The role of immediate CT in the management of acute cerebral ischemia/infarction is – (1) To diagnose or exclude intra cerebral hemorrhage (ICH) because the cause treatment, and prognosis of primary ICH differ from those of cerebral ischemia and (2) To identify the presence of an under lying structural lesion such as tumor, vascular malformation or Subdural heamatoma that can mimic ischemic episode clinically.

As very few reports of such studies is available and in 1957 a study group of World Health Organization has expressed the view that in order to get a comprehensive picture of disease in this case diagnostic tool ,more and more studies have to be carried out, Garg Narendra K. (1). This prompted the authors to under take this study to assess the efficacy of C.T. scan in diagnosis of the extent and nature of lesions in hemorrhagic cerebrovascular accident.

MATERIALS AND METHOD:

A study of 30 patients of both sexes and adult and older age groups with “cerebrovascular accident” diagnosed by CT scan was done. Patients were taken from the neurology wards of J.A. Group of Hospitals

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.

Data Collection:

The X-ray source (tube) and the detectors are placed opposite to each other on a movable gantry. The X-ray are well collimated in a fan shaped manner and are thrown upon the part of the patient to be scanned. There are 320 detectors in a in Toshiba TCT 80 A and 576 in Hitachi CTW 700. Detector containing high pressure Xenon gas, which detects the X-rays. The couch on which the patient is placed is movable in upwards, downwards, in wards and outwards directions.

The scanning operation begins with the X-ray generation whilst the X-ray tube and the detectors rotate 3600 around the patient patient body. In one complete rotation, 238 pulse, 400 pulse or 600 pulse X-rays are generated in 2.7 sec., 4.5 sec., or 9 sec. respectively to complete one scanning sequence. In case of Hitachi CTW 700 the pulse and scanning time are –

Pulse	246	400	600	800	1200
Scanning Time (In sec.)	1.9	3	4.5	6	9

Data Processing:

The data were obtained by 320 detectors, (576 in C/O Hitachi CTW 700). Converted to digital form (by A/D converter) and then transferred to the computer. Computer then store the data on a magnetic disc, which is an external memory unit.

(VI) After completion of each scanning, accurate absorption value of the human tissue at the slice plane is calculated by means of image reconstruction processing program, stored on the computer. The tomographic image data thus obtained is also stored on the magnetic disc for image display and processing.

The image data stored on the magnetic disc can be displayed at any time on the T.V. monitor of the console. Each displayed image has a 320-320 matrix and 64 shades of gray scale. (512 X 512 and 256 shades of gray scale in Hitachi CTW 700)

The CT values displayed can be set anywhere in the range between – 1000 to + 1000 and the window width can be set accordingly. In addition, it is possible to perform various kinds of image processing, such as displaying part of the reconstruction image in magnified form and also setting a particular region of interest to derive the average CT numbers and standard deviation for the region concerned. This system has the multiformat camera which is used to photograph the reconstructed images on X-ray films.

Attenuation coefficients and CT numbers for biolofical tissues at 6 KeV are.

Tissue	A.C. µ (cm.^-1)	CT No.
Bone	0.400	+ 1000
Blood	0.215	+ 1000 (Approx.)
Brain matter	0.210	+ 30 (Approx.)
CSF	0.207	+ 5 (Approx.)
Water	0.203	0
Fat	0.185	- 100
Air	0.0002	- 1000

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 ect.

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

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

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.

RESULTS:

On analysis of the collected data it has been observed that in all 30 haemorrhagic cases lesion was hyperdense and no hypodense (Table - I). Table further shows that there was oedema and Ventricular effacement in 21 and 30 haemorrhagic lesions respectively.There was no Calcification and loss of gray /white differentiation in haemorrhagig lesions.

Table – I Distribution of hemorrhagic cerebrovascular lesions according to CT findings

CT findings

Hemorrhagic

Hyperdense

Hypodense

Edema

Ventricular effacement

Loss of gray/white differentiation

Calcification

(Table - II) reveals that site of nvolvement in intracranial haemorrhage was in decreasing frequency - capsular 17 (28.3%), basal ganglia and lentiform nucleus - 16 (226.6%), lobar - 14 (23.3%) ,Thalamus - 4 (6.6%), brain stem - 1 (1.6%), vermis - 1 (1.6%), cerebellum -1 (1.6%).

Table – II Site and ventricular involvement of hemorrhagic cerebrovascular lesions

Site

Ventricular leak

Frequency of involvement

Lobar (hemispheric)

Capsular

Basal ganglia

Lentiform nucleus

Thalamus

Brain stem

Vermis

Cerebellum

(Table - III) In 30 haemorrhagic cases, 27 (67.5%) lesions were seen in the MCA territory and 4 (10%) in the ACA territory, 3 (7.5%) in the PCA territory and 6 (15%) in the posterior fossa.

Table – III Distribution of hemorrhagic cases according to vascular territory

Vascular Territory

Frequency of involvement

ACA

MCA

PCA

Posterior fossa

DISCUSSION:

Hypertensive ICH (Okajaki H, 1989) has a predilection for areas supplied by penetrating branches of the middle cerebral and basilar arteries Hypertensive ICH therefore preferentially involves the external capsule and putamen. Thalamus and Pons. About Two/Third of spontaneous intracerebral hematomas are located in the basal ganglia and often extend beyond the putamen to include the globus pellidus and internal capsule.

In posterior fossa, the cerebellum is relatively common site, the mid brain, medulla and spinal cord are rarely involved.

High-density basal ganglionic hematomas with or without intraventricular hemorrhage are the most common CY manifestations of acute hypertensive ICH, followed by thalamic and pontine hemorrhage. Leys D.et al (4) found the location of hemorrhage in decreasing order of frequency – putamen and external capsule 60 to 65%, thalamus 15 to 25%, pons 5 to 10%, cerebellum 2 to 5% and subcortical white matter 1 to 2%. In our study sites of intra cranial hemorrhage are internal capsule (28.3%), Basal ganglia and lentiform nucleus (26.6%), Lobar (23.3%), Thalamus (6.6%), brainstern (1.6%), vermis (1.6%), cerebellum (1.6%).

Atlas SW et al (2) found that acute subarachnoid hemorrhage due to ruptured saccular aneurysm, usually fills the basal cisterns and sylvian fissure first. When it mixes with CSF and spreads over the cerebral convexities. Subarachnoid blood appears as high density ‘feathered’ collection along the inter hemispheric fissure. Most aneurysm arises from the circle of Willis and Middle cerebral artery bifurcation. (Watanabe AT et al, 1992). Blood in the sylvian fissure may be due to an aneurysm on the ipsilateral internal carotid, posterior hemispheric blood is usually due to an anterior communicating artery aneurysm. Blood in the fourth ventricle is often caused by a posterior inferior cerebellar artery lesion. In our study out of 3 cases 2 sub arachnoid hemorrhages were seen in the right temporoparietal region and one had multiple location with B/L parietal, Rt frontal and posterior fossa location.

Mack Geu Bae et al (3) had mentioned the rapid expansion of hypertensive intra cerebral hemorrhage. It occurred in about 3% of 320 cases. The site of hemorrhage was the putamen in 6 patients and in thalamus in 4 patients. Repeat CT scan showed an increase of heamatoma volume that was twice as large in thalamic hemorrhage and about three times as large in putaminal hemorrhage.

Gilbert J Toffol (5) et al studied the computed tomographic findings of 72 patients with intra cerebral hemorrhage. The site of hemorrhage were – 41 lobar, 11 putaminal, 4 thalamic, 4 pontine, 4 intra ventricular, 2 caudate nucleus, 2 midbrain, 2 cerebellar, 1 globus pallidus and one corpus callosum hemorrhage. The main causes were ruptured AV malformation, arterial hypertention, Sympathomimetic drug abuse, hemorrhagic tumour, acute alcoholic intoxication, preeclampsia-dclampsia, superior sagittal sinus thrombosis and systemic lupus erythematoss. In our study intracerebral hemorrhage with ventricular leak was seen in 6 cases. One out of 14 in lobar, two out of 17 in capsular hemorrhage, 2 out of 8 in lenform nucleus and one out of four in thalamic hemorrhage.

Out of 30 hemorrhagic cases 27 (67.5%) lesions were seen in the middle cerebral artery territory, 4 (10%) lesions in the anterior cerebral artery territory, 3 (7.5%) lesions in the posterior cerebral artery territory and 6 (15%) lesions in the posterior fossa.

From above observations and discussion the authors reached to the conclusion that findings of the present study are more or less in accordance of the findings of the different studies conducted by different authors from time to time across the Globe.

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Received on 19.03.2011

Accepted on 30.03.2011

Research J. Pharmacology and Pharmacodynamics. 3(2): March –April, 2011, 88-91