Recent eLetters
Displaying 1-10 letters out of 26 published
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The death of the neuro exam: not so soon please!
Submit responseDear Editor,
I read the title of Dr. Hawkes’ editorial three times before I was certain I had read it correctly1. As a fourth year medical student about to apply for a neurology residency, I was initially bewildered. When I read on though, I was impressed not only with his candidness, but also by the validity of what he was saying; although I am a newcomer, it does not take long to appreciate that imaging is central to current diagnosis of neurological disorders. However, from the perspective of someone about to commence her career, I would like to make a plea to save the neurological examination.
Neurology traditionally has been a field which medical students find intimidating. Full of esoteric names, bizarre pathologies and a lengthy examination the significance of which is often unclear to us at our stage of training. As we go through our rotation, some like me are captivated by the complexity and organization of this supercomputer, when many of its secrets and pathologies are revealed after acquiring the necessary examination skills. The exam further provides us with an opportunity to feel like a true physician because it helps seal the doctor patient relationship, providing the healing touch if I may say.
Lastly, we find the neurological exam quirky and fun to practice on each other.Finally I do have a more pragmatic argument. After decades of experience, it makes sense that Dr. Hawkes feels confident diagnosing and treating certain patients without a formal exam. However, he himself notes that "the ability to take a history and examine simultaneously is a technique that takes a few years to acquire". This level of mastery is indeed something to strive for, but in the meantime it would be hugely irresponsible of me to neglect a thorough examination of my patients. And if those with such expertise as Dr. Hawkes sit back and let things change, how will the next generation of neurologists ever acquire the skill set necessary to practice the art of neurology?
References
1. Hawkes CH.
I’ve stopped examining patients!
Pract Neurol.2009 Aug; 9(4):192-4. -
The death of clinical neurology: not so soon please!
Submit responseDear Editor,
I read with interest the editorial by Dr. Hawkes titled “I have stopped examining patients!”1. The title appropriately has an exclamation mark at the end highlighting his shocking claim. I have to commend Dr. Hawkes for finally coming out and admitting boldly and maybe somewhat proudly what most neurologists already know but are afraid to accept.
Bedside clinical neurology is a dying art and I admit many times in the office I have been guilty of a cursory neurological examination. A brief flash of the pen light into the patient’s eyes, a tap with the reflex hammer here and there, stand up, walk and voila I am done. The founding fathers of our great art would surely be turning in their graves if they saw a modern neurologist like me at work today.But should we just sit back and let things change? Dr. Hawkes says yes and why not? It is for the best after all. Why swim against the tide?
I have a slightly different view. I still remember what made me choose neurology from among the various disciplines of medicine. The thrill of watching the big toe go up in a patient with a hemispheric stroke, the eye signs in a patient with multiple sclerosis and the first time I saw facial myokymia. My joy and fascination with neurology was unparalleled and remains to this day. James Parkinson in his short monograph on shaking palsy in 1817 described six patients in total. Parkinson was an astute observer, and his report contained observations from three patients he saw in his clinic and three individuals he observed on city streets. Much of the description of the longitudinal course of the illness was derived from his observations of a single case only. Till today the diagnosis of Parkinson’s disease remains a clinical diagnosis. One made after taking a history and examining the patient for the three cardinal signs namely resting tremor, rigidity and bradykinesia. None of the advanced neuroimaging capabilities at my disposal can improve my ability to diagnose this and many other neurological conditions.I am sure that Dr. Hawkes shall agree with me that the "joy" and "fun" of neurology lies in the examination. For that reason in itself we all should strive to save this dying art.
References
1. Hawkes CH.
I’ve stopped examining patients!
Pract Neurol.2009 Aug; 9(4):192-4. -
Careful Examination Irreplaceable
Submit responseDear Editor,
Perhaps because I don't have Dr. Hawkes' degree of experience (I have approximately 25 years of practice experience), I disagree very strongly with his conclusion. Careful examination remains the cornerstone of neurologic practice. I agree that a great deal of information is gleaned from informal examination - watching the patient walk into the exam room, etc. I agree as well that for paroxysmal disorders - migraine, epilepsy, TIAs, etc. - history is the most important aspect of the evaluation. But efficient and careful examination is indispensable. Lets look at one of the examples cited by Dr. Hawkes. No younger patient, for example, with typical migraine features should undergo imaging unless they have an examination abnormality. Deferring to patient wishes is a pallid excuse and leads to waste of tax dollars (this is true in the US and UK).
Indeed, imaging of all headache patients will result in identification of a significant number of unrelated and largely benign findings, additional imaging studies, and heightened patient anxiety. Polite discussion and deflection of patient requests for inappropriate imaging is better care.
At a time when we are likely to see increased emphasis on clinical evaluation and decision making, it would be an enormous mistake for neurologists to permit erosion of reliance on the powerful and distinctive method of clinical examination. -
Premature closure and other unintended consequences of omitting the clinical examination
Submit responseDear Editor,
The admission that a neurologist has stopped examining patients(1) is a disturbing one, given the fact that "the practice of medicine is the art of drawing conclusions from incomplete evidence"(2), thanks to the fact that, as clinicians, "we work in a probabilisic enviroment in which the evidence we gather bears an imperfect relationship to its cause"(3).
Accordingly, the evidence initially gathered from history taking has to undergo subsequent "fine tuning" through the medium of clinical examination, special investigations, and, in some intances, also through the medium of the literature search. We omit any of the stages of that work up to our peril, given the fact that "the dominant cause of error in the faulty data-gathering category [lies] in the subcategory of ineffective, incomplete, or faulty work up", exemplified by a missed diagnosis of subdural hematoma in a patient seen after a car accident because "the physical examination was incomplete"(4). A potential benefit of clinical examination is that it might reduce the risk of "premature closure" whereby the clinician fails to consider other possibilities once an intitial diagnosis has been reached(4). With the benefit of clinical examination, even a clinician who is guilty of premature closure can learn from the experience of recognising that "I didn't reassess the situation when things didn't fit"(5). Clinical examination also helps to cut down on the number of "blunderbuss" investigations,thereby releasing scarce resources such as computerised tomography(CT) and magnetic resonance imaging(MRI) for use in patients who are too old and frail to cooperate with meticulous and long-drawn out clinical examination.
These are the patients who "miss out" in the era of high-tech medicine. On the one hand,after presenting with atypical symptoms, they do not receive the benefit of even a cursory clinical examination. To compound diagnostic error, their atypical symptoms are then falsely attributed to old age, and, as a consequence, they are also denied the benefit of the high-tech investigations that are themselves supposed to be a short cut to diagnosis.
References
(1) Hawkes CH
I've stopped examining patients
Practical Neurology 2009;9:192-4(2)Apley J., McKeith R
The child and his symptoms
Oxford: Blackwell,1962:228(3) Kirwan JR., de Saintonge MC., Joyce CRB
Clinical judgment analysis
Quarterly Journal of Medicine New Series 76,No 281:9350949(4) Graber ML., Franklin N., Gordon R
Diagnostic error in internal medicine
Archives of Internal Medicine 2005;165:1493-1499(5) Scott I
Errors in clinical reasoning: causes and remedial strategies
British Medical Journal 2009;339:22-25 -
Bipartisanship
Submit responseDear 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) 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.
-
Leprosy
Submit responseDear 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 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.
REFERENCES
1. Hughes R.
Peripheral nerve diseases.
Pract Neurol 2008; 8: 396-405.2. Monrad-Krohn GH.
The neurological aspect of leprosy.
Christiania; Jacob Dybwad, 1923.3. Crawford CL.
Neurological lesions in leprosy.
Lepr Rev 1968; 39: 9-13.4. Crawford CL, Hobbs MJ.
Neurotrophic factors in diabetic neuropathy.
Trends Neurosci 1995; 18: 15.5. Crawford CL.
Diabetic Neuropathies.
Available at http://pn.bmj.com/cgi/eletters/7/2/ 82 Accessed 22 January 2009.6. Crawford CL, Hardwicke PMD, Evans DHL, Evans EM.
Granulomatous hypersensitivity induced by sensory peripheral nerve.
Nature 1977; 265: 457-459.7. 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. -
Clinical signs and symptoms emphasized.
Submit responseDear 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 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 -
Neurologic complications of celiac disease
Submit responseDear 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 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. -
"Functional" Vitamin B12 Deficiency
Submit responseDear 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 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.
References
1. Turner MR, Talbot K.
Functional vitamin B12 deficiency.
Practical Neurology 2009; 9:37-45.2. 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. -
"Ice-on-eyes" test
Submit responseDear 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%. 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.
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