The article on a neurological MRI menagerie by Jonathan Schott1 was a good read. I would like to highlight an important and potentially treatable differential diagnosis for the “eye of the tiger” sign, highlighted by Professor Patrick Chinnery in his interesting talk at the 29th Advanced Clinical Neurology Course in Edinburgh in May this year and recently published in Brain. Neuroferritinopathy produce...
The article on a neurological MRI menagerie by Jonathan Schott1 was a good read. I would like to highlight an important and potentially treatable differential diagnosis for the “eye of the tiger” sign, highlighted by Professor Patrick Chinnery in his interesting talk at the 29th Advanced Clinical Neurology Course in Edinburgh in May this year and recently published in Brain. Neuroferritinopathy produces similar neuroradiological changes to pantothenate kinase-associated neurodegeneration. In males and non-menstruating females, the serum ferritin will help to distinguish panthotenate kinase deficiency from neuroferritinopathy.
Sui H Wong
References
1. Schott JM. A neurological MRI menagerie. Pract Neurol 2007;7:186–90.
2. Chinnery PF. Clinical features and natural history of
neuroferritinopathy caused by the GTL1160InsA mutation. Brain 2007;130:110–19.
In Figure 1c, in Little et al’s article on diabetic neuropathy (1), there is a glove and stocking distribution of sensory loss, but with extensive involvement of the upper limbs. This is exactly the distribution of sensory loss in patients with leprosy, demonstrated in 1923 by Monrad-Krohn and shown in the Figure (2). This was a meticulous clinical examination of 63 Norwegian patients. While multiple...
In Figure 1c, in Little et al’s article on diabetic neuropathy (1), there is a glove and stocking distribution of sensory loss, but with extensive involvement of the upper limbs. This is exactly the distribution of sensory loss in patients with leprosy, demonstrated in 1923 by Monrad-Krohn and shown in the Figure (2). This was a meticulous clinical examination of 63 Norwegian patients. While multiple mononeuropathies are well described in leprosy, a sensory polyneuropathy is not recognised by
neurologists, despite a similar pattern of sensory loss being found in a group of leprosy patients in northern Nigeria, in a study carried out without prior knowledge of Monrad-Krohn’s findings (3).
Trophic ulcers, tapering of the heads of the metatarsals and Charcot’s joints are complications which occur in both diabetics and leprosy patients (4). For these reasons, and because of the similarity in the distribution of the sensory loss, an animal autoimmune model of non-lepromatous leprosy using sensory peripheral nerve as antigen (5), could be used to study the pathogenesis of diabetic neuropathy, especially as the ‘characteristic degenerative changes’ in the human disease do not develop in the streptozotocin-diabetic rat (6). There is, however, an important difference between the two disorders, in that postural hypotension is not a feature of leprous polyneuropathy (3) and hence adrenergic function is not impaired.
Little et al. state that the ‘spontaneous shooting and stabbing pains are small fibre sensations due to dysfunction of thinly myelinated A-gamma and unmyelinated C fibres’. (The thinly myelinated fibres are A-delta rather than A-gamma fibres). In the autoimmune peripheral nerve model, the conduction velocity and amplitude of A delta fibres were normal, whereas there was a diminished amplitude in the slower component of C fibres5. As only a highly selective group of neurons are affected in this autoimmune model, depletion of a growth factor may be
implicated, but is unlikely to be nerve growth factor (5,7) as adrenergic function is normal in leprosy polyneuropathy.
REFERENCES
1. Little AA, Edwards JL, Feldman EL. Diabetic neuropathies. Pract Neurol2007; 7: 82-92.
2. Monrad-Krohn GH. The neurological aspect of leprosy. Christiania; Jacob Dybwad,. 1923.
Thanks to Kevin Talbot for a wise and timely caution, prefaced by an apt quotation from Jeremy Bentham. Bentham also observed:
"He who thinks and thinks for himself, will always have a claim to thanks; it is no matter whether it be right or wrong, so as it be explicit. If it is right,
it will serve as a guide to direct; if wrong, as a beacon to warn. "
Thanks to Kevin Talbot for a wise and timely caution, prefaced by an apt quotation from Jeremy Bentham. Bentham also observed:
"He who thinks and thinks for himself, will always have a claim to thanks; it is no matter whether it be right or wrong, so as it be explicit. If it is right,
it will serve as a guide to direct; if wrong, as a beacon to warn. "
Given the crucial importance of evaluation of cognitive function for purposes such as assessment of capacity to make a will(1), the broadspectrum strategy employed by the Addenbrooke's Cognitive Examination(ACE)(2) will help overcome limitations of the Minimental State
Examination(MMSE) exemplified by the acknowledgement that "someone who scores 27/30 may lack capacity because of impaired judgment and...
Given the crucial importance of evaluation of cognitive function for purposes such as assessment of capacity to make a will(1), the broadspectrum strategy employed by the Addenbrooke's Cognitive Examination(ACE)(2) will help overcome limitations of the Minimental State
Examination(MMSE) exemplified by the acknowledgement that "someone who scores 27/30 may lack capacity because of impaired judgment and reasoning due to frontal lobe impirment, which is not tested by the mini-mental
state examination"(1). What the ACE now needs is validation of its diagnostic accuracy, using parameters such as sensitivity, specificity and positive predictive power(3) for each of the subtypes of demntia.
Furthermore, given the implications of quantification of the degree of severity of Alzheimer's disease for the purpose of assessing eligibility for certainn types of drug treatment(4)(5), the ACE needs to be sufficiently calibrated to distinguish between mild to moderate
Alzheimer's disease and more advanced forms of this disease.
Oscar M Jolobe
References
(1)Jacoby R., Steer P. How to assess capacity to make a will British Medical Journal 2007:335:155-7
(2)Bak TH., Mioshi E. A cognitive bedside assessment beyond the MMSE: the Addenbrooke's Cognitive Examination
Practical Neurology 2007:7:245-9
(3)Cullen B., O'Neill B., Evans JJ et al. A review of screening tests for cognitive impairment Journal of Neurology, Neurosurgery and Psychiatry 2007:78:790-99
(4) Loveman E., Green C., Kirby J et al. The clinical and cost-effectiveness of donepezil, rivastigmine,
galantamine and memantine for Alzheimer's disease
Health Technology Assessment 2006:10(1):iii-iv, ix-xi, 1-160
(5) Dyer O High court backs NICE's decision on Alzheimer's drugs British Medical Journal 2007:335:319
Although chronic daily headache is considered by some neurologists to be one of the least engaging parts of their job(1), the author, nevertheless did remarkable justice to the topic in his review(1). Among the recent developments in the evaluation of chronic headache, ranging from headaches which occured daily to headaches occuring 2 to 3 times a month, was a retrospective analysis of symptom outcome...
Although chronic daily headache is considered by some neurologists to be one of the least engaging parts of their job(1), the author, nevertheless did remarkable justice to the topic in his review(1). Among the recent developments in the evaluation of chronic headache, ranging from headaches which occured daily to headaches occuring 2 to 3 times a month, was a retrospective analysis of symptom outcome following interventional treatment of unruptured intracranial aneurysms in 49
patients who presented with preoperative chronic headache(including chronic daily headache)(2). All 49 had a history of chronic headache compliant with the definition used by the International Headache Society(3), and , in all 49 instances, comorbid neurological disorders(including giant aneurysms) which were potential causes of
chronic headache had been excluded, as were comorbid diseases such as psychosis and hepatic encephalopathy(2). Among the 49 patients meeting the strict inclusion criteria 32 experienced marked improvement in headache(by
2 or more grades) following interventional treatment of intracranial aneurysms. As the authors themselves state, these observations do however require cautious interpretation in view of the retrospective nature of the
study(giving rise to recall bias), and the possibility of a placebo effect(2). Furthermore, for the purposes of a review of chronic daily headache such as the one reported above(1), the authors did not specifically analyse the outcome in the subgroup of chronic headache patients in whom the headaches were of daily occurence(2).
(2)Kong D-S., Hong S-L., Jung Y-J., Kim JS. Improvement of chronic headache after treatment of unruptured intracranial aneurysms Headache 2007:47:693-7
(3)Headache Classification Subcommittee of the International Headache Society. The International Classification of Headache Disorders, 2nd Ed.
Cephalalgia 2004;24(suppl 1):9-160
This article highlights an important aspect of scientific training not only to neurologists, but to all clinicians. Advances in neuroimaging,genetic analysis and molecular biology constantly advance our understanding of disease and challenge our approach to treating patients.
This demands that even clinically oriented neurologists and neurosurgeons have not only a basic understanding of the process o...
This article highlights an important aspect of scientific training not only to neurologists, but to all clinicians. Advances in neuroimaging,genetic analysis and molecular biology constantly advance our understanding of disease and challenge our approach to treating patients.
This demands that even clinically oriented neurologists and neurosurgeons have not only a basic understanding of the process of rigourous scientific method, but also of the ethical and socio-economic impact of these changes. It is hoped that by doing a postgraduate degree,these goals might be achieved.
Post-graduate training has traditionally meant taking time out of clinical training to do one's degree.Frequently the research project that is undertaken has little bearing on the actual clinical impact the doctor will make in their careers. A research degree should have a clear practical application to the student who is going to undertake it. In that regard, the challenge for clinical neuroscientists is to develop projects that are career driven and clinically relevant.
As a neurosurgical trainee,I found that a Clinical Neuroscience MSc was a good foundation for neurological illness. However the degree whilst teaching the fundamentals of neurological disease and neurochemistry, had very little bearing on the practice of neurological surgery. It was of tremendous value to the psychologists and neurologists on the program. Thankfully,a thesis on brain tumours saved the day. The question, each trainee needs to answer is "Does this program provide me with skills to produce clinically meaningful research that will help my patient, further my profession and advance my career?". The challenge facing postgraduate boards is to provide this within the context of clinical training.On going research should be part of clinical training,at the end of which, a clinically oriented higher degree is the result.
For the sake of completeness, mention must also be made of the role of right to left shunts, exemplified by pulmonary arteriovenous malformations attributable to hereditary haemorrhagic telangiectasia(1)(2), and also exemplified by patent dusctus arteriosus with shunt reversal(3), in the aetiopathogenesis of recurrent bacterial meningitis, both meningococcal(1), and pneumococcal(3), as well as
cerebral...
For the sake of completeness, mention must also be made of the role of right to left shunts, exemplified by pulmonary arteriovenous malformations attributable to hereditary haemorrhagic telangiectasia(1)(2), and also exemplified by patent dusctus arteriosus with shunt reversal(3), in the aetiopathogenesis of recurrent bacterial meningitis, both meningococcal(1), and pneumococcal(3), as well as
cerebral abscess(1)(2), which may simulate partially treated bacterial meningitis. In a review of 31 instances of recurrent intracranial infection(including bacterial meningitis) attributable to intrapulmonary right to left shunts blood cultures were sterile in every single
instance(2). In the event of intrapulmonary right to left shunts being a risk factor for strile blood cultures in patients with suspected blood borne intracranial sepsis, this would entail greater reliance on the clinical index of suspicion for these disorders, an index of suspicion
that would embrace even more exotic causes of intrapulmonary shunts such as the hepatopulmonary syndrome, now acknowledged to be one of the rare risk factors fro metastatic cerebral abscess(4). This does not diminish the role of blood cultures in the "work up" of suspected bactrial meningitis(5), given the fact that in bacteraemic patients with pneumococcal meningitis, positive blood culture results can be obtained within 1.2 to 10.9 hours of being ordered(6). This could amount to a
decisive diagnostic advantage in cases where the initial cerebrospinal fluid is sterile and has low cellularity(7).
Oscar M Jolobe
References
(1) Hazouard E., Ritz-Quillacq L., Herbreteau D et al
Weber-Rendu-Osler disease:pulmonary arterio-venous malformation with shunt disclosed after 5 occurences of purulent meningococcal encephalitis(article in French: abstract in English)Revue des Maladies Respratoires 1999:16:95-7
(2) Press OW., Ramsey PG Central nervous system infections associated with hereditary hemorrhagic telangiectasia
American Journal of Medicine 1984:77:86-92
(3) Spencer SE., D'Cruz IA., Tenholder MF Recurrent meningitis and severe hypoxemia in a 77 year old man
CHEST 1997:112:1120-3
(4) Molleston JP., Kaufman BA., Cohen A et al
Brain abscess in hepatopulmonary syndrome Journal ogf Pediatric Gastroenterology 1999;29;225-6
(5) Schut ES., de Gans J., van de Beek D Community-acquired bacterial meningitis in adults Practical Neurology 2008:8:8-23
(6)Peralta G., Rodriguez-Lera MJ., Garrido JC et al
Time to positivity in blood cultures of adults with streptococcus pneumoniae bacteraemis BMC Infectious Diseases 2006:6:79
(7)Rapkin RH Repeat lumbar puncture in the diagnosis of meningitis Pediatrics 1974:54:34-6
I read with keen interest Dr. Davenport’s editorial” why can’t I make a neurological diagnoses anymore?” 1. I am currently in my second year of fellowship training in clinical neurophysiology in the USA and even though
I am heading down the path of superspecialization or rather subspecialization in neurology, as Dr. Davenport points out, I could not agree more with his comments.
I read with keen interest Dr. Davenport’s editorial” why can’t I make a neurological diagnoses anymore?” 1. I am currently in my second year of fellowship training in clinical neurophysiology in the USA and even though
I am heading down the path of superspecialization or rather subspecialization in neurology, as Dr. Davenport points out, I could not agree more with his comments.
Here in the USA, residency in neurology is for 3 years after one year of compulsory internship in general medicine. Fellowship training ranges in duration anywhere from one to three years with an average of one year.
It surprises me that now when I am applying for a job, I am more marketable as an epileptologist rather than as a general neurologist or rather generalist as Dr. Davenport refers to himself. Surely at least at this juncture by the virtue of the time spent in training, I am a more
competent general neurologist rather than an epileptologist. Maybe as time goes by and if I restrict myself to seeing only epilepsy patients, I would
become a competent epileptologist too. My only fear is that, then I would not know what to do if a patient with migraine walked through my office doors. I would surely need the expertise of a generalist like Dr. Davenport. Or maybe I would refer the patient to a headache specialist.
Neither of the extremes seem sensible to me and I agree with Dr. Davenport that the answer probably lies in a system that places emphasis on general neurologists, some with special interests in certain areas like epilepsy.
Nitin K.Sethi
The author reports no competing interests.
References
1. Davenport RJ. Why can't I make neurological diagnoses anymore? Pract Neurol 2008;8:74-76.
The history of celiac disease (CD) is very long. The cultivation of grains, developed in the Neolithic period after the last ice age, particularly in the “Fertile Crescent” of the Near East including the Tigris, the Euphrates and the Upper Nile. With the development of cooking, agriculture came into its own and wheat became a main support of the vast growth in population in successive millennia. Thus ar...
The history of celiac disease (CD) is very long. The cultivation of grains, developed in the Neolithic period after the last ice age, particularly in the “Fertile Crescent” of the Near East including the Tigris, the Euphrates and the Upper Nile. With the development of cooking, agriculture came into its own and wheat became a main support of the vast growth in population in successive millennia. Thus arose the possibility
of development of syndromes, including CD, reflecting intolerance of wheat. In this context is interesting that the generally accepted earliest description of CD, is attributed to “Aretaeus the Cappadocian” (I-II
century A.D.), and Cappadocia is a region in the eastern part of Turkey near to the ‘Fertile Crescent’. Further descriptions, which may have been of CD followed, by the Dutch physician Vincent Ketelaer, William Hillary
of Yorkshire, England, and others.
The origin of the modern history of CD is ascribed to Samuel Gee in a lecture in 1887 followed by his written account in the Saint Bartholomew’s Hospital Reports in 1888. He termed the condition ‘the Celiac Affection’
after the translation by Francis Adams, in 1856, of the description by Aretaeus. In a notably description, Gee refers to the appearance of the stools, the onset of the condition, the muscular weakness, the abdominal
distension and the chronic course of the disease.
Subsequent to the suggestion by Samuel Gee there were various attempts at dietary management which bore some relation to the eventual recognition of cereal grains as being responsible.
Herter in 1908 suggested that fats were better tolerated than carbohydrates, Still in 1918 drew attention to the poor tolerance of bread, Howland in 1921 recognised intolerance to carbohydrates and Haas in 1924 suggested a banana diet which, even though it contains carbohydrates,
excludes the damaging cereals.
The great breakthrough was by Wim Dicke of The Juliana Children's Hospital in The Hague. In his doctoral thesis of 1950 to the University of Utrecht he showed that exclusion of wheat, rye and oats from the diet led
to dramatic improvement in the general condition of the child and marked reduction in the fatty diarrhoea. Wheat starch did not have the same damaging effect. There are descriptions of how Dicke came across this association. During wartime the gruel supplied to children in hospital
might, at different times, have contained wheat or other plant products, depending on what was available, which would have provided the clue. Confirmation came with Dicke's laboratory colleagues Weijers and Van de
Kamer. With the chemical measurement of stool fat, it became possible to diagnose less severe cases showing that excluding wheat, rye, barley and oats led to reduction in the fat content of the stool and improvement in the clinical condition of the patient. French, showed that similar changes occurred in adults with otherwise unexplained steatorrhoea. Faecal fat is rarely estimated now because of the requirements for accurate diet and
prolonged collection of stools, and the associated expense.
Since wheat starch did not produce the effect, attention was drawn to the protein components of the relevant cereals, referred to as gluten since the work of Jacopo Bartolomeo Beccari in Bologna in 1745. At present
the etiology and pathogenesis of these disorders is uncertain.
In the recent years, same relevant studies concerning CD, are performed by Professor Giovanni Gasbarrini, Director to the Institute of Internal Medicine, Catholic University of Rome, and my chief. The research Group to Professor Gasbarrini, have been described pathophysiology
mechanisms and clinical manifestations of CD and published more than 140 articles, on this topic, available in pub-med. In the May issue, Dr Grossman highlighted the relationship between CD and neurological disorders (1). Our group reported, a case of brain perfusion
abnormalities, assessed by single photon emission computed tomography (SPECT) examination, in a 33-year-old CD patient with schizophrenia; regression of both cerebral hypoperfusion and schizophrenic symptoms was
observed after 6 months of a gluten free diet (GFD) (2). On the basis of this case we performed a SPECT study evaluating regional cerebral perfusion in untreated CD adult patients (age: 37±9 years), comparing them
with CD patients on GFD, and with healthy controls (3). The study showed the presence of regional cerebral hypoperfusion in 73% of the untreated CD patients, compared with only 7% of CD patients on GFD and none of the controls. An overall multivariate test showed a significant difference in cerebral perfusion among the three groups of subjects (p=0.01).
Considering each single region, a significant lower cerebral perfusion was found in untreated celiac patients compared to controls in seven of the 26 cerebral regions evaluated. Perfusion defects were predominant in the
superior and anterior areas of the frontal cortex with the involvement of the adjacent anterior cingulated cortex. We have been reported similar cerebral blood flow changes, in patients suffering from different neurological and psychiatric disorders (4,5). In according to the author,
I suggest to early investigate the presence of CD in patients with neurological abnormalities.
To conclude I want to give my gratitude to Professor Giovanni Gasbarrini, for his scientific commitment and to be a guide for us young researchers.
Figure legend
Professor Gasbarrini (first line, the 3rd from left ), coworkers (me, first line, the 2nd from right) and medicine school students
References:
1. Grossman G. Neurological complications of coeliac disease: what is the evidence? Pract Neurol. 2008; 8:77-89.
2. De Santis A, Addolorato G, Romito A, et al. Schizophrenic symptoms and SPECT abnormalities in a coeliac patient: regression after a gluten-free diet. J Intern Med 1997; 242: 421-23.
3. Addolorato G, Di Giuda D, De Rossi G, et al. Regional cerebral hypoperfusion in patients with celiac disease. Am J Med 2004; 116: 312-17.
4. Gabrielli M, Cremonini F, Fiore G, et al. Association between migraine and celiac disease. Am J Gastroenterol 2003; 98: 625-29
5. Addolorato G, Leggio L, D'Angelo C, et al. Affective and psychiatric disorders in celiac disease. Dig Dis. 2008; 26: 140-48.
Further to previous articles on the "ice-on-eyes" test or ice-pack test in myasthenia gravis,1,2 a prior report pooling six studies adjudged to have sufficient clinical and experimental detail (n = 76 patients with
myasthenia gravis, n = 77 non-myasthenic patients with ptosis), rather than just the two studies alluded to by Reddy & Backhouse,1 gave a test sensitivity of 89% and specificity of 100%....
Further to previous articles on the "ice-on-eyes" test or ice-pack test in myasthenia gravis,1,2 a prior report pooling six studies adjudged to have sufficient clinical and experimental detail (n = 76 patients with
myasthenia gravis, n = 77 non-myasthenic patients with ptosis), rather than just the two studies alluded to by Reddy & Backhouse,1 gave a test sensitivity of 89% and specificity of 100%. However, these specificity data should be viewed with some caution: in addition to
reports of false positive testing in non-myasthenic diplopia4 and Miller Fisher syndrome,2 false negative testing in myasthenia has also been reported.3 A negative ice pack test does not unequivocally exclude the
diagnosis of myasthenia, nor a positive test establish it.
References
1. Reddy AR, Backhouse OC. "Ice-on-eyes", a simple test for myasthenia gravis presenting with ocular symptoms. Pract Neurol 2007;7:109-11.
2. Reid JM, Morrison I, Gorrie G, Metcalfe R. Positive "ice-on-eyes" test in Miller Fisher syndrome. Pract Neurol 2008;8:193-4.
3. Larner AJ. The place of the ice pack test in the diagnosis of myasthenia gravis. Int J Clin Pract 2004;58:887-8.
4. Larner AJ, Thomas DJ. Can myasthenia gravis be diagnosed with the "ice pack test"? A cautionary note. Postgrad Med J 2000;76:162-3.
Dear Editor,
The article on a neurological MRI menagerie by Jonathan Schott1 was a good read. I would like to highlight an important and potentially treatable differential diagnosis for the “eye of the tiger” sign, highlighted by Professor Patrick Chinnery in his interesting talk at the 29th Advanced Clinical Neurology Course in Edinburgh in May this year and recently published in Brain. Neuroferritinopathy produce...
Dear Editor,
In Figure 1c, in Little et al’s article on diabetic neuropathy (1), there is a glove and stocking distribution of sensory loss, but with extensive involvement of the upper limbs. This is exactly the distribution of sensory loss in patients with leprosy, demonstrated in 1923 by Monrad-Krohn and shown in the Figure (2). This was a meticulous clinical examination of 63 Norwegian patients. While multiple...
Dear Editor,
Thanks to Kevin Talbot for a wise and timely caution, prefaced by an apt quotation from Jeremy Bentham. Bentham also observed:
"He who thinks and thinks for himself, will always have a claim to thanks; it is no matter whether it be right or wrong, so as it be explicit. If it is right, it will serve as a guide to direct; if wrong, as a beacon to warn. "
John M S Pearce
...Dear Editor,
Given the crucial importance of evaluation of cognitive function for purposes such as assessment of capacity to make a will(1), the broadspectrum strategy employed by the Addenbrooke's Cognitive Examination(ACE)(2) will help overcome limitations of the Minimental State Examination(MMSE) exemplified by the acknowledgement that "someone who scores 27/30 may lack capacity because of impaired judgment and...
Dear Editor,
Although chronic daily headache is considered by some neurologists to be one of the least engaging parts of their job(1), the author, nevertheless did remarkable justice to the topic in his review(1). Among the recent developments in the evaluation of chronic headache, ranging from headaches which occured daily to headaches occuring 2 to 3 times a month, was a retrospective analysis of symptom outcome...
Dear Editor,
This article highlights an important aspect of scientific training not only to neurologists, but to all clinicians. Advances in neuroimaging,genetic analysis and molecular biology constantly advance our understanding of disease and challenge our approach to treating patients. This demands that even clinically oriented neurologists and neurosurgeons have not only a basic understanding of the process o...
Dear Editor
For the sake of completeness, mention must also be made of the role of right to left shunts, exemplified by pulmonary arteriovenous malformations attributable to hereditary haemorrhagic telangiectasia(1)(2), and also exemplified by patent dusctus arteriosus with shunt reversal(3), in the aetiopathogenesis of recurrent bacterial meningitis, both meningococcal(1), and pneumococcal(3), as well as cerebral...
Dear Editor,
I read with keen interest Dr. Davenport’s editorial” why can’t I make a neurological diagnoses anymore?” 1. I am currently in my second year of fellowship training in clinical neurophysiology in the USA and even though I am heading down the path of superspecialization or rather subspecialization in neurology, as Dr. Davenport points out, I could not agree more with his comments.
Here in the U...
Dear Editor
The history of celiac disease (CD) is very long. The cultivation of grains, developed in the Neolithic period after the last ice age, particularly in the “Fertile Crescent” of the Near East including the Tigris, the Euphrates and the Upper Nile. With the development of cooking, agriculture came into its own and wheat became a main support of the vast growth in population in successive millennia. Thus ar...
Dear Editor
Further to previous articles on the "ice-on-eyes" test or ice-pack test in myasthenia gravis,1,2 a prior report pooling six studies adjudged to have sufficient clinical and experimental detail (n = 76 patients with myasthenia gravis, n = 77 non-myasthenic patients with ptosis), rather than just the two studies alluded to by Reddy & Backhouse,1 gave a test sensitivity of 89% and specificity of 100%....
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