asystole.
Seizures are frequently associated with hemorrhagic as well as ischemic stroke with cortical involvement. Up to 9% of patients will suffer from seizures after stroke with only about one quarter of them to develop epilepsy afterwards. 40% of all the seizures will occur within 24
hours after stroke onset (1). These early-onset seizures are possibly due to regional metabolic dysfunction and excitotoxic neurotransmitter release secondary to hypoxia. We propose that clinically unapparent focal seizures
might be the cause for recurrent ictal asystole in this patient.
Ictal bradycardia and asystole are rare, but well documented autonomic symptoms during epileptic seizures and may lead to life-threatening cardiac arrest, syncope and trauma. Electrical brain stimulation studies in humans show that variation in heart rate, mostly bradycardia, can be obtained by stimulation of the anterior cingulus,
frontal, temporal and insular cortex as well as the right uncus. Intracranial and scalp EEG data points towards EEG seizure origin in the temporal, insular as well as frontal cortex before the onset of ictal asystole or bradycardia (2). Current hypotheses state that seizures may
lead to stimulation of insula, cingulated cortex, amygdala or hypothalamus which regulate cardiac function through connections to brainstem and spinal cord nuclei (3).
Case series usually show auras or partial seizures preceding the ictal bradycardia and asystole, however ictal asystole with loss of consciousness can be the exclusive ictal semiology (4).
As post-stroke seizures can present in a variety of atypical forms including acute confusional state, slowing, behavioural change, and syncope of unknown origin a high index of suspicion is required for the correct and early diagnosis (5). We conclude that in this case during the
acute phase of a right temporo-insular stroke unapparent seizures may have been the cause for recurrent asystole. However the cause will remain elusive as the diagnosis of ictal asystole would have required the recording of a representative clinical event during simultaneous EEG/ECG
monitoring.
A. Strzelczyk and F. Rosenow
The authors report no competing interests.
References
1. Bladin CF, Alexandrov AV, Bellavance A, Bornstein N, Chambers B, Cote R, et al. Seizures after stroke: a prospective multicenter study. Arch Neurol 2000;57(11):1617-22.
2. Leung H, Kwan P, Elger CE. Finding the missing link between ictal bradyarrhythmia, ictal asystole, and sudden unexpected death in epilepsy. Epilepsy Behav 2006;9(1):19-30.
3. Oppenheimer S. Cortical control of the heart. Cleve Clin J Med 2007;74 Suppl 1:S27-9.
4. Strzelczyk A, Bauer S, Knake S, Oertel WH, Hamer HM, Rosenow F. Ictal asystole in temporal lobe epilepsy before and after pacemaker implantation. Epileptic Disord 2008;10(1):39-44.
5. Myint PK, Staufenberg EF, Sabanathan K. Post-stroke seizure and post-stroke epilepsy. Postgrad Med J 2006;82(971):568-72.
We read with great interest the report from Maks et al entitled: “Deep brain stimulation activation volumes and their association with neurophysiological mapping and therapeutic outcomes”. This paper supports previously published articles and the clinical experience of many centers by suggesting that the true therapeutic target for subthalamic DBS may include the white matter dorsal to the subthalamic...
We read with great interest the report from Maks et al entitled: “Deep brain stimulation activation volumes and their association with neurophysiological mapping and therapeutic outcomes”. This paper supports previously published articles and the clinical experience of many centers by suggesting that the true therapeutic target for subthalamic DBS may include the white matter dorsal to the subthalamic nucleus (STN) proper. We were surprised, however, that the authors failed to mention a striking
correlation within their data set, which is that all four patients who received a model 3389 DBS lead were categorized as poor responders. The correlation of a poor outcome with stimulation via the model 3389 lead is
statistically significant (Chi Square=6.67; P=0.01) in this data set.
The 3389 lead is equipped with four contacts as is the model 3387; however the inter-electrode spacing is reduced from 1.5 to 0.5 mm. Consequently the 3389 contacts span 7.5 mm of tissue as compared to 10.5 mm for the 3387 lead. The concept underlying the design of the 3389 lead is to increase stimulation coverage within the STN, the presumptive target of subthalamic DBS. The data presented in this report indicates that this goal was achieved as the four patients with model 3389 leads had the largest stimulation volumes within their respective STNs. Unfortunately, achieving this goal seems to have been disadvantageous. Previously, we reported the case of a patient who had experienced a sub-optimal response
to suthalamic DBS via a model 3389 lead1. In particular, significant levodopa-induced dyskinesia persisted on one side of her body. Rather than replace the lead, we merely withdrew it 3 mm in order to extend coverage dorsal to the nucleus. The dyskinesias abated immediately. The current
report supports our contention that the 3389 lead provides suboptimal coverage of the subthalamic region for the treatment of Parkinson’s disease, specifically by limiting stimulation dorsal to the nucleus.
References
1. Alterman RL, Shils J, Tagliati M: Immediate and sustained relief of levdopa-induced dyskinesias after dorsal relocation of a deep brain stimulation lead. Neurosurg Focus 17(1):39-42, 2004.
van Kooten et al. are to be commended for their outstanding recent contribution to the literature concerning the epidural blood patch.(1)
However, I would like to correct some historical comments made in their introduction regarding the original epidural blood patch technique by Dr. James B. Gormley.
van Kooten et al. incorrectly describe Gormley as “locating the epidural space with the “han...
van Kooten et al. are to be commended for their outstanding recent contribution to the literature concerning the epidural blood patch.(1)
However, I would like to correct some historical comments made in their introduction regarding the original epidural blood patch technique by Dr. James B. Gormley.
van Kooten et al. incorrectly describe Gormley as “locating the epidural space with the “hanging drop” or “loss of resistance” method”. In the sentinel 1960 report(2), Gormley is paraphrased by Editor Stuart C.
Cullen as performing a lumbar puncture at the same intervertebral space as a previous spinal anesthetic. Cerebrospinal fluid pressure was noted to be low (“not measurable by manometer”) and 15ml sterile saline was injected intrathecally. The needle was then “withdrawn approximately 2mm, until there was no further return flow from the spinal needle. It was presumed then to be in the epidural space.” Two milliliters of the patient’s blood
was then injected as a patch.
This method of locating the epidural space is important and may help explain Gormley’s serendipitously high rate of success (7 of 7 cases rather than 6 of 6 as reported by van Kooten) while utilizing such small volumes of blood (2-3 ml). As has been previously suggested, Dr. Gormley
(a general surgeon untrained in epidural techniques) may have actually performed a subdural, rather than epidural, blood patch.(3) Although the role of the subdural blood patch in the treatment of postdural puncture headache remains largely speculative, it has been repeatedly reported to be effective after failure of the standard epidural blood patch since being widely introduced by Shantha and Bisese.(4)
Finally, it is of interest to note that Gormley’s publication seems to have been largely dismissed. Any “debate” regarding the efficacy of the epidural blood patch, referred to by van Kooten, would likely not have
begun until the 1970s when the procedure was popularized through the work of DiGiovanni and Dunbar.(5)
These details are provided for the sake of historical accuracy to an otherwise superb article.
References
1. van Kooten F, Oedit R, Bakker SLM, Dippel DWJ. Epidural blood patch in post dural puncture headache: a randomized, observer-blind, controlled clinical trial. J Neurol Neurosurg Psychiatry 2008;79:553-558
2. Gormley JB. Treatment of postspinal headache. Anesthesiology 1960;21:565-566
3. Harrington BE. Postdural puncture headache and the development of the epidural blood patch. Reg Anesth Pain Med 2004;29:136-163
4. Shantha TR, Bisese J. Subdural blood patch for spinal headache. NEJM 1991;325:1252-1254
5. DiGiovanni AJ, Dunbar BS. Epidural injections of autologous blood for postlumbar-puncture headache. Anesth Analg 1970;49:268-271
We enjoyed the well-documented case of aceruloplasminemia by Skidmore et al.1 The authors may not have been aware, however, that Miyajima and colleagues (2001)2 drew a distinction between aceruloplasminemia (aCp) and
hypoceruloplasminemia (hCp), by describing three Japanese patients with the latter condition, highly resembling the phenotype and imaging reported by Skidmore et al. The Miyajima patients h...
We enjoyed the well-documented case of aceruloplasminemia by Skidmore et al.1 The authors may not have been aware, however, that Miyajima and colleagues (2001)2 drew a distinction between aceruloplasminemia (aCp) and
hypoceruloplasminemia (hCp), by describing three Japanese patients with the latter condition, highly resembling the phenotype and imaging reported by Skidmore et al. The Miyajima patients had cerebellar ataxia, dysarthria, and hyperreflexia and their brain MRI showed mild cerebellar
atrophy but no T2-weighted hypointensities in the basal ganglia, as would have been expected in aCp. Their ceruloplasmin (Cp) levels were at or barely below 10 mg/dl (within the “undetectable” range for several laboratories). These patients were heterozygous for a nonsense mutation of the Cp gene (Trp858ter).2 Conversely, the reported cases of aCp appear to exhibit a fairly constant triad of diabetes, retinal degeneration, and
neurological deficits, usually chorea with prominent craniofacial involvement (blepharospasm, grimacing, facial and neck dystonia). Brain MRI studies of aCP patients reveal uniform hypointensity in the globus pallidus, putamen, caudate and thalamus reflecting widespread iron
deposition.3 Patients are usually homozygous for truncating mutations in the Cp gene on chromosome 3q25.
Thus, the patient described by Skidmore et al appears to fit the description of hCp better than aCp both from a phenotypic (ataxia, hyperreflexia, no diabetes or retinal degeneration) and imaging (no iron deposition) perspectives. The lack of iron deposition can be explained by the fact that plasma iron turnover requires only 5% of normal Cp levels (which explains the normal iron homeostasis in Wilson’s disease). The distinction between aCp and hCp may be important as the latter may be
associated with milder disease course4 and perhaps better response to iron chelation than aCp patients.5
References
1. Skidmore FM, Drago V, Foster P et al. Aceruloplasminaemia with progressive atrophy without brain iron overload: treatment with oral chelation. J.Neurol.Neurosurg.Psychiatry 2008;79:467-70.
2. Miyajima H, Kono S, Takahashi Y et al. Cerebellar ataxia associated with heteroallelic ceruloplasmin gene mutation. Neurology 2001;57:2205-10.
3. McNeill A, Birchall D, Hayflick SJ et al. T2* and FSE MRI distinguishes four subtypes of neurodegeneration with brain iron accumulation. Neurology 2008;70:1614-9.
4. Moriai S, Daimon M, Susa S et al. Hypoceruloplasminemia in neurological diseases. Intern.Med. 2001;40:548-9.
5. Mariani R, Arosio C, Pelucchi S et al. Iron chelation therapy in aceruloplasminaemia: study of a patient with a novel missense mutation. Gut 2004;53:756-8.
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