With great interest, I read the letter by Dhollander et al. (1). The
authors report two cases with convexity subarachnoid hemorrhages,cortical
superficial siderosis (SS)and raised b-amyloid load on PIB-PET
examination. Based on the absence of micro- and macrobleeds in one
patient, they conclude that this case differs from cerebral amyloid
angiopathy (CAA). However, I would like to draw attention to recently
published fi...
With great interest, I read the letter by Dhollander et al. (1). The
authors report two cases with convexity subarachnoid hemorrhages,cortical
superficial siderosis (SS)and raised b-amyloid load on PIB-PET
examination. Based on the absence of micro- and macrobleeds in one
patient, they conclude that this case differs from cerebral amyloid
angiopathy (CAA). However, I would like to draw attention to recently
published findings that SS is very common in patients with histologically
proven CAA, and can even constitute the only pathological MRI finding in
these patients (2). Modified Boston criteria including SS as a criterion
have been proposed (2). In addition, there is upcoming evidence that in
elderly patients CAA is the most common underlying pathology for both
acute convexity subarachnoid hemorrhages and chronic cortical SS (3).
Based on the data available in literature, I conclude that the authors
present to typical cases of CAA (with or without additional Alzheimers
disease).
1 Dhollander I, Nelissen N, Van Laere K, Peeters D, Demaerel P, Van
Paesschen W, Thijs V, Vandenberghe R.In vivo amyloid imaging in cortical
superficial siderosis. J Neurol Neurosurg Psychiatry. 2010 Jul 28.
2 Linn J, Halpin A, Demaerel P, Ruhland J, Giese AD, Dichgans M, van
Buchem MA, Bruckmann H, Greenberg SM. Prevalence of superficial siderosis
in patients with cerebral amyloid angiopathy. Neurology. 2010;74:1346-50.
3 Kumar S, Goddeau RP Jr, Selim MH, Thomas A, Schlaug G, Alhazzani A,
Searls DE, Caplan LR.Atraumatic convexal subarachnoid hemorrhage: clinical
presentation, imaging patterns, and etiologies. Neurology. 2010;74:893-9.
The issue of orthostatic hypotension is a very common an important
diseable picture of many diseases, as Singer et al. points. Parkinson
disease and diabetic neuropathy are the most common clinical situation of
these cases, and even the very well controlled patient, with tilt-test
table measures to the choice of therapeutic strategies in most cases shows
frustanting results.
The issue of orthostatic hypotension is a very common an important
diseable picture of many diseases, as Singer et al. points. Parkinson
disease and diabetic neuropathy are the most common clinical situation of
these cases, and even the very well controlled patient, with tilt-test
table measures to the choice of therapeutic strategies in most cases shows
frustanting results.
This novel approach, with pyridostigmine, in this open study, is a
very important way to enlight the paths of this cases:I have used the
similar approach in a few patients, with all methods of observation and
control of side effects, and the results were similar of the paper
presented.
We need more research like those, with well-designed statistical and
evidence-based sources, to prescribe acetylcholinesterase inibition as the
prime indication.
Of course, this paper open a novel view of treatment of this kind of
hypotension, perhaps with other measures and/or drugs.
Like Dr Wedderburn and colleagues,1 we have investigated the clinical utility of the Cambridge Behavioural Inventory (CBI), but in patients attending memory clinics and not preselected for clinical diagnosis.
This pragmatic approach has shown that the difference in CBI global score (possible range 0-324) between patients diagnosed with dementia (range 20-239, mean 99.3 +/- 54.0) and without dementia...
Like Dr Wedderburn and colleagues,1 we have investigated the clinical utility of the Cambridge Behavioural Inventory (CBI), but in patients attending memory clinics and not preselected for clinical diagnosis.
This pragmatic approach has shown that the difference in CBI global score (possible range 0-324) between patients diagnosed with dementia (range 20-239, mean 99.3 +/- 54.0) and without dementia (range 10-120, mean 59.1 +/-
34.8) was statistically significant (t = 3.49, p < 0.001).2
However, as regards the ability of the CBI to discriminate between neurodegenerative diseases, specifically Alzheimer’s disease (AD) and frontotemporal dementia (FTD), as defined by NINCDS-ADRDA and Neary criteria respectively, our experience differs from that of the Cambridge group. In our combined cohort of patients (N = 159, dementia prevalence 63%), the difference between the CBI global scores for patients with AD (n= 79, range 20-239, mean 93.6 +/- 53.1) and FTD (n = 11, range 19-216,
mean 101.2 +/- 56.3) did not reach statistical significance (t = 0.44, p > 0.5).
Whilst these data do not speak to the question of Parkinson’s disease and Huntington’s disease, where clinical diagnosis is usually straightforward, they suggest that caution may be necessary before using
the CBI to differentiate between AD and FTD. This observation may simply be a reflection of the symptom overlap between AD and FTD as defined by clinical diagnostic criteria.3
Andrew J Larner
References
1. Wedderburn C, Wear H, Brown J et al. The utility of the Cambridge Behavioural Inventory in neurodegenerative disease. J Neurol Neurosurg
Psychiatry 2008;79:500-3.
2. Larner AJ. Cambridge Behavioural Inventory: diagnostic and differential diagnostic utility. J Neurol Neurosurg Psychiatry 2008;79:351-2 (abstract 61).
3. Varma AR, Snowden JS, Lloyd JJ et al. Evaluation of the NINCDS-ADRDA criteria in the differentiation of Alzheimer’s disease and frontotemporal dementia. J Neurol Neurosurg Psychiatry 1999;66:184-8.
Yates et al. (1) in their recent study have revisited the
epidemiology of head injuries as seen in the UK. They have reiterated the
points mentioned by Kay and Teasdale (2) in 2003 and added the risk
assessment based on the socioeconomic status. It is interesting to note
the high incidence of A&E visits amongst the under fives from people with
a lower socioeconomic background. There are a few...
Yates et al. (1) in their recent study have revisited the
epidemiology of head injuries as seen in the UK. They have reiterated the
points mentioned by Kay and Teasdale (2) in 2003 and added the risk
assessment based on the socioeconomic status. It is interesting to note
the high incidence of A&E visits amongst the under fives from people with
a lower socioeconomic background. There are a few additional points that
we would like to raise:
1. From a treatment point of view or a neurosurgical viewpoint it is
important to know how many of these ‘MSHI’ patients as mentioned by the
authors were transferred to neurosurgical care and had surgery on their
brain. It is generally accepted that 20% of all head injuries require
admission for observation and less than 5% are transferred to
neurosurgical care(2). Our experience is similar to these figures and it
would have been worth knowing what the authors’ experience was.
2. Retrospective data collection from the A&E records has its
problems. As far as we are aware the only means of doing so is the coding
system. One must bear in mind that the coding is done only at the very end
when the patient is being discharged from the A&E department and takes
into account all the investigations performed. This throws in a small
bias. We know very well lots of patients presenting to the A&E who have a
small scalp laceration and questionable loss of consciousness as a result
of a fall, on investigation turn out to have had a cerebrovascular event
which led o the collapse and fall and hence are coded as stroke rather
than head injury. The number of such patients could be substantial,
especially in the elderly population. The problem that this creates is
that these patients are investigated as a head injury and when the
investigations refute the initial diagnosis the coding is not head injury.
So, if data regarding scans or skull x-rays for head injuries is collected
from the A&E coding and also simultaneously from radiology request cards,
the data would be different because the coding has taken into
consideration the results of the scan or x-ray. We do not know of any ways
to deal with this problem, except prospective collection of data. We are
reasonably certain almost all studies which have published retrospective
data from the A&E with respect to NICE head injury guidelines must have
had the same problem, but none of the papers explicitly mention it. We
appreciate that Yates et al. (1) have mentioned it saying that diagnostic
codes may not reliably identify all head injuries. Hence we can never be
absolutely certain of these figures except those derived from a
prospective study, of which unfortunately there have not been any. It is
time that this issue was taken seriously and dealt with.
We believe that it is time for a prospective head injury database to
be set up to collect the required data from the A&E departments all over
the UK so that these questions can be answered once and for all.
References
1.Yates PJ, Williams WH, Harris A, Round A, Jenkins R. An epidemiological
study of head injuries in an UK population attending an emergency
department. J Neurol Neurosurg Psychiatry 2006;77:699-701.
2.Kay A, Teasdale G. Head injury in the United Kingdom. World J Surg
2001;25:1210-20.
Following acceptance
of the final version of our in vivo amyloid imaging paper in December 2009
(1), 2 subsequent papers (2,3) were published that used a different
methodology and design but were in full accordance with our findings. In
our paper, we report the clinical history, CT, MR and in vivo amyloid
imaging in 2 cases with cortical superficial siderosis. Both ca...
Following acceptance
of the final version of our in vivo amyloid imaging paper in December 2009
(1), 2 subsequent papers (2,3) were published that used a different
methodology and design but were in full accordance with our findings. In
our paper, we report the clinical history, CT, MR and in vivo amyloid
imaging in 2 cases with cortical superficial siderosis. Both cases had a
positive amyloid scan. The PIB pattern in our two cases with superficial
siderosis was closely similar to that typically seen in Alzheimer disease
(AD). We conclude that cortical superficial siderosis falls within the
spectrum of cerebral amyloid angiopathy (CAA) and Alzheimer disease (AD)
and constitutes an occasional complication of cerebral amyloidosis (1).
Following acceptance of our paper, a series of 38 pathologically
confirmed CAA patients was published (2), including 2 cases who had
superficial siderosis on MRI in the absence of microbleeds or
macrohemorrhages, similarly to our case 1 (Fig 1B). On that basis, Linn et
al. proposed in April 2010 to modify the criteria for CAA and include
superficial siderosis as one of the imaging criteria. If we apply the
modified criteria, our case 1 fulfills the modified Boston criteria of
possible CAA. As mentioned in the discussion (1), case 2 fulfills the
criteria of probable CAA according to the Boston criteria and also
according to the modified criteria (2010). In a third paper, Kumar et al.
(2010) published a consecutive series of 13 cases of atraumatic localized
convexal subarachnoid hemorrhage above 60 years of age (along with 16
younger cases who are not directly relevant to the current discussion)
(3). In 5-7 cases, the clinical history was remarkably similar to that
observed in our 2 cases, with stereotyped paroxysmal episodes of focal
neurological loss, sometimes with a migratory pattern. The CT image of
intrasulcal hemorrhage also closely resembled that shown in Fig 1A and C
(1). On the basis of the MRI findings (superficial siderosis, cortical
microbleeds or macrohemorrhage), Kumar et al. propose that convexal
subarachnoid hemorrhages in patients above 60 years of age, may be caused
by cerebral amyloid angiopathy. Taken together, these 3 papers provide
novel and converging evidence that, clinically, cerebral amyloid
angiopathy should be considered as a cause in patients above the age of 60
years with stereotyped episodes of focal neurological loss and cognitive
decline and superficial siderosis on MRI, even in the absence of other MRI
abnormalities, in particular if the distribution of the siderosis is
mainly supratentorial.
1. Dhollander I. et al., In vivo amyloid imaging in cortical
superficial siderosis. J Neurol Neurosurg Psychiatry 2010 doi
10.1136/jnnp.2009.194480
2. Linn J. et al., Prevalence of superficial siderosis in patients with
cerebral amyloid angiopathy. Neurology 2010; 74; 1346-1350
3. Kumar S. et al., Atraumatic convexal subarachnoid hemorrhage: clinical
presentation, imaging patterns, and etiologies. Neurology 2010; 74; 893-
899
Conflict of Interest:
PI of a GE Healthcare sponsored phase I and phase II study, as well as of therapeutic phase II and phase III trials sponsored by EliLilly, Medivation, Novartis and Pfizer.
We thank Dr Celio Levyman for his supportive comments.[1]
We fully agree
with him that, in patients with baroreflex failure, it is necessary to
adopt approaches to combat orthostatic hypotension without increasing
supine hypertension. It is also important to follow up an open study with
a blinded study. We expect to complete, within the next month, a double-
blind placebo controlled study, funded by...
We thank Dr Celio Levyman for his supportive comments.[1]
We fully agree
with him that, in patients with baroreflex failure, it is necessary to
adopt approaches to combat orthostatic hypotension without increasing
supine hypertension. It is also important to follow up an open study with
a blinded study. We expect to complete, within the next month, a double-
blind placebo controlled study, funded by NIH, on this subject. The study
has 4 arms: pyridostigmine; pyridostigmine + subthreshold dose of
midodrine (2.5 mg); and pyridostigmine + low dose (5 mg) midodrine;
placebo, in the treatment of neurogenic orthostatic hypotension.
Reference
(1) Levyman C. A new light to orthostatyc hypotension [electronic response to Singer et al Acetylcholinesterase inhibition: a novel approach in the treatment of neurogenic orthostatic hypotension] jnnp.com 2003http://jnnp.bmjjournals.com/cgi/eletters/74/9/1294#68
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.
Kuo et al report the usefulness of Transcranial Doppler (TCD) in
confirming brain death (BD) [1]. I found two points particularly
interesting.
First, the TCD showed “that there must be a time lag between the
cerebral circulatory arrest and the total loss of brain function [1].”
This suggests that in clinically diagnosed BD the loss of all critical
brain functions tested occurs before cere...
Kuo et al report the usefulness of Transcranial Doppler (TCD) in
confirming brain death (BD) [1]. I found two points particularly
interesting.
First, the TCD showed “that there must be a time lag between the
cerebral circulatory arrest and the total loss of brain function [1].”
This suggests that in clinically diagnosed BD the loss of all critical
brain functions tested occurs before cerebral circulatory arrest. Another
way of saying this is that clinically diagnosed BD may reflect an ischemic
penumbra phenomenon, and only later progress to cerebral circulatory
arrest (over the ensuing 36 hrs). This is what Coimbra claims when he
states that what may contribute to the irreversibility of BD is doing the
apnea test itself [2]. When the pC02 rises during an apnea test, the
intracranial pressure will rise, and this may convert an ischemic penumbra
to an irreversible circulatory arrest situation [2]. This has two major
implications. One is that doing an apnea test may be harmful. Two is
that early clinical BD may not be an irreversible state.
Second, in the discussion Kuo et al state that “in our series, no
flow was detected in …only two members of the control group (1.9%)” [1].
Table 4 shows that the specificity and positive predictive value of TCD
for BD using any of the vessels was 100%. These two findings do not seem
compatible. If the specificity was less than 100%, as in the Dosemeci et
al study (1/39 = 2.6% false positive rate), then TCD cannot be relied upon
to confirm death.
There is other data to suggest that BD may be due to a reversible
penumbra phenomenon. First, there are cases that fulfilled BD, with or
without an apnea test, that were reversible [3-8]. Second, there are
cases of brainstem encephalitis that fulfilled BD tests and were
reversible [9-12]. Third, there are reports of cerebral blood flow
studies in clinical BD progressing from flow, to a later study showing no
flow [13-15]. This suggests that when BD is clinically diagnosed it may
be a prognosis that irreversible BD will occur, but not that it has
necessarily already occurred.
References
1. Kuo JR, Chen CF, Chio CC, Chang CH, Wang CC, Yang CM, Lin KC. Time
dependent validity in the diagnosis of brain death using transcranial
Doppler sonography. J Neurol Neurosurg Psychiatry 2006;77:646-649.
2. Coimbra CG. Implications of ischemic penumbra for the diagnosis of
brain death. Braz J Med Biol Res 1999; 32: 1479-1487.
3. Bolton CF, Brown JD, Cholod E, Warren K. EEG and brain life. The
Lancet 1976;535.
4. Okamoto K, Sugimoto T. Return of spontaneous respiration in an infant
who fulfilled current criteria to determine brain death. Pediatrics
1995;96(3):518-520.
5. Green JB, Lauber A. Return of EEG activity after electrocerebral
silence: two case reports. J Neurol Neurosurg Psychiatry 1972;35:103-107.
6. Kato T, Tokumaru A, O’uchi T, Mikami I, Umeda M, Nose K, et al.
Assessment of brain death in children by means of P-31 MR Spectroscopy:
preliminary note. Radiology 1991;179:95-99.
7. Ashwal S, Smith AJK, Torres F, Loken M, Chou SN. Radionuclide bolus
angiography: a technique for verification of brain death in infants and
children. Journal of Pediatrics 1977;91(5):722-728.
8. Thompson JR, Ashwal S, Schneider S, Hasso AN, Hinshaw Jr DB, Kirk G.
Comparison of cerebral blood flow measurements by xenon computed
tomography and dynamic brain scintigraphy in clinically brain dead
children. Acta Radiologica Supplementum 1986;369:675-679.
9. Ragosta K. Miller Fisher Syndrome, a brainstem encephalitis, mimics
brain death. Clinical Pediatrics 1993;685-687.
10. Al-din ASN, Jamil AS, Shakir R. Coma and brain stem areflexia in
brain stem encephalitis (Fisher’s syndrome). BMJ 1985; 291:535-536.
11. Kohrman MH, Spivack BS. Brain death in infants: sensitivity and
specificity of current criteria. Pediatric Neurology 1990; 6(1):47-50.
12. Chandler JM, Brilli RJ. Brainstem encephalitis imitating brain
death. Crit Care Med 1991;19(7):977-979.
13. Facco E, Zucchetta P, Munari M, Baratto F, Behr AU, Gregianin M, et
al. HMPAO SPECT in the diagnosis of brain death. Intensive Care Med
1998; 24:911-917.
14. Kurtek RW, Lai KK, Tauxe WN, Eidelman BH, Fung JJ.
Hexamethylpropylene amine oxime scintigraphy in the diagnosis of brain
death and its implications for the harvesting of organs used for
transplantation. Clinical Nuclear Medicine 2000; 25(1):7-10.
15. de la Riva A, Gonzalez FM, Llamas-Elvira JM, Latre JM, Jimenez-
Heffernan A, Vidal E, et al. Diagnosis of brain death: superiority of
perfusion studies with HMPAO over conventional radionuclide cerebral
angiography. British Journal of Radiology 1992; 65:289-294.
I thank the editor for the opportunity to respond to a letter to the editor entitled 'Forget auditory nerve compression as a treatable cause for tinnitus' by Dr Folmer.
It states that in my editorial comment reality concerning tinnitus is distorted and, more specifically, that 1. many effective, non-surgical, non-pharmacologic management strategies are available and helpful for patients who experience tinnitus; 2. audit...
I thank the editor for the opportunity to respond to a letter to the editor entitled 'Forget auditory nerve compression as a treatable cause for tinnitus' by Dr Folmer.
It states that in my editorial comment reality concerning tinnitus is distorted and, more specifically, that 1. many effective, non-surgical, non-pharmacologic management strategies are available and helpful for patients who experience tinnitus; 2. auditory nerve compression is an
exceedingly rare cause of tinnitus; 3. therefore, microvascular decompression surgery for tinnitus should be undertaken in a similarly miniscule number of cases.
Based on his own work on tinnitus, Dr Folmer quotes 'proof' that many effective, non-surgical, non-pharmacologic management strategies are available and helpful for patients who experience tinnitus. These papers however do not seem to scientifically support his claims. One of the papers1 does not contain any data but only explains a flowchart that terminates in two endpoints: 1.'Employ management strategies and reassess at 1, 6 and 12 months' or 2. 'Reassure patient that condition is harmless'. These management strategies consist of individualized (as it should be) counseling and sound treatments. In other words, explaining how tinnitus develops combined with passive or active sound treatment, i.e. hearing aids or sound generators. In essence this is a variation of tinnitus retraining therapy or cognitive behavioral therapy plus sound treatment. The results of the second paper referenced2, dealing with the efficacy of ear-level devices, show exactly the same improvement without and with sound treatment 2, thus suggesting a placebo effect or effect of the counseling and therefore underscoring his rather surprising claim 'proven' efficacy. Furthermore, the claimed improvements might be statistically significant, but seem clinically irrelevant. The VAS intensity improves from 7.06/10 to 6.47/10, with most responses on the questionnaires improving from 3.4 to 3 (table 3, Folmer 2002)3. Moreover, the tinnitus associated depression scores remain unchanged in 112, worsen in 58 and improve in 28 patients, an outcome that would probably not satisfy neither patients nor tclinicians. Furthermore, these results are obtained in a way that is most likely non-sustainable at a population level. A first intake consultation takes 4 hours, and a follow up 2 hours, suggesting that only 2 patients can be evaluated per an eight-hour working day 3. This means that, following this treatment approach, for the 40.000.000 US citizens suffering from tinnitus 3, 1000 tinnitus specialists would spend 20.000 days, i.e. more than 60 years, just to do the first consultation. Thus Dr Folmer's statement that many effective and helpful treatments are available for people suffering from tinnitus, might be a distorted overoptimistic view of reality, and unrealistic to perform in routine clinical practice.
Everybody agrees that microvascular compressions are an uncommon cause for tinnitus. An epidemiological analysis demonstrates that the known incidences of other microvascular compression syndromes such as trigeminal neuralgia, hemifacial spasm, and glossopharyngeal neuralgia are related to the length of their respective CNS segments. Based on these data it has been estimated that microvascular compressions of the eighth cranial nerve result in an incidence of tinnitus of approximately 8/100.0004 , i.e. potentially more than 3000 patients in the US each year develop tinnitus based on a microvascular compression. For these patients it is known that the longer the tinnitus exists the worse the results of the surgical decompression5, and 4 years might be a treatment limiting factor6. Furthermore it is known that when no surgical decompression is performed a progressive deterioration of the nerve's integrity develops, as evidenced by a prolonging IPL I-III interval, and that this is associated with worsening of tinnitus intensity7. Therefore it is important to learn how to select this rare subgroup of causally treatable patients from the vast majority of unfortunately yet untreatable patients, before irreversible damage settles in. Thus it is essential that scientific journals publish reports, even on small amounts of patients, of successful treatments in very well selected specific subgroups. This will increase our understanding of how to better delineate tinnitus subgroups. If you do not look for it, you will not find it, and thus will not be able to treat it.
According to Dr Folmer we should leave a patient with a causally treatable tinnitus undiagnosed and untreated. The consequence of this attitude would be to stop any diagnosis in medicine and instead just apply some cognitive behavioral treatment for better accepting fate in life. This fatalistic philosophy progressively lost its grip on Western Society since the 12the century and especially since the scientific revolution of the 17th century. The concept 'Forget auditory nerve compression as a treatable cause for tinnitus' thus represents an unsustainable concept which is incompatible with contemporary medicine, even more so as it has become clear that there are many different subgroups of tinnitus and thus that there exists not one treatment, albeit individually adapted, that fits all.
If you only have a hammer, everything looks like a nail. The approach towards tinnitus treatment is rapidly evolving away from this concept. In this respect, the Tinnitus Research Initiative, promoting international multidisciplinary collaborations among clinicians and between clinicians and basic scientists has developed a flowchart (www.tinnitusresearch.org), permitting to separate tinnitus in its many subgroups, one of which is microvascular compressions. Specific treatments are being developed for each of the subgroups. This requires specialized tinnitus centers in which a truly multidisciplinary approach is available, combining the expertise of audiologists, psychologists, neurologists, psychiatrists, ENT surgeons and neurosurgeons.
It can therefore only be hoped that health care providers base their treatment approaches not only on statistics, but on the clinical relevance of the data and the proposed treatment and the practical reality of it. Moreover, progress and not personal, albeit well meant, opinions should guide the future of tinnitus treatments. Only by developing new treatments, and perfecting existing ones and their indications, will one day many effective (probably diverse) strategies become available and helpful for patients who experience tinnitus. These might, or might not, include surgical, pharmacologic options. For the time being, let us not forget that a limited amount of patients can already 'really' be helped, for instance in the case of microvascular compressions.
1. Folmer RL, Martin WH, Shi Y. Tinnitus: questions to reveal the cause, answers to provide relief. J Fam Pract 2004;53(7):532-40.
2. Folmer RL, Carroll JR. Long-term effectiveness of ear-level devices for tinnitus. Otolaryngol Head Neck Surg 2006;134(1):132-37.
3. Folmer RL. Long-term reductions in tinnitus severity. BMC Ear Nose Throat Disord 2002;2(1):3.
4. De Ridder D, Moller A, Verlooy J, Cornelissen M, De Ridder L. Is the root entry/exit zone important in microvascular compression syndromes? Neurosurgery 2002;51(2):427-33; discussion 33-4.
5. Moller MB, Moller AR, Jannetta PJ, Jho HD. Vascular decompression surgery for severe tinnitus: selection criteria and results. Laryngoscope 1993;103(4 Pt 1):421-7.
6. De Ridder D, Vanneste S, Adriaenssens I, Lee AP, Plazier M, Menovsky T, et al. Microvascular decompression for tinnitus: significant improvement for tinnitus intensity without improvement for distress. A 4-year limit. Neurosurgery;66(4):656-60.
7. De Ridder D, Heijneman K, Haarman B, van der Loo E. Tinnitus in vascular conflict of the eighth cranial nerve: a surgical pathophysiological approach to ABR changes. Prog Brain Res 2007;166:401-11.
I have read with interest the article written by Finsterer et al.
However, I do have several concerns and remarks in relation to it.
First, the authors describe a stenotic lesion at the L-ICA that I do not
actually see in the diagnostic angiogram. Moreover, this lesion was
treated wih a stent-graft.
Second, the image of the R-ICA corresponds to a classic carotid artery
dissection, probabl...
I have read with interest the article written by Finsterer et al.
However, I do have several concerns and remarks in relation to it.
First, the authors describe a stenotic lesion at the L-ICA that I do not
actually see in the diagnostic angiogram. Moreover, this lesion was
treated wih a stent-graft.
Second, the image of the R-ICA corresponds to a classic carotid artery
dissection, probably related to a minor trauma (abortion is referred in
the text, thus consider intubation, cervical hyperextention, coughing,
vomiting as etiological factors). The clinical presentation is classic of
a repetitive embolic phenomena.
Third, The pattern of fibromuscular dyaplasia is questionable.
Fourth, I do not agree with the implantation of stent graft for a disease
that can be easily managed with self expandable bare stents.
And last, the cervical surgical access to the carotid artery in order to
implant a stent in a young patient (straightforward arteries)seems
uneccessary when compared to the endovascular transfemoral route has been
the route of choice for years.
With great interest, I read the letter by Dhollander et al. (1). The authors report two cases with convexity subarachnoid hemorrhages,cortical superficial siderosis (SS)and raised b-amyloid load on PIB-PET examination. Based on the absence of micro- and macrobleeds in one patient, they conclude that this case differs from cerebral amyloid angiopathy (CAA). However, I would like to draw attention to recently published fi...
Dear Editor
The issue of orthostatic hypotension is a very common an important diseable picture of many diseases, as Singer et al. points. Parkinson disease and diabetic neuropathy are the most common clinical situation of these cases, and even the very well controlled patient, with tilt-test table measures to the choice of therapeutic strategies in most cases shows frustanting results.
This novel...
Dear Editor
Like Dr Wedderburn and colleagues,1 we have investigated the clinical utility of the Cambridge Behavioural Inventory (CBI), but in patients attending memory clinics and not preselected for clinical diagnosis. This pragmatic approach has shown that the difference in CBI global score (possible range 0-324) between patients diagnosed with dementia (range 20-239, mean 99.3 +/- 54.0) and without dementia...
Dear Editor,
Yates et al. (1) in their recent study have revisited the epidemiology of head injuries as seen in the UK. They have reiterated the points mentioned by Kay and Teasdale (2) in 2003 and added the risk assessment based on the socioeconomic status. It is interesting to note the high incidence of A&E visits amongst the under fives from people with a lower socioeconomic background. There are a few...
We thank J. Linn for her interest in our paper.
Following acceptance of the final version of our in vivo amyloid imaging paper in December 2009 (1), 2 subsequent papers (2,3) were published that used a different methodology and design but were in full accordance with our findings. In our paper, we report the clinical history, CT, MR and in vivo amyloid imaging in 2 cases with cortical superficial siderosis. Both ca...
Dear Editor
We thank Dr Celio Levyman for his supportive comments.[1]
We fully agree with him that, in patients with baroreflex failure, it is necessary to adopt approaches to combat orthostatic hypotension without increasing supine hypertension. It is also important to follow up an open study with a blinded study. We expect to complete, within the next month, a double- blind placebo controlled study, funded by...
Dear Editor
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...
Dear Editor,
Kuo et al report the usefulness of Transcranial Doppler (TCD) in confirming brain death (BD) [1]. I found two points particularly interesting.
First, the TCD showed “that there must be a time lag between the cerebral circulatory arrest and the total loss of brain function [1].” This suggests that in clinically diagnosed BD the loss of all critical brain functions tested occurs before cere...
I thank the editor for the opportunity to respond to a letter to the editor entitled 'Forget auditory nerve compression as a treatable cause for tinnitus' by Dr Folmer.
It states that in my editorial comment reality concerning tinnitus is distorted and, more specifically, that 1. many effective, non-surgical, non-pharmacologic management strategies are available and helpful for patients who experience tinnitus; 2. audit...
Dear Editor
I have read with interest the article written by Finsterer et al. However, I do have several concerns and remarks in relation to it.
First, the authors describe a stenotic lesion at the L-ICA that I do not actually see in the diagnostic angiogram. Moreover, this lesion was treated wih a stent-graft. Second, the image of the R-ICA corresponds to a classic carotid artery dissection, probabl...
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