It is not correct that the Democratic Party has historically been the
major underwriter of biomedical research in the USA. American science,
and biomedical science in particular, benefited historically from
substantial bipartisan support. The major increase in NIH funding of the
Clinton period owed at least as much to actions of moderate Republicans
like Rep. John Porter (Republican of Illinois) an...
It is not correct that the Democratic Party has historically been the
major underwriter of biomedical research in the USA. American science,
and biomedical science in particular, benefited historically from
substantial bipartisan support. The major increase in NIH funding of the
Clinton period owed at least as much to actions of moderate Republicans
like Rep. John Porter (Republican of Illinois) and Sen. Arlen Spector
(Republican of Pennsylvania) as it did to the Clinton administration. The
predominance of the hard right in the Republican Party, with its
marginalization of Republican moderates, and the anti-intellectualism of
the Bush administration had a deplorable effect on federal funding of
science. Bush administration science funding policies, however, are not
the historic norm of the Republican Party.
I write as a fervent Obama supporter and very, very left of center
Democrat - but fair is fair.
Richard Hughes does not include leprosy in his list of peripheral
nerve disorders.(1) While it is true that new cases of leprosy are
declining rapidly , as a result of effective anti-bacterial therapy, there
are still frequent numbers with residual disabilities in endemic
countries.
In neurological text books, a mononeuropathy or multiple
mononeuropathy is regarded as the sole neurolog...
Richard Hughes does not include leprosy in his list of peripheral
nerve disorders.(1) While it is true that new cases of leprosy are
declining rapidly , as a result of effective anti-bacterial therapy, there
are still frequent numbers with residual disabilities in endemic
countries.
In neurological text books, a mononeuropathy or multiple
mononeuropathy is regarded as the sole neurological lesion in leprosy. In
1923, Monrad-Krohn described a sensory polyneuropathy involving
superficial sensory modalities in patients with leprosy.(2) A similar
pattern of sensory loss was found in a group of northern Nigerian leprosy
patients, without prior knowledge of Monrad-Krohn’s observations.(3)
There are still no references to Monrad-Krohn’s findings in neurological
text books. This omission is serious because a patient with this sensory
polyneuropathy can develop trophic ulcers, mutilation of the extremities
and Charcot’s joints. Moreover, this polyneuropathy, because of the
distribution of the sensory loss, cannot be caused by direct invasion of
the peripheral nerves by Mycobacterium leprae
Sensory loss in leprosy can be acute in onset with simultaneous
involvement of all four limbs(3) and could be an autoimmune response to an
antigen in sensory peripheral nerve rather than a direct response to
M.leprae . In order to test this hypothesis, rabbits were injected with a
homogenate of human sensory peripheral nerve plus adjuvant and
electrophysiological recordings were made from the hind limb. It was found
there was a diminished amplitude in the slower component of C fibres but
the conduction velocity and amplitude of A delta fibres were normal.(4) An
animal model of diabetic neuropathy could be developed as a result of
these experiments.(5) Some of the rabbits previously injected with sensory
nerve developed a state of granulomatous hypersensitivity. ie. Skin
testing in sensitised rabbits results in the formation of a granuloma,(6)
with invasion of mononuclear cells into the endoneurium of dermal nerves,
together with axonal damage.(7) The antigen involved is a non-myelin
membrane fraction.(8) A similar antigen in the central nervous system
could be used to induce tolerance, which if successful could lead to a
vaccine against multiple sclerosis.(9)
The observations on the clinical aspects of leprosy may therefore
lead to a greater understanding of the pathogenesis of diabetic neuropathy
and multiple sclerosis, in which case it will reinforce the maxim that
there is no substitute for precise clinical examination, with no need for
auxiliary aids, apart from a pin and a piece of cotton wool.
7. Crawford CL, Hardwicke PMD. Somatic unmyelinated degeneration in
rabbits with granulomatous hypersensitivity produced by a non-myelin
antigen sensory peripheral nerve.
Acta Neuropath 1979; 45: 1-7.
8. Hardwicke PMD, Crawford CL. Nature of the antigen of human sensory
nerve that induces granulomatous hypersensitivity.
J Neurochem 1978; 30:
1609-1611.
9. Crawford CL. Is it possible to induce oral tolerance using a non-myelin
peripheral nerve antigen?
Available at
http://www.jci.org/eletters/view/32132 Accessed 22 January 2009.
I wish to commend the authors for their paper on functional vitamin
B12 deficiency.
It is important that despite the array of investigative tools that may be
available at the disposal of clinicians, clinical signs and symptoms are
given their due emphasis particularly in Vitamin B12 deficiency. The
authors report a case where the serum cobalamin was normal in the face of
anaemia and neurol...
I wish to commend the authors for their paper on functional vitamin
B12 deficiency.
It is important that despite the array of investigative tools that may be
available at the disposal of clinicians, clinical signs and symptoms are
given their due emphasis particularly in Vitamin B12 deficiency. The
authors report a case where the serum cobalamin was normal in the face of
anaemia and neurological damage, at the other end of the spectrum are
cases with normal haemoglobin levels but with significant morbidity. A
recent report by Rajkumar AP and Jebaraj P (1) was of a non anaemic
patient with psychosis who returned to complete self care following
treatment with Vitamin B12.
The diagnostic value of properly elicited clinical signs and symptoms
cannot be overemphasized.
Reference
1. Chronic Psychosis associated with Vitamin B12 deficiency.
J Assoc
Physicians India 2008 Feb; 56: 115-6
We read with great interest the review by Grossman on neurologic
complications of celiac disease in a recent issue of Pract Neurol.(1)
Using an evidence-based approach, the author has carefully and critically
analyzed articles published in the last decade on the most common
neurologic manifestations associated with celiac disease, namely ataxia,
epilepsy, and peripheral neur...
We read with great interest the review by Grossman on neurologic
complications of celiac disease in a recent issue of Pract Neurol.(1)
Using an evidence-based approach, the author has carefully and critically
analyzed articles published in the last decade on the most common
neurologic manifestations associated with celiac disease, namely ataxia,
epilepsy, and peripheral neuropathy.
Grossman has rigorously dissected the evidence for, and against, the
possible association of celiac disease with neurological manifestations.
The association, the review concludes, does not seem to hold up when
referral bias is considered or when strict criteria are applied.
While still leaving open the possibility of an association between celiac
disease and certain neurologic disorders, the author calls for well-
controlled and prospective studies to help clarify the issue.
We would like to call attention to a 2-year prospective study, which was
recently published.(2)
After a retrospective study of a cohort of celiac children, where we did
not find a correlation between neurologic manifestations and improvement
on gluten-free diet (3), we undertook a prospective study in an adult
celiac population in order to evaluate the incidence of neurologic
symptoms and examine the response to gluten-free diet.
Our prospective study enrolled 71 patients with histologically proven
celiac disease, who were prospectively followed for up to 28 months.
Of the 71 patients, 69 were consecutively referred to our centre from the
university’s gastroenterology department, whereas 2 directly sought
treatment at our clinic for neuropathic symptoms. Forty-two patients were
on gluten-free diet at recruitment. Adherence to the diet was assessed by
testing for anti-transglutaminase antibodies. All patients underwent
neurological and electrophysiological evaluation at recruitment and at
every follow-up visit.
The results of the prospective study showed that 3 patients were affected
by sensory-motor polyneuropathy. However, 2 of the 3 patients with
polyneuropathy had sought treatment at our clinic for neuropathic
symptoms. Considering this referral bias, only one of the 69 celiac
patients referred for evaluation was affected by neuropathy. Several other
manifestations affecting the nervous system were detected in our celiac
population (4 with headache, 4 with depression, 4 with entrapment
syndromes, 1 with facial hemispasm, and one of the 3 patients with
neuropathy was also affected by epilepsy). However, the relatively common
occurrence in the general population of headache, depression, and
entrapment neuropathies makes it difficult to conclude a likely
association with celiac disease.
Antibody reactivity to neural antigens was detected in 30/71 (42.2%)
patients, but there was no clear correlation between anti-neural
reactivity and active neurologic dysfunction.
Follow-up of 62 patients during gluten-free diet did not reveal
significant changes in electrophysiology. However, in 2 patients with
neuropathy, improvement in symptoms did correlate with the diet.
In conclusion, the results of our prospective study do not seem to support
a causal relationship between biopsy-proven celiac disease and neurologic
disease in the studied group of patients.
We agree with Grossman that further well-controlled studies are warranted
in order to clarify the relationship, as well as the effect of diet.
The use of proper outcome measures should be considered when evaluating
therapeutic efficacy of any intervention (e.g. diet) in such a
heterogeneous disease.(4)
While further research may end up refuting an association between celiac
disease and neurologic dysfunction, gluten sensitivity, as defined only on
the basis of presence of anti-gluten antibodies, might prove to have a
connection with certain neurologic and psychiatric deficits.(5)
The potential relevance and significance of elevated levels of these
antibodies in the absence of celiac disease deserve proper attention as
well and should not be overlooked.
References
1. Grossman G. Neurological complications of coeliac disease: what is
the evidence?
Pract Neurol. 2008;8:77-89.
2. Briani C, Zara G, Alaedini A, Grassivaro F, Ruggero S, Toffanin
E, Albergoni MP, Luca M, Giometto B, Ermani M, De Lazzari F, D’Odorico A,
Battistin L. Neurological complications of celiac disease and autoimmune
mechanisms: a prospective study.
J Neurommunol. 2008;195(1-2):171-5.
3. Briani C, Ruggero S, Zara G, Toffanin E, Ermani M, Betterle C,
Guariso G. Anti-ganglioside antibodies in children with celiac disease: correlation
with gluten-free diet and neurological complications.
Alimentary
Pharmacology and Therapeutics, 2004;20:231-235.
4. Hobart JC, Cano SJ, Zajicek JP, Thompson AJ. Rating scales as
outcome measures for clinical trials in neurology: problems, solutions,
and recommendations.
Lancet Neurol. 2007;6:1094-105.
5. Briani C, Samario D, Alaedini A. Celiac disease: from gluten to
autoimmunity.
Autoimmun Rev. 2008;7(8):644-50.
I read with interest the important case report of Turner and Talbot
describing clinical subacute combined degeneration in a patient with
“functional” vitamin B12 deficiency (defined by elevated levels of the B12
-dependent metabolites, methylmalonic acid and homocysteine, despite
normal serum B12 values).1 It is important to note that although their
patient did not improve with hydroxycobalamin the...
I read with interest the important case report of Turner and Talbot
describing clinical subacute combined degeneration in a patient with
“functional” vitamin B12 deficiency (defined by elevated levels of the B12
-dependent metabolites, methylmalonic acid and homocysteine, despite
normal serum B12 values).1 It is important to note that although their
patient did not improve with hydroxycobalamin therapy, progression of her
disease was halted. This pattern is consistent with B12 deficiency since
neurologic changes become irreversible if B12 therapy is delayed for more
than 6 months.2
Importantly, functional vitamin B12 deficiency may be far more
prevalent than classic B12 deficiency where serum vitamin B12 levels are
clearly depressed.3 Moreover, recent reports suggest that vitamin B12
therapy can indeed improve neuropathy in some patients with functional B12
deficiency as well as in some patients with normal B12, methylmalonic acid
and homocysteine values.3-5 Finally, B12, methylmalonic acid and
homocysteine values have been shown to fluctuate widely in untreated
individuals.3 Thus, when the clinical picture is consistent with B12
deficiency, therapeutic trials of B12 should be considered regardless of
the results of B12 and metabolite testing.
2. Chanarin I. The Megaloblastic Anaemias, 2nd Edition, Oxford, UK.
Blackwell Scientific Publications, 1979:287-290.
3. Solomon LR. Cobalamin-responsive disorders in the ambulatory care
setting” unreliability of cobalamin, methylmalonic acid and homocysteine
testing.
Blood 2005; 105:978-985.
4. Solomon LR. Disorders of cobalamin (vitamin B12) metabolism:
emerging concepts in pathophysiology, diagnosis and treatment.
Blood
Reviews 2007; 21:113-130.
5. Nardin RA, Amick ANH, Raynor EM. Vitamin B12 and methylmalonic acid
levels in patients presenting with polyneuropathy.
Muscle Nerve 2007;
36:532-535.
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.
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.
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.
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
Dear Editor,
It is not correct that the Democratic Party has historically been the major underwriter of biomedical research in the USA. American science, and biomedical science in particular, benefited historically from substantial bipartisan support. The major increase in NIH funding of the Clinton period owed at least as much to actions of moderate Republicans like Rep. John Porter (Republican of Illinois) an...
Dear Editor,
Richard Hughes does not include leprosy in his list of peripheral nerve disorders.(1) While it is true that new cases of leprosy are declining rapidly , as a result of effective anti-bacterial therapy, there are still frequent numbers with residual disabilities in endemic countries.
In neurological text books, a mononeuropathy or multiple mononeuropathy is regarded as the sole neurolog...
Dear Editor,
I wish to commend the authors for their paper on functional vitamin B12 deficiency.
It is important that despite the array of investigative tools that may be available at the disposal of clinicians, clinical signs and symptoms are given their due emphasis particularly in Vitamin B12 deficiency. The authors report a case where the serum cobalamin was normal in the face of anaemia and neurol...
Dear Editor,
We read with great interest the review by Grossman on neurologic complications of celiac disease in a recent issue of Pract Neurol.(1)
Using an evidence-based approach, the author has carefully and critically analyzed articles published in the last decade on the most common neurologic manifestations associated with celiac disease, namely ataxia, epilepsy, and peripheral neur...
Dear Editor,
I read with interest the important case report of Turner and Talbot describing clinical subacute combined degeneration in a patient with “functional” vitamin B12 deficiency (defined by elevated levels of the B12 -dependent metabolites, methylmalonic acid and homocysteine, despite normal serum B12 values).1 It is important to note that although their patient did not improve with hydroxycobalamin the...
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%....
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,
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
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...
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