Role of Computed Tomography in the Assessment of Extent and Nature of Lesions in Ischemic Cerebrovascular Accidents

 

Thakur J.R., Dhruv K.K., Bansal A.K., Meshram A. and Shrivastava P.K.

Govt. Medical College, Jagdalpur (Bastar) 494001, India.

 

ABSTRACT:

In 20 ischemic cases, site of involvement in decreasing order were Lobar and capsular 11 (39.2%) each, lentiform nucleus and thalamus 2 (7.1%) each, caudate nucleus and brain stem 1 (3.57%) each.

In 20 ischemic cases, 18 (61.4%) lesions were located in the MCA out of 20 ischemic cases 9 showed loss of gray/white differentiation and 2 showed obscuration of lentiform nucleus. Out of 20 ischemic cases 2 (10%) showed hyperdense middle cerebral artery sign.

 

KEYWORDS: Ischaemic lesion, Site, Vascular territory, Frequency of involvement.

 

 

INTRODUCTION:

Normal cerebral blood flow to the cerebral cortex is approximately 50ml./100gms./min. Once perfusion pressure falls below critical level, tissue ischemia results. In general the cerebral blood flow threshold for electrical activity of neurons is approximately 18ml./100gms./min.

 

Cerebral ischemia may be focal as a result of arterial disease embolisation, venous disease or global as a result of decreased cardiac output, decreased peripheral resistance, metabolic or haematologic disorders. The clinical spectrum of cerebral ischemia/infarction includes transient ischemic attacks (TIAs), reversible ischemic neurological deficit (RIND), partially reversible ischemic neurological deficit (PRIND) and stroke. TIAs are brief episodes of neurological dysfuctions that commonly resolve within minutes but may last as long as 24 hrs. RINDs are episodes of neurological dysfunctions that last longer than 24 hrs. and resolve completely in several days. A stroke implies an element of fixed neurological deficit.

The role of immediate CT in the management of acute cerebral ischemia is (i) to diagnose or exclude intracerebral hemorrhage. (ii) to exclude other lesionsuch as tumor, arteriovenous malformation, subdural heamatoma.

 

Although cerebral ischemia/infarction may be detected by CT scan within 6-8 hours of the ictus. They may not be evident unit upto 24 hours post ictus. CT scan is highly sensitive for cerebral ischemia/infarction, 24 hours post ictus.

 

As very few reports of clinical study available and in 1957 a study group of World Health Organization (W.H.O.) has expressed the view that in order to get a comprehensive picture of disease in this study, Diagnostic Tool, more and more studies have to be carried out, Garg Narendra K. (1). This prompted the authors to undertake this study to find out the role of Computed Tomography in the assessment of extent and nature of lesions in ischaemic cerebro vascular accidents.

MATERIAL AND METHODS:

A study of 20 patients of both sexes and adult and older age groups with “cerebrovascular accident” diagnosed by Computed Tomography (C.T.) scan was done.

 

 

Equipment – CT examination was carried out with (Toshiba) TCT 80A and (Hitachi) CTW – 700 whole body scanners. As a routine, 10 mm. slice thickness was taken. Wherever required 5 mm. slice thickness was also taken. Minimum of 10 contiguous sections were taken in all patients with orbitomeatal line as base. If needed patients were immobilized by diaxepam given intravenously.

 

TCT 80 A (Toshiba) and CTW – 700 (Hitachi) are 3rd generation scanners.

 

Prominent features are:

1.      The use of wide fan beam X-ray tube, enables         scanning to be achieved by means of extremely         simple rotatory motion, where by the X-ray tube in                combination with detector is fully rotated with respect    to the patient.

2.      Slice width can be varied (5 mm., 10 mm.).

3.      A shift mechanism is employed to vary the scanning              area.

4.      A pulsed X-ray beam is employed to reduce the X-ray           dose received by the patient.

5.      Tilting mechanism for oblique scan.

 

 

The CT findings were recorded on a devised proforma as follows: -

1.      Site of lesion – Whether the lesion is located in       temporal, frontal, parietal, occipital, basal ganglia,         thalamic region, intraventricular, cerebellar etc.

2.      Density of lesion – Hypodense, Isodense,                Hyperdense, mixed densities, calcification, perifocal         oedema, mass effect.

3.      Cerebral edema – Present or not if present then focal,            diffuse, or perilesional.

4.      Mid line shift –

5.      Status of cisterns – The term “compressed cistern” was applied if cisterns were still visible. Cisterns         which could no longer be seen are referred to as      obliterated cisterns.

6.      Hydrocephalus

7.      Calcification

8.      Others such as loss of gray/white matter    differentiation, hyperdense middle cerebral artery sign   etc.

 

 

Patients Selection: - Patients were taken from the neurology wards of J.A. Group of Hospitals, Gwalior (M.P.) with positive CT finding. Detailed neurological as well as other systemic examination of the patients was done with special attention to the symptoms like: -

-         Headache

-         Vomiting

-         Consciousness

-         Speech and Visual Disturbances

-         Weakness

-         Convulsion

-         Fever

-         Etc.

 

A special note was made of presence or absence of pre-existing or co-existing disease like hypertension, diabetes mellitus, cardiac illness, tuberculosis, syphilis, accidents/operations, previous episode of cerebrovascular accident and other chronic medical ailments.

Hb estimation, blood sugar, urine sugar, electro cardio gram, X-ray chest, was done in relevant cases.

 

RESULTS:

On analysis of the collected (Table - I) reveals that only two ischaemic cases showed Hyperdense middle cerebral artery sign while eighteen Hypodense.Intra lesional oedema found in five ischaemic cases . Table further reveals that Loss of gray / white differentiation was present in nine cases with lobar involvement.

 

Table – I: Distribution of Ischemic cerebrovascular lesions according to CT findings

CT findings

Ischemic

Hyperdense

Hypodense

Edema

Ventricular effacement

Loss of gray/white differentiation

Calcification

2

18

5

0

9

0

 

In 20 ischemic cases site of involvement in decreasing frequency were - Lobar and capsular 11 (39.2%) each, Lentiform nucleus and thalamus 2 (7.1%) each, Caudate nucleus and brain stem 1 (3.57%) each (Table- 2).Table further shows that there was no involvement of Vermis and Cerebellum.

 

Table – II: Site and Frequency of involvement of Ischemic cases

Site

Frequency of involvement

Lobar         (hemispheric)

Internal capsule

Caudate nucleus

Lentiform nucleus

Thalamus

Brain stem

Vermis

Cerebellum

11

11

1

2

2

1

0

0

 

(Table -3) shows that in 20 ischemic cases 18 (61.4%) lesions were seen in the MCA territory,6 (21.4%) in the ACA territory and 4 (14.2%) in the PCA territory. There was no lesion in the Posterior fossa.

 

Table – III: Ischemic cases according to vascular territory

Vascular Territory

Frequency of involvement

ACA

MCA

PCA

Posterior fossa artery

6

18

4

0

 

DISCUSSION:

HR Jager studied the early signs conventional CT of stroke patients. The early signs are obscuration of the lentiform nucleus, loss of the insular ribbon and loss of the differentiation between cortical gray and subcortical white matter. Blaurt ok Jos et al (1983) observed the CT findings of 10 patients with acute global central nervous system hypoperfusion. Findings were characterized as [1] Diffuse mass effect with effacement of cerebral sulci and of the brain stem cistern (9 patients). [2] Loss of the gray/white matter differentiation (6 patients). [3] Low density lesion of the basal ganglia bilaterally (5 patients). [4] Decreased gray matter density in watershed distribution bilaterally (2 patients). In our study out of 20 cases 11 showed loss of gray/white differentiation and only two showed obscuration of the lentiform nucleus.

 

Robert G. Hart et al (2) found that about half of all hemorrhagic infarctions are associated with presumed cardioembolic strokes. Hemorrhagic infarction are present in only 5% of CT performed within the first 24 hours, But in about 20% of CT performed 1-2 weeks after stroke. In our study, one hemorrhagic infarction was found, associated with hypertension and cardiomegaly.

 

According to TA Tomsic et al (6) the hyperdense middle cerebral artery sign (HMCAS) was detected in 6 (12%) out of 50 initial studies. All six patients with HMCAS positive developed large infact in the MCA distributions. Two of the 6 HMCAS positive developed infarct in the MCA distribution. None become hemorrhagic. De. Leys et al (4) performed CT scans within 12 hours after onset in 272 consecutive, unselected patients with a first acute cerebrovascular event. 73 patients had the hyperdense middle cerebral artery sign, prevalence of 26.8% in a whole group and 41.2% in patients with middle cerebral artery infarct. Specificity was 100% but sensitivity was only 30%. Mad A rouch et al (5) Studied 13 patients with hyper dense middle cerebral artery sign. History of hypertension, diabetes mellitus and hematocrit were obtained and compared with control group of patients without a hyperdense MCA. Patient with hyperdense MCA had a higher hematocrit and also a higher prevalence of hypertension and diabetes mellitus than patient without a hyper dense MCA. The higher hematocrit may have increased the density of the blood, while both DM and HT are associated with calcification within blood vessel walls. So hyperdense MCA is not a reliable indicator of occlusion of MCA or subsequent infarction. In our study, 2 cases (out of 20 ischemic events) of hyper dense MCA were found.

 

Clarles L. Truwit et al (8) found that in MCA stroke, less than 6 hours old, therer was Loss of definition of the gray/white interface in the lateral margin of insula. Loss of the insular ribbon was detected in 12 cases out of 16 prospective cases, and in all 11 retrospective cases. Loss of the insular ribbon is a reflection of acute edema due to infarction. Noriaki Tomura et al (7) observed the CT findings of 25 patients with embolic cerebral infarction, scans were obtained within 6 hours of ictus and analysed for (a) obscured outline of lentiform nucleus (b) decresed tissue density (c) effacement of cortical sulci. One or more findings were recognized in 23 out of 25 patients (92%). In our study decreased tissue density seen in 18 ischemic cases while obscuration of lentiform nucleus seen in 2 cases (10%).

 

A Kapila (2) followed up three patients with CT documented. Non hemorrhagic cerebral infarction. In the first patient, calcification was first seen in the infracted area 12 months later. The second patient was found to have calcification in the infracted area 41 months after his stroke. In the third case, calcification was first seen 4 months later.

In our study calcification was not seen in any ischemic cases.

 

Out of 20 ischemic cases lesions as shown in compared tomography, the Site of involvement in decreasing order was Lobar and capsular 11 each ()39.2%, Lentiform nucleus and thalamus 2 each (7.1%), Caudate nucleus and brain stem 1 each (3.57%).

 

Out of 20 ischemic cases 16 lesions were located in MCA territory, 5 in ACA territory, 2 in PCA territory. No ischemic lesion was detected in posterior fossa.

From above observations and discussion the authors reached to the conclusion that the inferences drawn from this study are more or less similar to that of other studies conducted across the globe from time to time.

 

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Received on 26.04.2011

Accepted on 15.05.2011     

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Research J. Pharmacology and Pharmacodynamics. 3(3): May –June, 2011, 98-101