eLetters

65 e-Letters

published between 2019 and 2022

  • Tetanus-induced rhythmic seizures mimicking the clinical and electroencephalographic presentation of status epilepticus

    I read this paper with great interest and congratulate the authors on consideration of tetanus in this case. I would point out that the EEG in Figure 1 was recorded with a low pass filter of 30 Hz, which could make EMG artifact look like the fast activity labeled as wicket spikes. If the raw EEG data are still available, examination at a low pass filter of 70 Hz would resolve the issue.

    Tetanus does not in and of itself alter consciousness, so one might infer that she had suffered hypoxia during her spasms to cause her coma on presentation, which likely led to the idea that this was status epilepticus. Her eventual cognitive recovery attests to the skill and persistence of her medial team.

    Culturing C. tetanii from a wound does not prove the diagnosis of tetanus, as the spores are ubiquitous, and only antitetanus antibodies from vaccination prevent the disease. However, I have no doubt about the diagnosis on clinical grounds. Did she receive tetanus toxoid in addition to human tetanus immune globulin? There are unfortunately cases of recurrent tetanus if active immunization is not pursued.

    Ref: Birch TB, Bleck TP. Tetanus (Clostridium tetani). In Bennett JE, Dolin R, Blaser MJ (eds), Mandell, Douglas, and Bennett’s Principles and practice of infectious diseases (ed 9). Philadelphia: Elsevier, 2020, pp. 2948 – 2953.

  • Ref: bcr-2021-242073.R2 - Very Late Onset Friedreich’s Ataxia with rapid course mimicking as Possible Multiple System Atrophy Cerebellar Type. Rapid Response from Dr. Stefan M. Pulst, Professor & Chair, Neurology, University of Utah

    Respected Editor and Dr. Pulst,


    Thank you for your interest in our case. We agree with your comment that Friedreich ataxia (FRDA) is an autosomal recessive neurodegenerative disease caused by bi-allelic expansion of an intronic GAA repeat in the frataxin (FXN) gene, but our patient had eight GAA repeats on allele-1 and 37 repeats (pre-mutated allele) on allele-2. The pre-mutated allele can be responsible for the disease, in
    rare cases, by causing somatic expansion or pre-mutation in cell populations. But this occurs only when in the setting of the second allele in the clear pathogenic range of expansion. This intronic GAA expansion further silences the FXN gene, resulting in pathologically suppressed levels of the frataxin protein. As per the respected reader, even though the patient had the probability of compound
    heterozygous mutation with a pathogenic point mutation in one allele, the second allele would not be pathogenic at 37 GAA repeats.

    Usually, individuals with ataxia who are heterozygous for an expanded GAA repeat (> 66) may contain a separate loss-of-function mutation in the FXN gene copy over the allele with normal GAA repeat length. In the relevant clinical context, these patients should be considered to have Friedreich ataxia. [1] However, in populations where the prevalence of Friedreich ataxia carriers is high, such an
    individual may have a different disorder responsible for ataxia apart from being a carrier for Fr...

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  • Burden of organdonation after euthanasia: better exclude it than reduce it

    Maes et al suggest that the burden of organdonation related issues in organdonation after euthanasia (ODE) patients is well tolerable or may even be neglegible. They present two cases with untreatable psychiatric disorders who requested for euthanasia and expressed their deathwish to combine with postmortal organdonation. The burden relates to the patient, his family and the professionals involved in euthanasia. They propose that all psychiatric patients whom euthanasia is granted should be informed about the possibility of postmortal organ donation(1).
    First, we state that the burden can even be minimized further: it is not necessary for the patient to have his euthanasia performed in the hospital. These patients can be given the sense of dying at home and transported thereafter using an anesthesia bridge to the hospital, as we have shown to be feasible(2).
    Second, it is not fair to use the experience of these two evident highly for ODE motivated psychiatric patients and their families as a reference for comparable euthanasia patients who are unaware of the option of post mortal organdonation.
    But third, of perimount importance, we criticize the opinion that the amount of burden for ODE patients may reach a point to be neglegible. In our opinion this burden should not be minimized, but excluded. The suggestions of Maes et al are motivated by utilistic ethical considerations and the existence of waitinglists for transplantation. The act of organdonation h...

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  • Ref: bcr-2021-242073.R2 - Very Late Onset Friedreich’s Ataxia with rapid course mimicking as Possible Multiple System Atrophy Cerebellar Type. Rapid Response from Dr. Stefan M. Pulst, Professor & Chair, Neurology, University of Utah

    Response from Tushar Vidhale, MD (Dated: July 8th, 2022)

    Respected Editor and Dr. Pulst,
    Thank you for your interest in our case. We agree with your comment that Friedreich ataxia (FRDA) is an autosomal recessive neurodegenerative disease caused by bi-allelic expansion of an intronic GAA repeat in the frataxin (FXN) gene, but our patient had eight GAA repeats on allele-1 and 37 repeats (pre-mutated allele) on allele-2. The pre-mutated allele can be responsible for the disease, in
    rare cases, by causing somatic expansion or pre-mutation in cell populations. But this occurs only when in the setting of the second allele in the clear pathogenic range of expansion. This intronic GAA expansion further silences the FXN gene, resulting in pathologically suppressed levels of the frataxin protein. As per the respected reader, even though the patient had the probability of compound
    heterozygous mutation with a pathogenic point mutation in one allele, the second allele would not be pathogenic at 37 GAA repeats.

    Usually, individuals with ataxia who are heterozygous for an expanded GAA repeat (> 66) may contain a separate loss-of-function mutation in the FXN gene copy over the allele with normal GAA repeat length. In the relevant clinical context, these patients should be considered to have Friedreich ataxia. [1] However, in populations where the prevalence of Friedreich ataxia carriers is high, such an individual may have a different disorder respon...

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  • Not Visceral, but Localized Leishmanial Lymphadenopathy

    Dear Editor:
    We have read with interest this case, but we do not agree with the authors about considering this case as a visceral leishmaniasis (VL). This is a typical case of localized leishmanial Lymphadenopathy (LLL), as we and others described in several series of cases (1,2). This not-well known form of presentation of leishmaniasis is more common in Middle-East region, caused by dermatotropic strains like L. tropica or L. major, but isolated cases are described in Mediterranean region caused by L. infantum, as probably this case.
    In last decade, we suffered in Southern urban cities of Madrid, mainly Fuenlabrada, an important outbreak of leishmaniasis. More than 1000 cases of leishmaniasis were reported, and we could describe several cases of LLL (2).
    LLL is a form of presentation of leishmaniasis in patients without cellular immunosuppression, which presented with lymphadenopathy as the only form of presentation, and without systemic manifestations (no fever, no splenomegaly, no kytopenias, and normal acute phase reactants). Some LLL patients can refer lesions of cutaneous leishmaniasis (CL) near the adenopathy that had been previously spontaneously resolved or not, showing adenopathies as a local inflammatory rather than a systemic disease. Median duration of the adenopathy was 3 months in our patients. None of these patients, some of them without treatment, progressed to VL.
    We think it is important to distinguish LLL from VL because of crit...

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  • A supporting case for this profound presentation

    Jiang presents a very interesting and unique case of bilateral corneal decompensation in a patient with COVID pneumonitis. We would like to offer a similar case to support their hypothesis of viral endotheliitis. These cases demonstrate an ocular manifestation of COVID-19 infection which was previously unknown. This manifestation is important to be aware of as the subsequent visual impairment may be profound, though likely amenable to treatment.

    Jiang pointed out the unclear onset for their case and possible delayed presentation from 34 days of ventilation. While we cannot assume the onset time of Jiang’s patient, our patient provides an interesting comparison. Our case describes a male patient who developed significant and painless overnight vision loss. He had gone to bed with only cough as a symptom of COVID infection and awoke to find himself only able to perceive light and gross motion. This patient presented to our local accident and emergency department with this sudden and profound bilateral loss of vision. He required admission due to his inability to self-care.

    On examination the patient was found to have significant bilateral corneal oedema. Both eyes were white with no evidence of local infection, inflammation, or ocular surface trauma. There was no epithelial uptake with fluorescein in either eye. Intraocular pressure was within normal limits and symmetrical. No corneal dystrophy could be seen with biomicroscopy. The patient was started on topi...

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  • Prof

    Dear Sir/Madam.

    Thanks for your interest in our case report and the literature review on CeAD and spinal manipulation, which is the most important element of patient care.
    All clinicians would like to have a positive outcome for their patients using evidence-based practice.
    Unfortunately, the patient in this case had a near fatal outcome by a chiropractor practising in a major metropolitan region of China. The chiropractor is a graduate of a traditional Chinese medical university. The patient could only recall heavy massage and possibly using an equipment (activator? we did not put in the paper because of the uncertainty).
    The side effect with this mode of chiropractor treatment is extremely rare as what we have reviewed. This mode of treatment can certainly be the risk factors for the outcome (we ruled out most of the other risk factors presented in our case). We are sharing this case purely for education purpose without the intention of criticising any individual and the chiropractor profession. We did not want to see any more similar cases with an almost fatal outcome. We do appreciate that the whole profession of chiropractors constantly reviews their practice to ensure the delivery of evidence-based practice for treatment effectiveness of various aches and pain (shoulder girdle and neck pain in our case), which all health professionals should practice routinely.

    Hope the response helps to clarify the queries.

    kind regards

    ...

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  • Paradoxical reactions in neurotuberculosis – what is the optimal management?

    Sindgikar et al. report a severe paradoxical reaction in a 15-year-old HIV-uninfected patient with stage III tuberculous meningitis, during her fifth month of treatment. After improving with re-initiation of corticosteroids, the paradoxical reaction worsened after the prednisolone was weaned over 8 weeks. The patient continued 4 months of corticosteroids in addition to 13 months anti-TB treatment (ATT) with significant morbidity at one year follow up, including permanent disability.

    Whilst corticosteroids are the mainstay of treatment for paradoxical reactions, their effectiveness for this difficult-to-treat complication has not been assessed in randomised controlled trials (RCT)(1). TNF-alpha is a key cytokine implicated in the exaggerated inflammatory response underlying paradoxical reactions (2,3). We have used infliximab, a monoclonal antibody targeting TNF-alpha, in the management of severe paradoxical reactions in paediatric central nervous system TB with positive outcomes (4,5). Anti-TNFα monoclonal antibodies, including infliximab, have also been used with encouraging results in adults for this indication (6,7). Thalidomide, another anti-TNF-alpha therapy was evaluated in an RCT of children with stage II and III tuberculous meningitis (8), however, this trial was ceased early due to increased deaths and adverse outcomes with a thalidomide dose of 24 mg/kg/day. A subsequent case series of 38 children treated with low-dose thalidomide (3-5 mg/kg) with life-th...

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  • Letter to the Editor regarding “Obstetric rectal laceration in the absence of an anal sphincter injury”

    Dear Editor,

    We read, with interest, “Obstetric rectal laceration in the absence of an anal sphincter injury” by Awomolo et al in your journal [1]. We commend the authors on reviewing this rare injury.

    We appreciate your detailed case report and were pleased to read that your patient recovered well from her injury. We agree that these rare injuries require careful repair with experience, good surgical technique and detailed knowledge of perineal anatomy. Your extensive literature review found other similar cases, many of which we included in our most comprehensive case series [2], but we were surprised to see that our case series was not included in your paper. Although rectal buttonhole tears are rare they are now defined in many National guidelines in the world [3]. What our paper also adds is a standardised approach for repair of isolated rectal tears and follow up, with a video demonstration on a porcine specimen. In addition, we have highlighted that rectal button hole tears can occur concomitantly with a third or 4th degree tear when there is intact bridge of anorectal mucosa between the two injuries.

    We appreciated the insufficiencies in training regarding classification, diagnosis and repair of obstetric anal sphincter injuries (OASIS) over 20 years ago and began the first hands-on course in 2000 (www.perineum.net). We have also introduced the Prevention and Repair Of perineal Trauma Episiotomy through Co...

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  • Misrepresentation of chiropractic in a case of carotid artery dissection

    We read with interest the case report by Yap et al regarding “A near-fatal consequence of chiropractor massage: massive stroke from carotid arterial dissection and vertebral arterial oedema,”(1) which describes a 35-year-old man with a massive stroke purportedly caused by massage. Cerebrovascular disease is an invested topic for manual therapists, considering such providers are responsible for recognizing emergent signs/symptoms of a cervical artery dissection (CeAD) and referring accordingly,(2) however, we are concerned about appropriate and accurate reporting of details of the case including several inconsistencies and evident biases.

    We believe this case report likely misclassifies the treating provider as a chiropractor. The report does not specify the credentials of the person providing massage during the business trip. As pointed out by the authors, there is limited regulation and licensing of chiropractic in China.(3) Furthermore, spinal manipulation is by far the most common treatment intervention provided by chiropractors(4) but the authors did not mention its use in the case presentation.

    We request the authors clarify the credentials of the massage provider, and elaborate on treatment interventions, specifically if cervical spinal manipulation was performed. Previous case reports have misrepresented the treating provider as a chiropractor when describing potential adverse events.(5) This practice is spurious and adds to over-reporting of adverse...

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