Rapid resolution of symptoms and signs of intracerebral haemorrhage: case reports
BMJ 1998; 316 doi: https://doi.org/10.1136/bmj.316.7143.1495 (Published 16 May 1998) Cite this as: BMJ 1998;316:1495
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Gunatilake reported two patients with intracerebral haemorrhage and resolution of symtoms and signs within 24 hours (1). Previously, Aparicio et al and Alvarez reported other two patients with similar clinical course( 2,3), one due to anticoagulant therapy (3),
On the other hand, Rey et al (4) reviewed all the clinical trials in which aspirin was used in the secondary and primary prevention of ischemic stroke and there was an increased risk associated with the use of aspirin as a compared to a placebo with respect to a intracerebral haemorrhage (Odd ratio= 2,08; IC 95%=1,32-3,29; p=0,0009).
In conclusion, it is felt that a cranial CT should be also mandatory before starting antiplatelet therapy and should be performed within 6 hours after the symptoms onset. Bogousslavsky et al (5) reported 15 patients with cerebral intra-infarct haematoma (type 2 of cerebral haemorragic infarct) in whom cranial CT showed no bleeding within 6 hours of stroke onset but showed intracerebral haemorrhage less than 18 hours later. The findings in the second cranial CT sugessted intracerebral haemorrhage in a review by two radiologist and two neurolgist whom were blinded to the first cranial CT. In these patients a primary infarct was suspected only because they had a cranial CT within 6 hours after the infarct onset.
REFERENCES:
1. Gunatilake SB. Rapid resolution of symtoms and signs of intracerebral haemorrhage: case reports.
2. Aparicio A, Sobrino J, Arboix A, Torres M. Hematoma intraparenquimatoso que simula un accidente isquémico transitorio. Med Clin ( Barc) 1995; 104: 478-479.
3. Alvarez J. Hematoma intraparenquimatoso que simula un accidente isquémico transitorio. Med Clin ( Barc) 1995; 105: 598.
4. Rey A, Martí-Vilalta. Enfermedad cerebrovascular yatrogénica. Rev Neurol 1995; 23(Supl 1): 131-146.
5. Bogousslavsky J, Regli F, Uské A, Maeder P. Early spontaneous hematoma in cerebral infarct: is primary cerebral hemorrhage overdiagnosed?. Neurology 1991; 41: 837-840
Competing interests: No competing interests
Gunatilake [1] illustrates the importance of obtaining imaging studies in cases of transient neurological events prior to starting anti-platelet agents, by reporting 2 cases of putaminal haemorrhage, which were associated with rapidly resolving neurological deficits. Presentation of intracerebral haemorrhage with transient neurological deficits is uncommon in younger age groups [2,3], but can occur in the setting of cerebral amyloid angiopathy (CAA) in the elderly [4,5]. CAA is a major cause of spontaneous lobar haemorrhages in the elderly. Greenberg and colleagues [4] reported 7 cases of CAA, which were not associated with hypertension, trauma or other antecedent causes. 5 of these cases were associated with transient neurological events. The transient neurological events in such cases may be due to either focal seizures relating to petechial haemorrhages or true short-lived neurological deficits.
References
1. Gunatilake SB. Rapid resolution of symptoms and signs of intracerebral haemorrhage: case reports. BMJ 1998; 316: 1495-1496.
2. Sohn YH, Kim SM, Kim JS, Kim DI. Benign brainstem hemorrhage simulating transient ischemic attack. Yonsei Med J 1991 Mar;32(1):91-93
3. Chen WH, Liu JS, Wu SC, Chang YY. Transient global amnesia and thalamic hemorrhage. Clin Neurol Neurosurg 1996 Nov;98(4):309-311
4. Greenberg SM, Vonsattel JPG, Stakes JW et al. The clinical spectrum of cerebral amyloid angiopathy: Presentations without lobar hemorrhage. Neurology 43: 2073 -
5. Smith DB, Hitchcock M, Philpott PJ. Cerebral amyloid angiopathy presenting as transient ischemic attacks. J Neurosurg 1985; 63: 963-964
Competing interests: No competing interests
The diagnosis of "transient ischaemic attack" needs re-examining
observing rapid resolution of symptoms and signs of intracerebral
haemorrhage (May 16, p 1495).1 On my opinion, author's concept is funded
on two erroneous statements.
First statement: "…no one has reported resolution of the symptoms and
signs of intracerebral haemorrhage within 24 hours, although the
possibility has been recognised". Obviously, the author chose to ignore a few
published data showing rapid resolution of neurological deficit following
intracerebral haemorrhage.2-5
Second statement: "Intracerebral haemorrhage… is not included in the
differential diagnosis of transient ischaemic attacks."
In his capital work "Vascular disease of the central nervous system"
R.W. Ross Russell says the following: "With CT scanning it is now possible
to be sure that a brief reversible focal disturbance is not due to a minor
haemorrhage or to a cerebral tumour". He emphasises that statement with an
illustration of diagnostic algorithm (clinical screening) of patients with
transient ischaemic attacks (TIA), which includes CT scan in
differentiating between ischaemia and haemorrhage.6
TIA is universally agreed to be an episode of focal neurologic
deficit in a vascular distribution, sudden in onset and resolving without
residual deficit within 24 hours. Beyond this arbitrary limit, another
diagnosis must be made. It was Fisher (and Millikan, too) who popularised
TIA as a marker for risk of cerebral infarction. This opinion persisted
beyond the introduction of new diagnostic and explanatory methods:
computed tomography, magnetic resonance imaging, positron emission
tomography, etc. These methods revealed that even in persons with normal
findings on a neurologic examination there were often prolonged
morphologic, physiologic and/or metabolic disturbances. Therefore, the
question should be made: should we classify these patients as having a TIA
(on the basis of hysteria data and absence of neurological signs and
symptoms) or as having a cerebral infarction (on the basis of
neuroimaging)? Additionally, the unexpected frequency with which other
causative factors - which imitate TIA - are revealed using mentioned new
neuroimaging techniques has created a need to redefine the differential
diagnosis of TIA.
Whether a patient has residual neurologic abnormality is also a vague
determination. We have no applied instruments for identifying and
quantifying transitory cognitive and behavioural changes. Thus, accepted
criteria for TIA of vanishing of event and absence of residual signs are -
at least partly - obsolete.
The best illustration is shown in the result of our prospective
investigation (1991-1997): "The relationship between transient ishaemic
attack and meteorological stress" (project 3-01-229, funded by Croatian
Ministry of Science). During the mentioned period we have identified
totally 134 patients with clinically approved diagnosis of TIA (according
to the criteria recommended by Landi) who were admitted in Department of
Neurology as an emergency. Although we tried to use very strict criteria,
the percent of misclassified patients - on the basis of CT scanning - was
23 % (Table 1.)
Obviously, what we need is a re-examination of the concept of TIA.
Table 1. CT findings in patients with clinical diagnosis of TIA (1991
-1997)
Normal 103 (76,9%)
Cerebral infarction 19 (14,2%)
Cerebral tumour 7 (5,2%)
Cerebral parasites 2 (1,5%)
Subdural haematoma 2 (1,5%)
Cerebral haemorrhage 1 (0,7%)
Total 134 (100%)
Literature:
1. Gunatilake SB. Rapid resolution of symptoms and signs of
intracerebral haemorrhage: case reports. BMJ 1998; 316:1495-6.
2. Chen WH. Liu JS. Wu SC. Chang YY . Transient global amnesia and
thalamic hemorrhage. Clinical Neurology & Neurosurgery 1996; 98(4):309
-11.
3. Aparicio A. Sobrino J. Arboix A. Torres M. Hematoma
intraparenquimatoso que simula un accidente isquemico transitorio.
Medicina Clinica 1995; 104(12):478-9.
4. Sohn YH. Kim SM. Kim JS. Kim DI . Benign brainstem hemorrhage
simulating transient ischemic attack. Yonsei Medical Journal 1991;
32(1):91-3.
5. Weisberg LA. Lacorte WS . Computerized tomographic abnormalities
in patients with transient episodes of focal neurological dysfunction.
Computerized Radiology 1985; 9(4):247-54.
6. Ross Russell RW. Transient cerebral ischaemia. In: Ross Russell
RW(ed). Vascular disease of the central nervous system. Edinburgh:
Churchill Livingstone, 1983: 205-223.
Lušic Ivo, MD, PhD
Neurologist
Department of Neurology
Clinical Hospital Split
Adress:
Clinical Hospital Split
Department of Neurology
Spinciceva 1
21000 Split
Croatia
Competing interests: No competing interests