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Recent eLetters

Displaying 1-10 letters out of 241 published

  1. Comment on the paper "Transient global amnesia following a whole-body cryotherapy session"

    Dear Editor,

    We read with interest the case report concerning a transient global amnesia (TGA) in an individual who was previously submitted to a session of whole body cryotherapy (WBC).1

    The scientific literature is already sufficiently wide to realize that the WBC is a safe procedure, while it could seem apparently dangerous due to very low temperature of the air used in the chambers during treatment.2 Only burns owing to sweat or water traces are reported as adverse events, considering some pathological, universally accepted, conditions as exclusion criteria for the treatment.3-9

    It is possible that some rare adverse events are neither known nor described in literature, thus possible pathological modifications of metabolism or behaviour can be important. However, in the case report,1 in order to build on a robust hypothesis about WBC-induced TGA, we believe that additional findings are needed. The patient previously underwent to WBC, thus the direct cause-effect relationship is in doubt; we outline that a standard treatment is based on two or three weeks (10-15 sessions). Moreover, the type of treatment should be more deeply detailed: was that a classical cryochamber doing a whole-body treatment or, instead, a cryosauna which is used to treat the body but the head; in the latter case the nitrogen could partially escape possibly causing nervous symptoms.

    The anamnestic evaluation lacks of drugs eventually taken by the individual and of mental reactivity and cognition evaluation, in order to exclude early sign of cognitive impairment due to Alzheimer or similar diseases. Furthermore, since the speculative association between WBC and TGA, it should be also taken into account the possible side effects (i.e., amnesia) of the proton pump inhibitors (PPI, e.g., omeprazole), taken by the patient, which were previously reported by Fireman et al.10 More recently, Feng et al. also reported about the psychotic symptoms of dissociative disorder, including amnesia, in a patient treated with clarithromycin and the PPI rabeprazole.11 Hence, if cold could be a risk factor for TGA, as reported by the authors,1 also the PPI use cannot be excluded as a potential trigger.

    The description of the case is important to outline the impact of WBC on nervous system, since this procedure is now indicated for the symptomatic treatment of nervous and psychiatric disorders, after the successful symptomatic treatment of chronic inflammatory ones.12,13 However, care should be taken in associating this universally considered safe procedure with possibly spurious, and not surely associated, adverse events.

    References

    1. Carrad J, Lambert AC, Genn? D. Transient global amnesia following a whole-body cryotherapy session. BMJ Case Rep. Epub Aehad of Print. doi: 10.1136/bcr-2017-221431

    2. Lombardi G, Ziemann E, Banfi G. Whole-Body Cryotherapy in Athletes: From Therapy to Stimulation. An Updated Review of the Literature. Front Physiol 2017;8:258. doi:10.3389/fphys.2017.00258

    3. Cholewka A, Stanek A, Sieron A, Drzazga Z. Thermography study of skin response due to whole-body cryotherapy. Skin Res Technol 2012;18(2):180-7. doi:10.1111/j.1600-0846.2011.00550.x

    4. Hausswirth C, Schaal K, Le Meur Y, et al. Parasympathetic activity and blood catecholamine responses following a single partial-body cryostimulation and a whole-body cryostimulation. PloS One 2013;8(8):e72658. doi:10.1371/journal.pone.0072658

    5. Demoulin C, Vanderthommen M. Cryotherapy in rheumatic diseases. Joint Bone Spine 2012;79(2):117-8. doi:10.1016/j.jbspin.2011.09.016

    6. Louis J, Schaal K, Bieuzen F, et al. Head Exposure to Cold during Whole-Body Cryostimulation: Influence on Thermal Response and Autonomic Modulation. PloS One 2015;10(4):e0124776. doi:10.1371/journal.pone.0124776

    7. Pournot H, Bieuzen F, Louis J, et al. Time-course of changes in inflammatory response after whole-body cryotherapy multi exposures following severe exercise. PloS One 2011;6(7):e22748. doi:10.1371/journal.pone.0022748

    8. Kruger M, de Marees M, Dittmar KH, et al. Whole-body cryotherapy's enhancement of acute recovery of running performance in well-trained athletes. Int J Sport Physiol Perform 2015;10(5):605-12. doi:10.1123/ijspp.2014-0392

    9. Schaal K, Le Meur Y, Louis J, et al. Whole-Body Cryostimulation Limits Overreaching in Elite Synchronized Swimmers. Med Sci Sports Exerc 2015;47(7):1416-25. doi:10.1249/MSS.0000000000000546

    10. Fireman Z, Kopelman Y, Sternberg A. Central nervous system side effects after proton pump inhibitor treatment. J Clin Gastroenterol 1997;25(4):718.

    11. Feng Z, Huang J, Xu Y, et al. Dissociative disorder induced by clarithromycin combined with rabeprazole in a patient with gastritis. J Int Med Res 2013;41(1):239-43. doi: 10.1177/0300060513475384.

    12. Bettoni L, Bonomi FG, Zani V, et al. Effects of 15 consecutive cryotherapy sessions on the clinical output of fibromyalgic patients. Clin Rheumatol 2013;32(9):1337-45. doi: 10.1007/s10067-013-2280-9.

    13. Bouzigon R, Grappe F, Ravier G, Dugue B. Whole- and partial-body cryostimulation/cryotherapy: Current technologies and practical applications. J Therm Biol. 2016;61:67-81. doi: 10.1016/j.jtherbio.2016.08.009.

    Conflict of Interest:

    None declared

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  2. Deaths are rare in neurocysticercosis

    I read with interest the case report about a fatal case of neurocysticercosis. I want to emphasize that deaths are rare in neurocysticercosis and in neurocysticercosis there is no malignant course. Lesion load seems to be quite low. In fact the patient not fully worked up for more likely diagnosis. For example miliary tuberculosis and miliary secondary malignancy. The CSF should have examined for malignant cells and Mycobacterium tuberculosis. X-ray chest would have revealed miliary lesions in lungs as well. Multiple tiny parenchymal rim-enhancing lesions are characteristically not seen in neurocysticercosis.

    Another point I want to mention is that neurocysticercosis can not occur via direct consumption of infected pork because a human is a definitive host and pork consumption will produce adult worms in human intestine. It will not lead to larval spread to brain.

    Conflict of Interest:

    None declared

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  3. Q: Retrospectively identified in the CT images?

    Sirs,

    I wonder whether that plastic toy could be spotted in the CT images by a reader who has been informed about it. Did the radiology department comment about this?

    I am pretty shure the cone cannot be detected on a plain x-ray. The ABS polymer used by toy manufacturers like Playmobile or Lego seems to have x-ray attenuation properties very near to human tissue (Saps et al., World J Clin Pediatr 2014, PMC4173203).

    Best Regards, Peter Koehler (Konstanz, Germany)

    Conflict of Interest:

    None declared

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  4. PFO and Stroke in Sickle Cell Re Dattani and Jackson

    Dear Sir, We read with great interest the case report by Dattani and Jackson detailing a case of potential cardioembolic stroke in a young man with sickle cell anemia (SCA), without significant cerebral vasculopathy but with PFO. We have conducted a controlled clinical study to determine the prevalence of potential left-to-right shunting (intracardiac or intrapulmonary) in children with SCA and overt clinical stroke using contrasted echocardiography in 147 children with SCA +overt stroke and a control group of 123 children without SCA or stroke. Right-to-left shunting was defined as any potential shunting detected by any method (conventional 2D, Doppler, or contrasted echocardiogram, with 2 contrast injections without Valsalva and 2 injections with Valsalva). We found that the prevalence of potential right-to-left shunting was significantly higher in the SCA+stroke group than in controls (45.6% vs 23.6%, p< 0.001). In post hoc analyses, the SCA+stroke group had a higher prevalence of intrapulmonary (23.8% vs 5.7% p<0.001) but not intracardiac shunting (21.8% vs 18.7%, p=0.533) (Dowling, et al., 2016).

    We agree with the Dattani and Jackson, that adults and children with SCA, while at high risk for stroke from SCA-specific risk factors such as sickle vasculopathy, are also at risk for stroke from the "traditional" risk factors for stroke in adults, including potentially treatable risk factors such as paradoxical embolization across a PFO (Dowling and Ikemba, 2011).

    Common SCA related conditions such as acute chest syndrome or pulmonary hypertension, as well as anemia itself, can increase right heart pressures, favoring right-to-left shunting and thus favoring paradoxical embolization. In patients without SCA, hypercoagulable states predispose to paradoxical embolization in adults with potential shunting and SCA is itself a hypercoagulable state. Studies of fat embolization syndrome in SCA also support the role of paradoxical embolization syndrome in SCA. Thus, we concur that both children and adults with SCA and stroke warrant more extensive clinical evaluation for "traditional" risk factors for stroke, particularly as they may be amenable to treatment.

    We suspect that similar mechanisms may be involved in the etiology of at least some of the "silent cerebral infarctions" that can be detected by MRI in up to 40% of children with SCA. We concur that further research is needed in this area but applaud the authors for highlighting the need for exploration of alternative etiologies for stroke in patients with SCA, and raising the clinical awareness of other potentially treatable stroke etiologies in this high risk population.

    Michael Morgan Dowling, MD, PhD, MSCS Departments of Pediatrics and Neurology & Neurotherapeutics University of Texas Southwestern Medical Center, Dallas, Texas

    Fenella J Kirkham, MD, FRCP, FRCPCH Developmental Neurosciences UCL Institute of Child Health London, UK

    References

    Dattani A, Jackson A, The cause of the stroke: a diagnostic uncertainty. BMJ Case Rep. 2017 doi:10.1136/bcr-2016-218358.

    Dowling, M.M. & Ikemba, C.M. (2011) Intracardiac shunting and stroke in children: a systematic review. Journal of Child Neurology, 26, 72-82.

    Dowling MM, Quinn CT, Ramaciotti C, Kanter J, Osunkwo I, Inusa B, Iyer R, Kwiatkowski JL, Johnson C, Rhodes M, Owen W, Strouse JJ, Panepinto JA, Neumayr L, Sarnaik S, Plumb PA, Dlamini N, Kirkham F, Hynan LS; PFAST Investigators. Increased prevalence of potential right-to-left shunting in children with sickle cell anaemia and stroke. Br J Haematol 2017 Jan;176(2):300-308

    Disclosures The authors were supported by the Doris Duke Charitable Foundation. They have no other disclosures and no conflicts of interest to report.

    Conflict of Interest:

    None declared

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  5. Mg dose with 3 TBSP Epsom Salts is over 4000 mg -- Way too HIGH

    It is important to consider the very high dose of elemental magnesium (Mg) in this case of severe livery injury due to Epsom salt intake (1).

    Using information from the Epsom Salt Council that Epsom Salts is 10% elemental Mg by weight, and that one pound of Epsom Salts = 32 Tbsp, I calculate that 3 Tbsp. Epsom Salts would deliver 4,250 mg elemental Mg.

    This amount of supplemental Mg is definitely excessive for only one day let alone as a daily dose for 15 days.

    The adult male RDA for Mg is 420 mg/day, one tenth of the daily dose given in this case study (2). It is amazing that drug withdrawal and adequate hydration were enough for an uneventful recovery with normalization of liver function test after 38 days, showing how safe oral Mg supplementation can be. However, even though quite safe, such excessive doses (> 1,000 mg Mg/day) of this essential nutrient should be avoided.

    References 1. Philips CA, Paramaguru R, Mahadevan P, et al. Severe liver injury due to Epsom salt naturopathy. BMJ Case Rep 2017;2017 doi: 10.1136/bcr-2017- 221718 [published Online First: 2017/10/04] 2. Institute of Medicine. Dietary reference intakes for calcium, phosphorus, magnesium, vitamin D, and fluoride. Washington, D.C.: National Academy Press 1997.

    Conflict of Interest:

    None declared

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  6. A plastic traffic cone masquerading as bronchial carcinoma

    I felt that the article was highly informative. We as nurses and doctors see many patients each day and on some occasions we do not have answers for peculiar symptoms or pains a patient may complain of. In my opinion, the pains and symptoms, are there because there is a cause but the cause is not known to the examiner or the patient. It is my view that we do our best but we seldom go far enough before we label a pain or a symptom as being "idiopathic" or "no known reason". It is my view that if we were more diligent, it may be possible to find the causes of those idiopathic pains etc. Sometimes, being a health care professional is like an investigator searching for a needle in a haystack.

    Conflict of Interest:

    Employee of Doctors at Palmerston Pty Ltd.

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  7. Thoracic heat exchange

    I enjoyed the important and educational case report submitted by Dr. Little, and congratulate him on a successful outcome using aggressive resuscitation techniques. One additional option to transfer heat efficiently to the patient's core is via a device recently introduced that allows warming through the esophagus using a closed-system silicone tube connected to standard water blanket heat exchanger.[1] This approach has been shown to provide sufficient heat to patients to avoid hypothermia in the operating room during challenging burn cases that are prone to substantial heat loss.[2] As such, esophageal warming may allow avoidance of a more invasive thoracotomy in some patients, although in the extreme case described, it is likely that adding esophageal rewarming using this modality would instead be supplementary to the thoracotomy.

    1. Kulstad E, Metzger AK, Courtney DM, Rees J, Shanley P, Matsuura T, McKnite S, Lurie K: Induction, maintenance, and reversal of therapeutic hypothermia with an esophageal heat transfer device. Resuscitation 2013, 84(11):1619-1624. 2. Williams D, Leslie G, Kyriazis D, O'Donovan B, Bowes J, Dingley J. Use of an esophageal heat exchanger to maintain core temperature during burn excisions and to attenuate pyrexia on the burns intensive care unit. Case Rep Anesthesiol. 2016;2016:6.

    Conflict of Interest:

    Co-inventor of a device, and equity holder in Attune Medical developing device mentioned in response.

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  8. Rest tremor due to hypoglycaemic injury?

    Title Page: Rest tremor due to hypoglycaemic injury? 1Halil Onder, 2 Javid Jahanroshan

    1Department of Neurology, Yozgat State Hospital, Yozgat, Turkey 2Department of Neurology, Hacettepe University Hospital, Turkey

    Corresponding author: Halil Onder Department of Neurology, Yozgat State Hospital, Yozgat, Turkey Post Code: 66000 Telephone number: 4442066 email: halilnder@yahoo.com

    Key words: Hypoglycaemic injury; Rest tremor; Neuroimaging; Pathophysiology. Manuscript word count: 555

    Rest tremor due to hypoglycaemic injury? Letter to Editor: We read with great interest the article by Boylan et al. in which they report an interesting patient with severe hypoglycaemic injury presenting with continuous symmetric low amplitude 3-4 Hz pill-rolling type rest tremor of both hands (1). We agree with the interesting aspect of this patient, however, I would like to comment on the article for a better understanding of the report and avoid misleading conclusions. First, as the authors state, rest tremor in deep coma is an unexpected finding as only one prior case has been reported showing rest tremor in a patient following brain death (2). Therefore, for reporting such an atypical presentation, detailed documentation of the clinical manifestations is crucial to make a proper diagnosis. For instance, propriospinal myoclonus, a form of spinal myclonus is known to involve limbs with a frequency of 1-6 Hz which is similar to the frequency range of the described movements in this case (3). Another type of myoclonus is anoxic myoclonus that is a widely recognized finding after cardiac arrest and viewed as an ominous sign (4). Remarkably, myoclonus has also been reported to be present in hypoglycaemic encephalopathy in addition to hypoxic brain injury (5, 6). Although the underlying mechanisms and responsible neurons are not properly understood, generally, myoclonus has been associated with abnormal function of either cortical and/or subcortical structures (7). On the other hand, epileptiform discharges have been reported to lead anoxic-myoclonus in some sub-group of patients and EEG monitoring is suggested to be performed in early anoxic myoclonus for determination of underlying possible ictogenesis well as neuroprognostication of the patients (4, 8). Taken together these knowledges, we think that diagnosing the defined movement disorder (low- amplitude, 3-4 Hz) as 'rest tremor' can be strictly challenging. Hence, we think that electrophysiologic evaluation of the defined symptoms in this patient might give substantial contributions in identification of the abnormal movements in terms of phenomenological aspect. Also, EEG recording which is lack in the report might also give important insights regarding the underlying mechanisms as also mentioned by Elmer et al (4). Based on these points, we think that there may be some crucial limitations in the documentation of this manifestation, as tremor video was unavailable in the report. Second, I would like to remark the devastating neuroimaging findings, affecting prominently striatum, cerebral cortex (including occipital cortex) and hippocampus. However, unlike hypoxic damage, occipital cortex and hippocampus have rather been resistant to hypoglycaemic injury (9), which was not the case in this case. Hence, I wonder if the authors might state if there had been a concurrent hypoxic injury or not in this case. Finally, although the points mentioned above need to be clarified, I agree with the strictly interesting aspect of this report mentioning a patient with rest tremor due to hypoglycaemic injury. As there are some major hypotheses trying to explain the pathophysiology of rest tremor, such as basal ganglia and the cerebello-thalamo-cortical circuitry dysfunctions, the exact mechanims remain to be unknown (10). Besides, rest tremor occurring secondary to a brain lesion is an extremely rare entity, as not a detailed documentation of such a patient is present in literature. Future reports of these rare manifestations of movement disorders in symptomatic circumstances may add substantial contributions to our currently understanding of underlying pathophysiologies. Bullet Points - Were electrophysiologic evaluations of the defined movement disorders conducted? - Might a video demonstration of the defined 'rest tremor' be involved ? - Might the authors state if there had been a concurrent hypoxic injury or not in this case?

    Acknowledgements: None. Conflict of interest: None. References 1. Boylan LS. Hypoglycaemic injury spares thalamus, spoils striatum and leaves only a rest tremor. BMJ Case Rep. 2016;2016. 2. Araullo ML, Frank JI, Goldenberg FD, Rosengart AJ. Transient bilateral finger tremor after brain death. Neurology. 2007;68(16):E22. 3. Kojovic M, Cordivari C, Bhatia K. Myoclonic disorders: a practical approach for diagnosis and treatment. Ther Adv Neurol Disord. 2011;4(1):47 -62. 4. Elmer J, Sandroni C. A nuanced view of post-anoxic myoclonus. Resuscitation. 2017;115:A4-A5. 5. Kida Y, Sawada T, Naritomi H, Kuriyama Y, Ogata J, Kashiwagi A, et al. [A case of hypoglycemic coma associated with myoclonus, periodic synchronous discharges and progressive cerebral atrophy resembling Creutzfeld-Jakob disease]. Nihon Naika Gakkai Zasshi. 1988;77(3):419-24. 6. Nicoli F, Bartolomei F, Swiader L, Gastaut JL. [Diffuse, segmental, asynchronous myoclonus, manifestations of severe hypoglycemia]. Presse Med. 1991;20(36):1783-4. 7. Gupta HV, Caviness JN. Post-hypoxic Myoclonus: Current Concepts, Neurophysiology, and Treatment. Tremor Other Hyperkinet Mov (N Y). 2016;6:409. 8. Aicua Rapun I, Novy J, Solari D, Oddo M, Rossetti AO. Early Lance-Adams syndrome after cardiac arrest: Prevalence, time to return to awareness, and outcome in a large cohort. Resuscitation. 2017;115:169-72. 9. Cho SJ, Minn YK, Kwon KH. Severe hypoglycemia and vulnerability of the brain. Arch Neurol. 2006;63(1):138. 10. Helmich RC, Hallett M, Deuschl G, Toni I, Bloem BR. Cerebral causes and consequences of parkinsonian resting tremor: a tale of two circuits? Brain. 2012;135(Pt 11):3206-26.

    Conflict of Interest:

    None.

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  9. Re:Antenatal management of Cystic Pulmonary adenomatoid malformation

    Dear Dr Kumar,

    Thank you for your letter.

    In relation to the points raised:

    1. Much of the evidence for successful use of steroids in CPAMs relates to microcystic lesions. In this case, the lesion was a large macrocystic CPAM. The case was discussed at an antenatal MDT, and the decision not to treat with steroids was reached.

    2. We thank you for your comment on measuring baseline and subsequent cyst volume ratio, to monitor progression/resolution. That was not measured in this case.

    Conflict of Interest:

    None declared

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  10. Antenatal management of Cystic Pulmonary adenomatoid malformation

    We read case report by Cullen et al and found it very interesting. It was a successfully managed case however, I have certain queries regarding management in the index case.

    1. In a prenatally detected CPAM (previously known as CCAM) with hydrops detected prior to 32 weeks, there is a well-defined role of maternal steroids.(1) Even multiple courses of betamethasone can be tried. Whether it was thought off in index case or not.

    2. Instead of two-dimensional size, measurement of baseline, as well as subsequent Cyst volume ratio (CVR), is a good indicator of progression/ resolution of the cyst.

    References: 1. David M, Lamas-Pinheiro R, Henriques-Coelho T. Prenatal and Postnatal Management of Congenital Pulmonary Airway Malformation. Neonatology. 2016 Apr 13;110(2):101-15.

    Conflict of Interest:

    None declared

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