In the presence of risk factors for thromboembolism, a focal
neurological episode which has a sudden onset should be assumed to be
embolic until proved otherwise. Whether or not that episode is purely
ischaemic, or whether or not it undergoes subsequent hamorrhagic
transformation is a separate issue which should not detract from the
urgency to identify the embolic source by means of echocardiography. That
is why I am so...
In the presence of risk factors for thromboembolism, a focal
neurological episode which has a sudden onset should be assumed to be
embolic until proved otherwise. Whether or not that episode is purely
ischaemic, or whether or not it undergoes subsequent hamorrhagic
transformation is a separate issue which should not detract from the
urgency to identify the embolic source by means of echocardiography. That
is why I am so surprised that echocardiography was not performed as a
matter of urgency in this patient(1). The "mantra" of "thromboembolism
until proved otherwise" is one which has stood the test of time in other
contexts, notably in the context of acute abdominal pain(attributable to
mesenteric embolism) in the presence of risk factors for thromboembolism
such as atrial fibrillation, myocardial infarction, and infective
endocarditis(2). "Frequently, [however], acute occlusive mesenteric
ischemia remains unrecognised, initially, so that specific treatment is
delayed for > 24 hours"(3). This is, arguably, attributable, at least
in part, to underrecognition of the diagnostic utility of the "mantra",
and the same might be true of the delayed recognition of the embolic
nature and the embolic source in the case reported by the authors(1).
Where the index of suspicion is sufficiently high, it should also be
recognised that normal intensity anticoagulation is no bar to
thromboembolism, as shown by the graph depicting occurence of embolic
stroke despite chronic anticoagulat therapy in patients with non valvular
atrial fibrillation, some of whom had international normalized ratios in
the range 2-3.4(4)
References
(1) Nieuwkamp DJ., Kirkels JH., Rinkel GJE
Multiple intracerebral haematomas during normal intensity anticoagulation
Practical Neurology 2010;10:45-47
(2)Jolobe,O
Intestinal ischaemia(letter)
British journal of Hospital Medicine 2002;63:695
(3)Menke J., Luthje L., Kastrup A., Larsen J
Thromboembolism in atrial fibrillation
Am J Cardiol 2010;105:502-10
(4)Hylek EM., Skates SJ., Sheehan MA., Singer DE
An analysis of the lowest effective intensity of prophylactic
anticoagulation for patients with non rheumatic atrial fibrillation
N Engl J Med 1996;335:540-6
Many thanks to Ramadan and his colleagues for this article about
neurology in the land of Mesopotamia. I have few notes:
1. The author has not mentioned other neurologists who participated
substantially in the creation of the subject "neurology in Iraq," and
these are Muhammed Tawfiq, Fadhil Al-Hadithy, and Adnan Al-Araji; Ajeeb
Ali practiced neurology in a city in the north of Iraq and was away from
the teachi...
Many thanks to Ramadan and his colleagues for this article about
neurology in the land of Mesopotamia. I have few notes:
1. The author has not mentioned other neurologists who participated
substantially in the creation of the subject "neurology in Iraq," and
these are Muhammed Tawfiq, Fadhil Al-Hadithy, and Adnan Al-Araji; Ajeeb
Ali practiced neurology in a city in the north of Iraq and was away from
the teaching environment of Baghdad. All of them were Members/Fellows of
the Royal Colleges of Physicians. One only, Khalid Ibrahim (who was
assassinated during the period of sectarian violence in Iraq, 2006) was
certified by the Arab board of Medicine. Therefore, the three names
mentioned in the article were not alone and the credit should also be
given to their neurology colleagues.
2. The so-called Scientific Council of Neurology (which is part of
the Iraqi Board of Medical Specializations; IBMS) collapsed totally in
late 2006 (the peak of the sectarian violence) after the immigration of
its founding members. Its post-graduate students were left alone facing
their unknown future; many of its trainees left Iraq. The IBMS then
brought three names to fill in the gap within 2 years; all of them were
locally trained and certified. One might ask, "Three individuals only
train, supervise researches, and examine 10 (more or less) post-graduate
students?"; misuse and abuse of those trainees occurred and occurs for
several reasons, which are beyond the scope of this article.
4. One of the authors himself (which is a neurologist) fled Iraq just
few months prior to the US-lead war against Iraq in 2003 and returned back
for unknown reasons in 2006; he did not return to his previous hospital,
but to a city in the north of Iraq. Some neurologists left Iraq after 2003
not because of the current disastrous situation in Iraq, but as part of
the immigration wave, which started in 2005 to deliberately empty Iraq
from its resources.
In short, adult clinical neurology in Iraq, instead of moving forward
after the "liberation of Iraq," has regressed profoundly and declined in
efficiency to a very counterproductive way. Many people travel to a nearby
country if they get a neurological disease; simply, they don't trust the
"new generation of Iraqi neurologists."
By no means, this article or any eLetter would cover this subject.
Anyway, as the author said, we hope that Iraq will re-take its position in
the lead.
Larner wrote an interesting article on morning headaches.1 We would
like to react to the statement 'Onset of subarachnoid haemorrhage during
sleep is extremely rare, if it occurs at all.'
In October 2008 a 62 year old woman was seen on the emergency department.
She reported moderately severe headache on awakening with chills and a
slight dizziness. There was a history of ulcerative colitis and she smoked
5 cigarettes a da...
Larner wrote an interesting article on morning headaches.1 We would
like to react to the statement 'Onset of subarachnoid haemorrhage during
sleep is extremely rare, if it occurs at all.'
In October 2008 a 62 year old woman was seen on the emergency department.
She reported moderately severe headache on awakening with chills and a
slight dizziness. There was a history of ulcerative colitis and she smoked
5 cigarettes a day. General, neurological, and laboratory examinations
were unremarkable. Because of the chills a possible viral infection with
headache was presumed. The patient was reassured and went home. The next
morning her husband found her in bed unresponsive and took her to the
emergency department urgently. She was comatose, with a Glasgow Coma Scale
Score of E1M3V1, fixed dilated pupils and bilateral extensor plantar
responses. CT showed a massive subarachnoid haemorrhage with intracerebral
and subdural blood and CTA a middle cerebral artery aneurysm. Despite
surgical decompression with clipping of the aneurysm, the patient died the
next day.
Our patient had an aneurysmal bleeding during sleep in two successive
nights. Although aneurysmal subarachnoid haemorrhage often is considered
to be triggered by strenuous activities, onset during non-strenous
activities and even sleep is not rare. In a series of 141 patients, onset
of SAH occurred during sleeping, resting, sitting, eating, or drinking in
38 patients ( 27%).2 In a series of 513 patients it occurred during
sleeping or resting in 41 (8%),3 and in a series of 500 patients during
sleep in 45 (9%).4
In conclusion, onset of subarachnoid haemorrhage during sleep is not
extremely rare. Not considering aneurysmal subarachnoid haemorrhage in
patients awakening with unusual headache is dangerous.
References
1. Larner AJ. Not all morning headaches are due to brain tumours. Pract
Neurol 2009;9:80-84
2. Ferro JM, Pinto AN. Sexual activity is a common precipitant of
subarachnoid hemorrhage. Cerebrovasc Dis 1994;4:375
3. Matsuda M, Watanabe K, Saito A, Matsumura K, Ichikawa M. Circumstances,
activities, and events precipitating aneurysmal subarachnoid hemorrhage. J
Stroke Cerebrovasc Dis 2007;16:25-29
4. Schievink WI, Karemaker JM, Hageman LM, van der Werf DJM. Circumstances
surrounding aneurysmal subarachnoid hemorrhage. Surg Neurol 1989;32:266-272
I am very grateful to Dr Amin's interest in this short letter and his
useful comments.
The aim of this letter was to inform PN readers about difficulties of
Iraqi doctors especially neuroscience clinicians been through in light of
successive damaging wars inflicted in to this country.
Dr Amin himself, names he mentioned and others (locally and overseas
trained) are among distinguished hardworking neurologists in...
I am very grateful to Dr Amin's interest in this short letter and his
useful comments.
The aim of this letter was to inform PN readers about difficulties of
Iraqi doctors especially neuroscience clinicians been through in light of
successive damaging wars inflicted in to this country.
Dr Amin himself, names he mentioned and others (locally and overseas
trained) are among distinguished hardworking neurologists in Iraq. Whilst
every single one of them deserves a credit and recognition for continuing
practicing under hostile and dangerous circumstances, it's beyond the
scope and aim of this article to mention every single neuroscience
clinician.
I agree with him, so many clinicians left Iraq after recent war and
only few dedicated neurologist left with challenging responsibility to
continue to train young neurologists.
When dealing with movement disorders which are associated with
subnormal caeruloplasmin levels, account should be taken, not only of
Wilson's disease(as was the case in a recent review)(1) where
neurological features are attributable to copper deposition in the basal
ganglia(2), but also of acaeruloplasminaemia, where neurological features
are attributable to iron deposition in the basal ganglia, thalamus,
dentate nucleus, an...
When dealing with movement disorders which are associated with
subnormal caeruloplasmin levels, account should be taken, not only of
Wilson's disease(as was the case in a recent review)(1) where
neurological features are attributable to copper deposition in the basal
ganglia(2), but also of acaeruloplasminaemia, where neurological features
are attributable to iron deposition in the basal ganglia, thalamus,
dentate nucleus, and motor cortex(3)(4). Unlike Wilson's disease, where
the cardinal feature of the genotype is the occurence of mutations
associated with copper-transporting ATPases(3), acaeruloplasminaemia is
charcterised by mutations in the caeruloplasmin gene itself(3), with
resulting failure of hepatic biosynthesis of the caeruloplasmin precursor
apocaeruloplasmin(2). Acaeruloplasminaemia merits inclusion in the
differential diagnosis of movement disorders because iron chelator
treatment with desferrioxamine has been shown, in at least one instance,
to produce a reduction in severity of blepherospasm, grimacing, and
rigidity, thereby suggesting that early chelator treatment may prevent or
decisively ameliorate neurological symptoms in this disorder(5).
Both Wilson's disease and acaeruloplasminaemia have to be distinguished
from a third disorder charactrised, this time, by serum caeruloplasmin
levels which are either subnormal or at the lower limit of the normal
range, in association with movement disorders such as tremor and
dystonia(6). By 1993, thirteen such cases had been described. In
two instances where investigation included magnetic resonance imaging
of the brain, no heavy metal deposition was detected in the basal
ganglia(6).
References:
(1) Fuller G
Hyperkinetic movement disorders: shakes, jumps, and jolts
Practical Neurology 2010;10: 114-123
(2)Miyajima H
Genetic disorders affecting proteins of iron and copper metabolism:
Clinical implications
Internal Medicine 2002;41:762-769
(3)Miyajima H., Takahashi Y., Kono S
Acaeruloplasminaemia, an inherited disorder of iron metabolism
Biometals 2003;16:205-213
(4)Miyajima H., Adachi J., Kohno S., et al
Increased oxysterols associated with iron accumulation in the brains and
visceral organs of acaeruloplasminaemia patients
QJMed 2001;94:417-422
(5)Miyajima H., Takahashi Y., Kamata T et al
Use of desferrioxamine in the treatment of aceruloplasminemia
Ann Neurol 1997;41:404-407
(6) Wierzbicki AS., Patel N., Evans K., Lascelles PT
Copper-64 metabolism in two patients with non-Wilsonian movement disorders
and copper deficiency
J Neurological Sciences 1993;119:84-90
The cautionary tale of miscalculation of the corrected QT
interval(1) highlights the extent to which clinicians and their patients
can become hostages to fortune when they base important clinical decisions
on "numbers" churned out by electronic gadgets whose validity has not been
"cross checked" manually. The sometimes indiscriminate use of oscillometric
devices for blood pressure measurement is another case in point. My
anx...
The cautionary tale of miscalculation of the corrected QT
interval(1) highlights the extent to which clinicians and their patients
can become hostages to fortune when they base important clinical decisions
on "numbers" churned out by electronic gadgets whose validity has not been
"cross checked" manually. The sometimes indiscriminate use of oscillometric
devices for blood pressure measurement is another case in point. My
anxiety is that, notwithstanding the inaccuracy of this technology in the
presence of atrial fibrillation(2), many patients with this arrhythmia may
have their blood pressures monitored using oscillometric devices for the
purpose of documenting their "vital" signs. This would bear out the
observation that "the measurement of blood pressure is likely the
clinical procedure of greatest importance that is performed in the
sloppiest manner"(3). And it does not get any better when it comes to
uncritical reliance on "numbers" churned out by "spread sheets" such
as the Framingham Risk Score for stroke(4) for the purpose of
evaluating indications for initiating antihypertensive therapy. A
potential consequence is that swathes of relatively young hypertensive
adults aged less than 45, principally black, might, on the basis of current
evidence(5), be at risk of falling victim to stroke during their wage-
earning years simply because they were underrepresented in the original
Framingham cohort upon which risk stratification is based(6). Even in the
updated version(7), prediction of cardiovascular risk is limited to 10
years(7), notwithstanding the fact that "ten years is not a
lifetime"(8), and also notwithstanding the fact that "in the absence
of intervention...long term exposure to an increased rsk may lead to a
high and partly irreversible risk situation in middle age"(9)
References:
(1)Chadwick D., Jelen P., Almond S
Life and death diagnosis
Pract Neurol 2010;10:155-9
(2) Pickering TG., Hall JE., Appel LJ et al
Recommendations for blood pressure measurement in humans and experimental
animals. Part 1 Blood pressure measurement in humans
AHA Scientific Statement
Circulation 2005;111:697-716
(3) Kaplan NM
commentary on the sixth report of the Joint National Committee(JNC-6)
Am J Hypertens 1998;11:134-6
(4) Wolf PA., D'Agostino RB., Belanger AK., Kannel WB
Probability of stroke. A risk profile from the Framingham Study Stroke
1991:22:312-318
(5) Pathak EB., Sloan MA
Recent racial/ethnic disparities in stroke hospitalisation and outcomes
for young adults in Florida 2001-2006
Neuroepidemiology 2009;32:302-311
(6) Kannel WB., Wolf PA., Verter J et al
Epidemiologic assessment of the role of blood pressure in stroke. The
Framingham Study 1970
JAMA 1996;276:1269-1278
(7) Marma AK., Lloyd -Jones DM
Systematic examination of the updated Framingham Heart Study. General
Cardiovascular Risk Profile
Circulation 2009;120:384-390
(8) Nambi V., Ballantyne CM
"Risky Business"
Ten years is not a lifetime
Citculation 2009;119:362-4
(9) Mancia G., De Packer G., Dominiczak A et al
The Task Force for the management of arterial hypertension of the European
Society of Hypertension(ESH) and European Society of Cardiology(ESC)
2007 Guidelines for the management of arterial hypertension
J Hypertens 2007;25:1105-1187
Accurate measurement of the QT interval is relevant, not only for the
diagnosis of long QT interval syndromes(1), but also for the recognition
of short QT syndromes which are familial disorders now recognised to be
characterised by complications such as a trial fibrillation, syncope, and
sudden death, in the absence of structural heart disease(2)(3). The
typical electocardiographic "signature" is a short QT interval associate...
Accurate measurement of the QT interval is relevant, not only for the
diagnosis of long QT interval syndromes(1), but also for the recognition
of short QT syndromes which are familial disorders now recognised to be
characterised by complications such as a trial fibrillation, syncope, and
sudden death, in the absence of structural heart disease(2)(3). The
typical electocardiographic "signature" is a short QT interval associated
with "peaking" of the T waves(4). Although a QT interval of 300 ms was
originally proposed as a diagnostic criterion(5), a novel form of
short QT interval syndrome wassubsequently reported in patients with a
corrected QT(QTc) interval up to 320 ms(6). Consequently the question
"whether the diagnosis of short QT syndromes should be based on QT or
QTc and what the sensitivity and specificity of different QT/QTc
interval cut-off values are is still unresolved"(4), a truly worrying
state of affairs given the potential lethality of this disorder.
References:
(1)Chadwick D., Jelen P., Almond S
Life and death diagnosis
Practical Neurology 2010;10:155-159
(2)Gaita F., Giustetto C., Bianchi F et al
Short QT syndrome . A familial cause of sudden death
Circulation 2003;108:965-970
(3)Schimpf R., Wolpert C., Gaita F., Giustetto C., Borggrefe M
Review
Short QT syndrome
Cardiovascular Research 2005;67:357-366
(4)Napolitano C., Bloise R., Priori S
Long QT syndrome and short QT syndrome: how to make correct diagnosis and
what about eligibility for sports activity
Journal of Cardiovascular Medicine 2006;7:250-256
(5)Gussak I., Brugada J., Wright RS., et al
Idiopathic short QT interval: a new clinical syndrome?
Cardiology 2000;94:99-102
(6)Priori SG., Pandit VS., Rivolta I et al A novel form of short QT
syndrome(SQT3) is caused by a mutation in the KCNJ2 gene
Circ Res 2005;96:800-80
Although no mention of subdural haematoma was made by the
authors(1), the occurence of reversible urinary retention, even in a
patient who is awake and ambulatory, can be a feature of bilateral chronic
subdural haematoma, as was the case in an 87 year old woman reported
by Lang et al(2). On the basis of the fact that she regained full bladder
control after evacuation of the haematoma, the authors proposed that there
might be...
Although no mention of subdural haematoma was made by the
authors(1), the occurence of reversible urinary retention, even in a
patient who is awake and ambulatory, can be a feature of bilateral chronic
subdural haematoma, as was the case in an 87 year old woman reported
by Lang et al(2). On the basis of the fact that she regained full bladder
control after evacuation of the haematoma, the authors proposed that there
might be a supratentorial micturition centre located in the region of the
frontal convexity cortex and anterior portion of the interhemispheric
fissure(2). Instead of urinary retention, some patients with bilateral
chronic subdural haematomas have urinary incontinence, and this, too,
is not necessarily associated with obtundation(3)(4). In one report
somnolence and stupor was a feature in only three of the six patients
with
the association of bilateral chronic subdural haematoma and urinary
incontinence. All six patients had "excellent recovery" after
evacuation of the haematomas(3). In another report, a 71 year old
woman with bilateral chronic subdural haematomas presented with
ataxia, paraparesis(although he could still walk), and incontinence of
the bladderand bowel. Although his level of consciousness was not
specifically documented, his speech was reported as being "slow and
superficial, but clear, distinct, and without aphasia". After
evacuation of the haematoma "he was discharged from the hospital
asymptomatic on the 9th postoperativeday"(4). Accordingly, "clinicians
should be aware that urinary incontinence may be a symptom of subdural
haematoma....and that its
occurence in patients who are reasonably alert should prompt a
detailed documentation of its onset in relation to head injury and its
resolution in relation to evacuation of subdural haematoma so as to
advance our understanding of this phenomenon"(5)
References:
(1) Panicker JN., Fowler CJ
Uro-neurology
Practical Neurology 2010;10:178-185
(2)Lang EW., Chesnut RM., Hennerici M
Urinary retention and space-occupying lesions of the frontal cortex
European Neurology 1996;36:43-47
(3)Goto I., Kuroiwa Y., Kitamura K
The triad of neurological manifestations in bilateral chronic subdural
hematoma and normal pressure hydrocephalus
J Neurosurg Sci 1986;30:123-128
(4)Bortnick RJ., Murphy JP
Paraparesis with incontinence of bowel and bladder
A syndrome of bilateral subdural hematoma
J Neurosurgery 1963;20:352-353
(5) Jolobe OMP
Urinary incontinence may be a feature of bilateral subdural haemorrhage in
patients who have no lateralizing signs(letter)
Journal of the American Geriatrics Society 2010;58:403
I read with interest the editorial by Dr. Warlow (1). It follows the
earlier editorial by Dr. Hawkes titled "I have stopped examining
patients" (2). That editorial evoked a fury of concerned responses
from both neurologists and neurologists to be. The editorial by
Dr.Warlow will be far less controversial and I feel aptly balances the
debate between examining and not examining neurologists. Dr....
I read with interest the editorial by Dr. Warlow (1). It follows the
earlier editorial by Dr. Hawkes titled "I have stopped examining
patients" (2). That editorial evoked a fury of concerned responses
from both neurologists and neurologists to be. The editorial by
Dr.Warlow will be far less controversial and I feel aptly balances the
debate between examining and not examining neurologists. Dr. Warlow
lays forth the argument for examining at least some aspects of the
neurological system in selected patients guided by their history.
This if I remember rightly is what is called a focussed examination.
Dr. Warlow lists 10 reasons in no particular order of importance to
defend the value of a neurological examination. To his comprehensive
10, I should like to add a couple of my own, again in no particular
order of importance:
1.It makes me feel like a doctor: neurologists at least here
in the United States have already surrendered the stethoscope to the
internists. If I surrender my neurological examination skills too, I
risk losing my very identity as a neurologist.
2.It makes my office day less monotonous and
gives me a reason to get away from the electronic medical chart on the
computer and get some much needed exercise. A well performed motor
examination is actually quite a decent workout!
For the above reasons and the many others so eloquently listed by Dr.
Warlow, I shall never stop examining patients.
References:
1. Warlow C. Why I have not stopped examining patients. Pract Neurol. 2010 Jun; 10(3):126-8.
2. Hawkes CH. I have stopped examining patients!. Pract Neurol. 2009 Aug;9(4):192-4.
Professor Warlow is to be congratulated on his masterly restatement
of the core values of clinical medicine, in general, and neurology, in
particular(1). As a corollary to his observation regarding "whether
what you find on imaging is relevant to the problem or is merely
incidental"(1), recognition should be made that the scan, itself, may
generate images which are either falsely normal(2), or too
nonspecifically abnormal...
Professor Warlow is to be congratulated on his masterly restatement
of the core values of clinical medicine, in general, and neurology, in
particular(1). As a corollary to his observation regarding "whether
what you find on imaging is relevant to the problem or is merely
incidental"(1), recognition should be made that the scan, itself, may
generate images which are either falsely normal(2), or too
nonspecifically abnormal to form the basis of an unequivocal
diagnosis(2)(3)(4). At the other extreme there may be a "surfeit" of
potentially significant images, generating the possibility of dual
pathology as the underlying cause of a single neurological disorder(4)(5).
All these scenarios are encountered during evaluation of the underlying
causes of temporal lobe epilepsy and partial complex seizures.
In one series, where 19 patients were identified as having gangioglioma as
the underlying cause of partial complex seizures, there were two
instances where "the MRfindings were normal", leading the
investigators to
conclude that CT should also be performed to recognise calcifications
that may be missed on MR imaging(2). Even where MR is abnormal
stigmata of ganglioglioma may be nonspecific, ranging from signal
hypointensity or even isointensity, to hyperintensity relative to gray
matter(3)(4). Diagnostic uncertainty is compounded by the fact that
ganglioma-related MR images may sometimes fail to enhance after
administration of contrast(6), and that, even in the event of contrast
enhancement, the pattern of enhancement may be non specific(4), an
observation which resonates with the view that, in this disorder, "CT
and MR findings [are] not specific"(2). At the other extreme there is
the problem of dual pathology as the potential underlying cause of
either temporal lobe or partial complex epilepsy. This was exemplified
by a
study where two of the twenty four patients with partial complex
epilepsy and ganglioglioma were identified as having coexisting
ipsilateral hippocampal sclerosis(4),and also by a study where other
potential causes coexisted with
hippocampal sclerosis(5). The final twist is where two lesions are
present, either or both of which could be an underlying cause of
temporal lobe epilepsy but only one of the lesions is epileptogenic.
This was the case in a 25 year old man in whom CT scan showed a
calcified left temporal lobe lesion which was characterised, on MR, by
heterogenous signal intensity suggestive of ganglioglioma.
Concurrently, also on MR, he had a right temporal lobe lesion
characterised by loss of gray-white matter demarcation, and by increased
signal intensity on the STIR(short tau inversion recovery) image
suggestive of a right-sided seizure focus. On intracranial EEG and on
intraoperative electrocorticography, however, only the right-sided lesion
was shown to be epiliptogenic. Pathological examination of the excised
right-sided lesion revealed stigmata of cerebral microdysgenesis(7), a
"pathological entity with clinical relevance[in the context of drug-
resistant epilepsy"(8).
References:
(1) Warlow C
Why I have not stopped examining patients
Practical Neurology 2010;10:126-128
(2) Tampieri D., Moumdjian R., Melanson D et al
Intracerebral gangliogliomas in patients with partial complex seizures: CT
and MR imaging findings
Am J Neuroradiol 1991;12:749-755
(3) Castello M., Davis PC., Takei Y., Hoffman JC
Intracranial ganglioglioma:MR.CT,and clinical findings in 18 patients
Am J Neuroradiol 1990;11:109-114
(4) Adachi Y., Yagishita A
Gangliogliomas: characteristic imaging findings and role in tempopral lobe
epilepsy
Diagnostic Neuroradiology 2008;50:829-834
(5) Salanova V., Markand O., Worth R
Temporal lobe epilpsy: analysis of patients with dual pathology
Acta Neurol Scand 2004;109:126-131
(6) Zentner J., Wolf HK., Ostertun B et al
Gangliogliomas: clinical, radiological, and histopathological findings in
51 patients
J Neurol Neurosurg Psychiatry 1994;57:1497-1502
(7) Adachi Y., Yagishita A., Arai N
White matter abnormalities in the anterior temporal lobe suggests the side
of the seizure foci in temporal lobe epilepsy
Neuroradiology 2006;48:460-464
(8) Pasquier B., Peoc'h M., Fabre-Bocquentin B et al
Surgical pathology of drug-resisteant partial epilepsy. A 10 year
experience with a series of 327 consecutive resections
Epileptic Disorders 2002;4:99-119
In the presence of risk factors for thromboembolism, a focal neurological episode which has a sudden onset should be assumed to be embolic until proved otherwise. Whether or not that episode is purely ischaemic, or whether or not it undergoes subsequent hamorrhagic transformation is a separate issue which should not detract from the urgency to identify the embolic source by means of echocardiography. That is why I am so...
Many thanks to Ramadan and his colleagues for this article about neurology in the land of Mesopotamia. I have few notes:
1. The author has not mentioned other neurologists who participated substantially in the creation of the subject "neurology in Iraq," and these are Muhammed Tawfiq, Fadhil Al-Hadithy, and Adnan Al-Araji; Ajeeb Ali practiced neurology in a city in the north of Iraq and was away from the teachi...
Larner wrote an interesting article on morning headaches.1 We would like to react to the statement 'Onset of subarachnoid haemorrhage during sleep is extremely rare, if it occurs at all.' In October 2008 a 62 year old woman was seen on the emergency department. She reported moderately severe headache on awakening with chills and a slight dizziness. There was a history of ulcerative colitis and she smoked 5 cigarettes a da...
I am very grateful to Dr Amin's interest in this short letter and his useful comments. The aim of this letter was to inform PN readers about difficulties of Iraqi doctors especially neuroscience clinicians been through in light of successive damaging wars inflicted in to this country.
Dr Amin himself, names he mentioned and others (locally and overseas trained) are among distinguished hardworking neurologists in...
When dealing with movement disorders which are associated with subnormal caeruloplasmin levels, account should be taken, not only of Wilson's disease(as was the case in a recent review)(1) where neurological features are attributable to copper deposition in the basal ganglia(2), but also of acaeruloplasminaemia, where neurological features are attributable to iron deposition in the basal ganglia, thalamus, dentate nucleus, an...
The cautionary tale of miscalculation of the corrected QT interval(1) highlights the extent to which clinicians and their patients can become hostages to fortune when they base important clinical decisions on "numbers" churned out by electronic gadgets whose validity has not been "cross checked" manually. The sometimes indiscriminate use of oscillometric devices for blood pressure measurement is another case in point. My anx...
Accurate measurement of the QT interval is relevant, not only for the diagnosis of long QT interval syndromes(1), but also for the recognition of short QT syndromes which are familial disorders now recognised to be characterised by complications such as a trial fibrillation, syncope, and sudden death, in the absence of structural heart disease(2)(3). The typical electocardiographic "signature" is a short QT interval associate...
Although no mention of subdural haematoma was made by the authors(1), the occurence of reversible urinary retention, even in a patient who is awake and ambulatory, can be a feature of bilateral chronic subdural haematoma, as was the case in an 87 year old woman reported by Lang et al(2). On the basis of the fact that she regained full bladder control after evacuation of the haematoma, the authors proposed that there might be...
Dear Editor,
I read with interest the editorial by Dr. Warlow (1). It follows the earlier editorial by Dr. Hawkes titled "I have stopped examining patients" (2). That editorial evoked a fury of concerned responses from both neurologists and neurologists to be. The editorial by Dr.Warlow will be far less controversial and I feel aptly balances the debate between examining and not examining neurologists. Dr....
Professor Warlow is to be congratulated on his masterly restatement of the core values of clinical medicine, in general, and neurology, in particular(1). As a corollary to his observation regarding "whether what you find on imaging is relevant to the problem or is merely incidental"(1), recognition should be made that the scan, itself, may generate images which are either falsely normal(2), or too nonspecifically abnormal...
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