129 e-Letters

  • Missing a trick

    I enjoyed this article on this important area of non-traumatic non-aneurysmal convexity SAH. The authors seems to have not recognised the literature that points to convexity/Sulcal subarachnoid haemorrhage in the context of ipsilateral carotid artery stenosis, which in some case series make up a significant proprtion of the cases (10-50%, references below). Also I would be cautious about having dichotomoised age as a rule, but better as a guide. In the case of carotid artery stenosis this is seen in the under 60s sometimes.

    Geraldes et al J Stroke Cereb Dis 23:e23-30, 2014.
    Zhao et al J Int Med Res 2017 45:1870.
    Renou et al 2012 Cerebrovasc Dis. 2012;34(2):147-52.
    Forman et al; J Stroke Cerebrovasc Dis. 2019;28(12):104473.

  • Amantadine is a N-metyhl-d-aspartate (NMDA) antagonist.

    Amantadine is not a N-metyhl-d-aspartate (NMDA) receptor agonist as stated in the paper, as it's a NMDA antagonist.

    - Vanle B, Olcott W, Jimenez J, Bashmi L, Danovitch I, IsHak WW. NMDA antagonists for treating the non-motor symptoms in Parkinson's disease. Transl Psychiatry. 2018 Jun 15;8(1):117. doi: 10.1038/s41398-018-0162-2. PMID: 29907742; PMCID: PMC6003962.,
    - Kornhuber J, Weller M, Schoppmeyer K, Riederer P. Amantadine and memantine are NMDA receptor antagonists with neuroprotective properties. J Neural Transm Suppl. 1994;43:91-104. PMID: 7884411.

    Note from the editors:
    an erratum will be published

  • Response

    I read the article by Alvar Paris et al. with great interest. The consumption of nitrous oxide (N2O) has recently surfaced as an exponentially growing form of recreational abuse, particularly among students, due to its euphoric effects and accessibility. The European Monitoring Centre for Drugs and Drug Addiction has expressed concern in a recent report about the recreational use of N2O in Europe. 1
    The most common neurological complications associated with N2O consumption are toxic polyneuropathy and subacute combined degeneration of the spinal cord (N2O-SACD), which may occur concurrently— a critical aspect that should not be overlooked. Initial clinical descriptions of N2O-SACD were reported in 2015 and complicated episodic use mediated through canisters. 2 Recently, the market for N2O distribution has expanded with diverse consumption accessories. The introduction of larger cylinders facilitates the consumption of significant amounts of N2O, posing younger individuals at an elevated risk of early and severe Vitamin B12 deficiency along with systemic complications. Consequently, new complications associated with N2O intoxication have been described, and their wide-ranging effects are regularly emphasized in the literature.
    Beyond psychiatric symptoms like hallucinations, cognitive impairments including Gayet-Wernicke's encephalopathy have been recently reported. 3 These deficiencies are mediated by Vitamin B1 levels, suggesting a risk of broader deficie...

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  • erratum to the article

    The authors of this article would like to apologise for omitting a reference to The Northwick Park Integrated Care Pathway (ICP) for Management of Hemiplegic Shoulder Pain. Further information about the pathway, its tools and ongoing development, may be found here (https://www.kcl.ac.uk/cicelysaunders/resources/management-of-hemiplegic-...) and in the following 2 citations:

    D. Jackson, L. Turner-Stokes, A. Khatoon, H. Stern, L. Knight & A. O'Connell (2002). Development of an integrated care pathway for the management of hemiplegic shoulder pain, Disability and Rehabilitation, 24:7, 390-398,

    Jackson D, Turner-Stokes L, Williams H, Das-Gupta R. Use of an integrated care pathway: a third-round audit of the management of shoulder pain in neurological conditions. J Rehabil Med. 2003 Nov;35(6):265-70.

  • Orbital bruits

    I was interested to read the article by Andrew Larner in Practical Neurology suggesting that listening for orbital bruits is “useful for impressing students but is not very rewarding”.

    I had not heard of Charles Warlow’s challenge before.

    My mentor as a trainee, Bernard Gilligan, would routinely listen to carotids and orbits and often femoral arteries as well - we saw a lot of large vessel arterial disease in those days – and I got into the habit of auscultating at least carotids and orbits.

    It paid off at least once: I enclose extracts from a letter I wrote in 2001.

    Thank you for referring this most interesting 30 year old lady. She has had migraines from her early twenties. Initially they were quite occasional but severe when they occurred. They tended to be triggered by exams or stress.

    She moved to Australia about 3 years ago and since then has had unusual episodes of bouts of migraine. In the first of these she had migraine every day for a week or so. Since then the attacks seem to be becoming more frequent and more prolonged so that the most recent one which finished about 2 weeks ago had lasted for 3 weeks or more.

    Typically at the start of a bout she will have aura symptoms consisting of numbness of the left finger, arm and face and blurred vision in the left visual field. In the early days of a bout there may be no headache following this. However then a pattern establishes with headache occurring on a virtually...

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  • Preventing vision loss in giant cell arteritis

    In their review on vision loss in giant cell arteritis (GCA), the authors point out that anterior arteritic ischaemic optic neuropathy is the most common ophthalmic manifestation of the disease, followed by central retinal artery or cilioretinal artery occlusion and posterior ischaemic optic neuropathy. We do agree that these ocular findings must be quickly diagnosed to prevent devastating visual consequences. When diagnosed, however, not much can be done to restore the visual function. We rather believe that more emphasis should be given to other ophthalmic features that can occur as the initial manifestation of GCA and, when unrecognized, can result in an unfortunate late diagnosis. These include amaurosis fugax, uveitis, anterior or posterior scleritis and ocular pain. Awareness of these uncommon ocular conditions as the presenting signs of impending visual loss in GCA should prompt clinicians to consider this diagnosis in any elderly patient presenting with ophthalmic manifestations other than permanent visual loss, especially if other signs of GCA are detectable.

  • Pain in locked-in Guillain-Barré syndrome: pathophysiological and therapeutic thoughts

    I read with great interest the excellent paper by Kumta and colleagues1 and the accompanying editorial2 concerning a patient with severe Guillain-Barré syndrome (GBS) requiring mechanical ventilation, who provided his experiences during the 31-day period of locked-in syndrome. I wish to open up some insights on the reported pain.
    Physical therapy, in particular the passive stretching of calf and masseter muscles, provoked him intense pain, the patient’s description being very impressive: “It felt like they were trying to tear the muscles off the bone … I’ve never known pain like it” 1. Pain due to peripheral nerve damage is basically divided into two major types: dysesthetic pain and nerve trunk pain, the distinction between them being based upon clinical observation and experience3. Reported aching characteristics in the current patient (excruciating, deep, and provoked by nerve stretch) points to nerve trunk pain.
    Pain is an integral manifestation of GBS. In a series of 55 consecutive GBS patients, Moulin and colleagues analysed pain features4, which could be summarised as follows: i/ 49 (89%) patients described pain during the course of their illness; ii/ in around half of them, it was described as excruciating; and iii/ pain preceded weakness by a mean of 5.3 days in 14, and both symptoms appeared simultaneously in seven. Furthermore, in “pure” motor GBS syndromes, usually classified as acute motor axonal neuropathy (AMAN), nerve trunk pain may occur in a h...

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  • Phenytoin in trigeminal neualgia

    Your artclce mentions phenytoin as a treatment that has been tried in open label studies. When I began as a neurologist I'd not heard of its use but was put on to it by a senior colleague. I do use carbamazepine as first line but have found phenytoin far superior to other second line agents. I draw the interested reader to the excellent article by Hellelink and Schatman (J Pain Res. 2017; 10: 1663-6 doi: 10.2147/JPR.S141896) which puts a case for phenytoin being considered first line.

  • Response to article by Rowe et al

    To the editor

    Although Rowe and colleagues make it clear that the most important purpose of their review is to cover the neglected aspect of management of Progressive Supranuclear Palsy (1) they also describe the disorder’s clinical symptoms and signs and its differential diagnosis in some detail. In this section of the article they fail to mention two simple bedside tests which I have found particularly useful over the years in making me more certain about my diagnosis. In those patients where Parkinson’s disease is the main differential diagnosis sequential finger tapping for 20 seconds is frequently informative. A progressive reduction in speed and amplitude ( ‘the sequence effect’) is a sine qua non for Parkinson’s disease but is rarely found in Progressive Supranuclear Palsy where marked reduction in amplitude of finger taps without decrement and preserved speed of movement is much more usual (2). Utilisation and imitation behaviour (3, 4) and the applause sign (5), all indicative of prefrontal lobe dysfunction, are very common in fully established Richardson’s syndrome but I have also found them to be sometimes present early on particularly when abulia or behavioural abnormalities are presenting complaints. The grasp reflex on the other hand is not commonly observed
    The diagnosis of Progressive Supranuclear Palsy is difficult and uncertainty is common particularly in the early stages. To retract a diagnosis of Progressive Supranuclear Palsy is tri...

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  • Response to Response by A Lees

    To the Editor,

    We agree with Andrew Lees on the value of the applause sign (i.e. ask a PSP patient to clap 3 times, and they typically perseverative by clapping more than 3 times) and a lack of decrement on hypokinesia tests (e.g. sequential finger tapping or in micrographic writing, without a progressive reduction in amplitude) to differentiate Progressive Supranuclear Palsy from Parkinson’s disease. Both are very useful, easy bedside tests.

    We also agree that there are cases where one is unsure. A diagnosis of Progressive Supranuclear Palsy is not to be given lightly, as for any other disease. But, patients with Progressive Supranuclear Palsy have suffered disproportionately from delays and diagnostic hesitation, often long past any reasonable doubt. It does not help a patient or family to live with a wrong diagnosis, or no diagnosis, for a large part of their illness. Across many countries, the diagnosis of PSP is made at around three years from symptom onset (Murley et al, 2021; Cosseddu et al 2017; Mamarabadi et al, 2018). In other words, halfway from onset to death. This is unnecessarily long. Greater awareness and simple clinical skills can reduce the diagnostic delay by more than a year (Mamarabadi et al, 2018). Through our article, we hope our colleagues can become more confident, early and accurate in making the diagnosis of PSP as a gateway to better care.

    James Rowe, Tim Rittman and Negin Holland


    Mamarabadi M, R...

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