Acute stroke
BMJ 2000; 320 doi: https://doi.org/10.1136/bmj.320.7239.920 (Published 01 April 2000) Cite this as: BMJ 2000;320:920All rapid responses
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Competing interests: No competing interests
Dear Sir,
In their first table, Bath and Lee state that patients with transient
ischemic attacks (TIA) lasting 1 hour or more, patients with more than one
TIA within a week, and patients presenting to hospital should be admitted
to hospital. They also assert that patients should be admitted to hospital
at the request of the general practitioner. I am not aware of any data to
support these recommendations. I am particularly disappointed that the
BMJ, a paragon of evidence-based-medicine has opted to publish these
recommendations despite the absence of any supporting evidence. This is
all the more disturbing given the rather high cost that would be incurred
in implementing the authors' proposals.
By definition, a person who has suffered a TIA has returned to
his/her baseline. Accordingly, there will be no need for in-hospital
physiotherapy or occupational therapy. Imaging and other investigations
can be performed on ambulatory basis. The fact that a patient has come to
hospital for assessment and advice does not, in itself, mandate
hospitalization. And, a general practitioner's request for admission to
hospital is just that - a request. My role, as consultant, is to make the
final determination.
I have no competing interests.
Yours sincerely,
Steven L. Shumak MD, FRCPC
Director, Division of General Internal Medicine
University of Toronto
Competing interests: No competing interests
Dear Sir,
Professors Philip Bath and Kennedy Lees in providing an excellent overview
of acute stroke1 have omitted to mention the metabolic abnormality of
hypoglycaemia as an important and treatable condition that can mimic a
cerebrovascular event. Various reversible and permanent neurological
manifestations of neuroglycopenia are recognised to be associated with
acute hypoglycaemia2. Transient hemiparesis can be precipitated by acute
hypoglycaemia in all age groups but elderly subjects are particularly
vulnerable, in whom neurological features such as impaired motor co-
ordination and slurring of speech are more prominent than in younger
adults. In elderly people these symptoms may be misinterpreted as
representing cerebral ischaemia, and are commonly misdiagnosed as
transient ischaemic attacks.
Rarely, severe and protracted neuroglycopenia can cause permanent
neurological damage resulting in hemiparesis, focal motor and sensory
abnormalities, and brainstem syndromes. Other permanent manifestations of
severe hypoglycaemia include epilepsy, persistent vegetative state, and
movement disorders such as ataxia and choreathetosis2. These are
presumably caused by mechanisms such as direct focal cerebral damage from
glucopenia, acute thrombotic occlusion secondary to the haemodynamic,
haematological and haemorrhological effects of hypoglycaemia or by
cerebral ischaemia provoked by changes in regional cerebral blood flow in
the brain. In one series of 778 cases of drug-induced hypoglycaemia,
permanent neurological deficit was described in 5% of the survivors3.
Because hypoglycaemia should be considered as a potential cause of
neurological dysfunction, we would suggest that measurement of blood
glucose should be included in the initial investigation of a stroke.
Yours sincerely
Dr Vincent McAulay
Clinical Research Fellow
Dr Brian M Frier
Consultant Physician
Department of Diabetes,
Royal Infirmary of Edinburgh,
Lauriston Place,
Edinburgh
EH3 9YW
References
1. Bath PMW, Lees KR. ABC of arterial and venous disease. Acute
stroke. BMJ 2000; 320: 920-3.
2. Perros P, Deary IJ. Long-term effects of hypoglycaemia on
cognitive function and the brain in diabetes. In: Frier BM and Fisher BM
(eds), Hypoglycaemia in Clinical Diabetes. John Wiley & Sons Ltd,
1999; pp.187-210.
3. Seltzer HS. Severe drug-induced hypoglycaemia: a review.
Comprehensive therapy 1979, 5: 21-9.
Competing interests: No competing interests
Some important risk factors are missing
dyslipidemia are modifiable risk factors for ischaemic stroke,(1,2) though
the role of serum cholesterol remains uncertain. These factors have been
brought out in the subsequent clinical review article which appeared in
BMJ 2000, 320:991-4.
Hence we feel that blood glucose and serum lipid profile should form part of the
investigations of stroke.
Prof. L.C.Thakur, Head, Dept. of Neurology
Prof. K.M. Prabhu, Dept. of Biochemistry
Dr. Jaspreet Kaur
Dr. J.K.Gambhir
Univ. Coll. of Med. Sciences & GTB Hospital
Delhi - 110 095.
INDIA
Competing interests: No competing interests