“Comparison of Clinical Stroke Scores and Ct Brain

“COMPARISON OF CLINICAL STROKE SCORES AND CT

BRAIN IN THE DIAGNOSIS OF INTRACEREBRAL

HAEMORRHAGE AND

INFARCT IN ACUTE STROKE PATIENTS”

Dissertation submitted to

The Tamil Nadu Dr.M.G.R. Medical University

In partial fulfillment of the regualtions for

The award of the degree of

M.D. General Medicine [Branch – 1]

K.A.P.VISWANATHAM GOVERNMENT MEDICAL COLLEGE

& M.G.M. GOVERNMENT HOSPITAL,

TIRUCHIRAPPALLI.

THE TAMIL NADU DR.M.G.R. MEDICAL UNIVERSITY

CHENNAI

2016 CERTIFICATE

This is to certify that the dissertation entitled “COMPARISON

OF CLINICAL STROKE SCORES AND CT BRAIN IN THE

DIAGNOSIS OF INTRACEREBRAL HAEMORRHAGE AND

INFARCT IN ACUTE STROKE PATIENTS” is a bonafide original work of Dr. RAMYAPRASAD in partial fulfillment of the requirements of M.D., General Medicine [Branch- 1] examination of THE

TAMILNADU Dr. M. G. R. MEDICAL UNIVERSITY to be held in April

2016.

Prof.Dr.P.KANAGARAJ.M.D Prof.Dr.M.K.MURALIDHARAN.M.S.,Mch HOD & UNIT-1 CHIEF DEAN Department of Medicine K.A.P.V. Govt. Medical College K.A.P.V. Govt. Medical College M.G.M. Govt. Hospital, M.G.M. Govt. Hospital, Tiruchirappalli. Tiruchirappalli.

DECLARATION

I Solemnly declare that the dissertation titled “COMPARISON OF

CLINICAL STROKE SCORES AND CT BRAIN IN THE

DIAGNOSIS OF INTRACEREBRAL HAEMORRHAGE AND

INFARCT IN ACUTE STROKE PATIENTS” is done by me at

K.A.P. VISWANATHAM GOVT MEDICAL COLLEGE,

TIRUCHIRAPPALLI under the guidance and supervision of

Prof. Dr. P. KANAGARAJ. M.D., This dissertation is submitted to The

Tamilnadu Dr. M.G.R. Medical University towards the partial fulfillment of requirements for the award of M.D Degree (Branch-1) in

General Medicine.

Place: Tiruchirappalli Dr. RAMYAPRASAD Date: Post Graduate Student M.D. General Medicine K.A.P.V. Govt Medical College & M.G.M. Govt Hospital Tiruchirappalli.

ACKNOWLEDGEMENT

I express my sincere gratitude to The DEAN

Prof. Dr. M.K. MURALIDHARAN M.S.,Mch., for allowing me to utilize the clinical material for this study.

I am extremely grateful to Prof. Dr. P. KANAGARAJ M.D.,

Professor and Head of the Department, Department of Internal Medicine,

K.A.P.V. Govt Medical College and M.G.M. Govt Hospital for permitting me to carry out this study and for his constant encouragement and guidance.

I whole heartedly thank Prof. Dr. M.ANGURAJ M.D., D.M.,

(Neuro), HOD i/c, Department of Neurology, for his constant motivation and valuable guidance throughout my dissertation work.

I express my sincere thanks to Prof. Dr. G. Anitha M.D.,

Prof. Dr. K.Parimaladevi M.D., Prof. Dr. N.K. Senthilnathan M.D.,

Prof. Dr. A. Sethuraman M.D., and Prof. Dr. D. Nehru M.D., for their valuable guidance and motivation.

I express my sincere gratitude to Prof. Dr. R. RAVI (Radiologist),

HOD Department of Radiology for his support.

I express my sincere gratitude to DR. E.ARUNRAJ M.D., D.M.,

(Neuro) Assistant Professor of Neurology, for his guidance and help during this study.

I thank my unit Assistant Professors Dr.RAJAMAHENDRAN

M.D., Dr.THENMOZHI M.D., and Dr.M.SUBRAMANI M.D., for their continuous motivation and valuable guidance throughout my work. I whole heartedly thank my family, colleagues, friends and staff of our hospital for their support.

I owe my sincere thanks to all the patients for their kind cooperation throughout the study.

CONTENT

S.NO TITLE PAGE NO

1 INTRODUCTION 1

2 REVIEW OF LITERATURE 3

3 AIMS AND OBJECTIVES OF STUDY 38

4 MATERIALS AND METHODS 40

5 RESULTS 48

6 SUMMARY 64

7 DISCUSSION 70

8 CONCLUSION 76

9 BIBLIOGRAPHY 78

10 ANNEXURES

1. MASTER CHART 87

2.PROFORMA 89

3. ABBREVIATIONS 90

4.ETHICAL COMMITTEE APPROVAL 93

5.PLAGIARISM REPORT 94

INTRODUCTION

Cerebrovascular accident / stroke, the second leading cause of death in the World1, is also an important cause of morbidity. Because of the varied epidemiological factors, the burden of stroke keeps increasing in the developing countries2, including India. Early diagnosis and prompt treatment can help in preventing the morbidity and also mortality. The prompt management of stroke depends on the correct diagnosis of its subtypes, mainly ischemic or hemorrhagic, so that thrombolytic therapy can be instituted for the needed.

CT Brain is a safe and accurate diagnostic tool for the differentiation of ICH and Ischemic Stroke. However, a relatively good number of patients in developing countries have only poor access to CT or could not afford for

CT. The clinical features of ICH and IS has much overlap3 and hence making the clinical differentiation difficult. Several clinical scoring systems were designed for their differentiation.

SIRIRAJ SCORE4 AND ALLEN SCORE5are among the various scores. The aim of this study is to compare and validate the two scores and to assess their predictive accuracy by comparing them with CT Brain.

REVIEW OF

LITERATURE

REVIEW OF LITERATURE

A cerebrovascular accident is defined as an abrupt onset of a neurological deficit, that is attributable to a focal vascular cause1.Thus stroke is more of a clinical diagnosis, which is supported by imaging studies.

The definition of TIA needs that all neurologic signs and symptoms resolve within 24 hours without any evidence on brain imaging 1.when it lasts for more than 24 hours or the brain infarction is demonstrable, then it implies that stroke has occurred.

The 24 hours time limit differentiating TIA and stroke is important, because both do not have the same differential diagnosis. TIA, is never caused by intracerebral haemorhage and stroke is more uniformly defined and more likely to be reported than TIA, but the investigations being almost identical for both.

As per WHO, about 15 million people suffer from stroke each year worldwide. Among them, about 5 million die and about 5 million suffer permanent disablement. In US, stroke is the third leading cause of death, with about three quarters of all strokes occurring among people more than

65 years .

In India, the incidence rate being 119- 145 per lakh. Prevalence rate among rural population being 334 – 424 per lakh and urban being 84 – 262 per lakh 6.

Average age being 15 years younger for stroke patients in india, when compared to developed nations and about one fifth being below 40 years.

However the mean age for stroke being 66-67 years in India. The age standardized incidence rate being higher in men than women, that is, 162 per lakh person years for men, against 142 per lakh person years in women.

Stroke occurs in relatively older age in women than men.(68.9 years in women and 63.4 years in men).

Among the stroke subtypes, ischemic stroke being common than haemorhagic Stroke. The main risk factors for stroke in India being hypertension, diabetes mellitus, hypercholesterolemia and smoking.

On comparing urban and rural populations, the annual incidence was higher among rural population, the main contributing factors being smoking and the presence of multiple risk factors together. On the contrary, the number of patients undergoing imaging was significantly lower in rural population .

RISKFACTORS :

AGE :

Age is the strongest risk factor for stroke, with the stroke in people aged 75 to 84 years being 25 times more common than in people aged 45 to

54 years .

SEX :

Small excess incidence in males is observed .

BLOOD PRESSURE :

There seems to be a log linear relationship between the usual diastolic blood pressure and stroke throughout the normal range ,with no evidence of a threshold below which the risk becomes stable . This applies even to patients, who have already experienced cerebrovascular symptoms7.

The association between increasing blood pressure and stroke seems to become less in the elderly, when compared to middle age. In the very elderly, stroke may be associated with low blood pressures, with the low blood pressure being a reflection of pre existing cardiovascular and other diseases 8.

SMOKING :

There seems to be a dose response relationship, with both the males and females being equally affected .There seems to be association with passive smoking also9,10.Ex smokers have a sustained excess risk of stroke for some years 11.

BLOOD LIPIDS :

Increased serum lipoprotein (a) carries risk for stroke .There seems to be a negative association of cholesterol with intracranial haemorhage, which obscures any positive association with the ischemic stroke in studies of ‘all strokes’12.

DIABETES MELLITUS :

The presence of diabetes mellitus almost doubles the stroke risk when compared with non diabetics .Also strokes in diabetics are likely to be fatal13. Among the hemostatic variables, increasing fibrinogen, raised factor

VII coagulant activity, raised tissue plasminogen activator antigen, raised vwf seems to be risk factors for stroke14.

ATRIAL FIBRILLATION

By virtue of forming clot in the left atrium and its appendage, atrial fibrillation is the most frequent potential cardiac source of embolism to the

13 brain, with the non rheumatic atrial fibrillation contributing more than the rheumatic atrial fibrillation, with the lone AF (i.e., without other cardiac disease ) also being a risk factor. Among the fibrillating population, further high risk exists for those with a previous embolic event, hypertension, diabetes mellitus, increasing age and left ventricular dysfunction15.

ALCOHOL :

Heavy alcohol consumption being an independent risk factor, more for haemorhagic than ischemic stroke 16. Alcohol raises blood pressure, affects blood lipids, can cause cardiomyopathy and atrial fibrillation and could contribute to stroke in these ways also.

OBESITY:

Increased risk for stroke, because of associated hypertension, dyslipidemia and insulin resistance17.

DIET :

Deficiency of fresh fruits and vegetables, vitamin E, vitamin C, beta carotene, flavanoids (antioxidants) are the proposed risk factors. High intake of potassium reduces and excessive salt intake increases stroke risk.

Lack of Exercise has association with stroke18. Parental history of stroke is also a risk factor19. Type A personality, stress, depression, sleep apnea, snoring, high body stores of iron, low bone density, low serum albumin have all been postulated as possible associations.

As the atheroma in one arterial system is often accompanied by atheroma in other arteries as well, Coronary artery disease (i.e., angina or myocardial infarction) is associated with ischemic stroke. Also cardiac failure and left ventricular hypertrophy are associated with stroke20.

In the same way, Claudicants and those with asymptomatic peripheral vascular disease are at excess risk for stroke. Carotid and supraclavicular arterial bruits are risk factors for subsequent stroke. A TIA patient has an excess risk of stroke, about 5 – 10 times greater than that of a non TIA patient of the same age .

BLOOD SUPPLY OF THE BRAIN21

The brain which is only 2 percent of total body weight, receives 20 percent of the cardiac output and consumes about 20 percent of total inspired oxygen .Arterial supply is via two internal carotid arteries and

15 two vertebral arteries which anastomose to form the Circle of Willis, at the base of brain, with the carotid arteries supplying the anterior and the vertebrobasilar arteries supplying the posterior portions of the brain.

The common carotid artery bifurcates at the level of the thyroid cartilage into internal and external carotid arteries. The internal carotid artery starts as the carotid sinus, runs up the neck without any branches and at the base of skull, passes through the foramen lacerum to enter the carotid canal in the petrous bone.

From the carotid canal, the internal carotid artery passes through the cavernous sinus forming the carotid siphon, pierces the dura and just medial to the anterior clinoid process, bifurcates into the anterior cerebral artery and the larger middle cerebral artery.

- The ophthalmic artery is the first major branch arising in the

cavernous sinus.

- Posterior communicating artery is the next branch, which passes to

join the posterior cerebral artery to form the circle of Willis.

- Anterior choroidal artery arises from the last section of the internal

carotid artery.

- Anterior cerebral artery passes horizontally and medially to enter

the interhemispheric fissure, where it anastomoses with its

counterpart via the ACoA, curves around the genu of corpus

callosum, supplying the anterior and medial parts of the cerebral

hemisphere.

- The Middle cerebral artery after entering the sylvian fissure,

divides into 2 to 4 branches, which supply the lateral cerebral

hemispheres. A medial and lateral group of tiny lenticulostriate

arteries arise from its main trunk, pass upwards to penetrate the

base of the brain, to supply the basal ganglia and internal

capsule22.

COLLATERAL BLOOD SUPPLY OF BRAIN23

The development of effective collateral channels is more likely if the occlusion develops gradually rather than suddenly. Also when compared with the normal cerebral blood vessels, the functional capacity to respond to changes in the perfusion pressure is limited for the collateral vessels.

Collaterals may develop via :

 The circle of Willis formed by the proximal parts of the two anterior

cerebral arteries connected by ACoA and the proximal part of the two

PCAs, which are connected to the distal ICAs by the PCoA .

 Around the orbit, between branches of ECA and the ophthalmic

artery, if ICA is severely stenosed .

 Muscular branches of the vertebral artery may receive blood from

occipital, ascending pharyngeal arteries, with the vertebral

obstruction.

 Leptomeningeal anastomoses

 Dural anastomoses

 Anastomoses between Anterior choroidal artery, a branch of ICA,

with the posterior choroidal artery, a branch of PCA.

THE REGULATION OF CEREBRAL BLOOD FLOW

In normal humans, cerebral blood flow is 50 ml per 100 mg of brain per minute. Studies have shown that CBF, CBV, CMRO2 are all higher in grey than in white matter24. CBF is much influenced by small changes in

PaCO2. A 1mm Hg acute rise of PaCO2 causes about 5 % increase in CBF due to dilatation of cerebral resistance vessels, whereas in chronic respiratory failure, adaptation occurs and CBF is normal despite hypercapnia. But in case of PaO2, only when it falls below 50 mmHg, the cerebral vascular resistance falls and CBF rises.

CBF is inversely related to the blood viscosity, the main determinant of which is the haematocrit. The reason being, the higher O2 content of high haematocrit blood, reduces the flow and so maintains normal oxygen delivery to the tissues to meet normal metabolic demands.

CBF depends on cerebral perfusion pressure and the cerebrovascular resistance. The CPP is the difference between the systemic arterial pressure at the base of the brain, when in the recumbent position and the venous pressure at the exit from the subarachnoid space, which is equated to the intracranial pressure. Normally, CBF remains almost constant when the systemic blood pressure lies between 50 to 170 mmHg .

The maintenance of a constant CBF during changes in CPP constitutes

Autoregulation. Within the autoregulatory range of blood pressure, as the

CPP falls, there is vasodilation of the cerebral resistance vessels within seconds, leading to a rise in CBV and hence CBF remains constant .

In chronic hypertension, there is an upward shift in the autoregulatory range so that the fall in CBF and ischemic symptoms occur at higher systemic blood pressure than normal25.Hence sudden lowering of blood pressure is more likely to cause ischemic symptoms in chronic hypertensives.

Whereas in case of hypertensive encephalopathy, which likely occurs in acute hypertension, the upper limit of autoregulation remains the same, which causes symptoms to occur once the autoregulatory range is exceeded.

PATHOPHYSIOLOGY OF ACUTE CEREBRAL ISCHEMIA

The brain derives energy from the oxidative metabolism of glucose normally. But, as there are only negligible stores of glucose in brain, when

CBF falls, the brain becomes ischemic, a series of changes which are dependent on the oxidative metabolism of glucose to provide energy in the form of ATP occur before cell death.

Cerebral blood flow

>50 ml/100g of brain /mt Normal flow , Normal function.

Low flow , Raised O2 extraction , 20 – 50 ml/100 g /mt Normal function

Ischemia without infarction.

< 20 ml/100g /mt Infarction could be prevented

if blood flow restored.

< 16 – 18 ml/100g/mt Infarction within an hour

Zero flow Death of brain tissue in 4- 10 minutes .

Increasing ischemia leads to,

 Impaired protein synthesis which is the earliest detectable metabolic

change, and

 Inefficient anaerobic metabolism of glucose, rise in lactate and fall in

pH.

 Impaired phosphocreatine and ATP synthesis and hence energy failure

 Failure of ion pumps (energy dependent) , which leads to water ,Na,

Cl ,Ca2+to enter the cells and K + leaks out.

 Neurotoxic excitatory neurotransmitters (glutamate and aspartate ) are

released, as also free O2 radicals.

 Activation of proteases occur26

 Acute inflammatory response with recruitment of inflammatory cells

occur.

The brain has the ability to resist ischemic infarction, if it has been

‘preconditioned’ with brief episodes of ischemia within the previous few hours .

THE ISCHEMIC PENUMBRA :

Around and as islands within the infarcted brain, is the ischemic penumbra. Here, there is viable tissue with ‘misery perfusion’, that is blood flow is low, function depressed, OEF high, in other words, the metabolic needs of brain are not fulfilled .

The death or recovery of the tissue depends on the speed and extent of

blood flow restoration.

The ischemic damage to the brain can be prevented, when the blood flow is restored in ‘therapeutic time window’. Irreversible damage to brain tissue occurs, if the window period is exceeded. In that area, OEF is low, indicating that flow is in excess of metabolic requirements, which is called ‘luxury perfusion’ .

Hence early recanalisation may be good (less tissue necrosis), while late recanalisation may be bad ( cerebral edema and haemorrhage).

TYPES OF STROKE – ISCHEMIC / HEMORRHAGIC

HEMORRHAGIC STROKE ISCHEMIC STROKE

Ischemic edema is partly Cytotoxic and partly Vasogenic. Ischemic edema reaches its maximum in 2 to 4 days and subsides over a week or two .

Cytotoxic edema Vasogenic edema

-Starts early within minutes of -Starts few hours late, after onset of stroke. onset of stroke.

-Affects Grey > white matter -Affects white > grey matter

-Intracellular water accumulation, -Damage to blood brain barrier, due to damaged cell membrane. causing plasma constituents to enter

the ECF.

Cerebral edema not only compromises further blood flow, but also causes mass effect, leading to death in the first week of infarction. The already damaged brain is very sensitive to secondary insults, such as, hypoxia, hypotension, raised ICT, dehydration, rising hematocrit, hyperglycemia and fever etc.,

Also, acute or chronic brain injury may cause effect in remote areas of the brain by reducing neuronal inputs, metabolic activity and hence blood flow, the so called ‘diaschisis’.

CAUSES OF ISCHEMIC STROKE :

Brain ischemia, followed by infarction are usually caused by occlusion or stenosis of artery , which can be the result of ,

 Disease in the arterial wall

 Embolus from the heart

 Haematological diseases and

 Other rare causes.

DISEASES OF ARTERIAL WALL :

Among the diseases of the arterial wall, the foremost is the Atheroma, which when complicated by thromboembolism accounts for the most frequent cause of cerebral ischemic stroke. Atheroma commonly affects larger and medium sized arteries, especially at the sites of arterial branching

(bifurcation) ,tortuosity (carotid siphon) and confluence (basilar artery)27, which are the sites of hemodynamic shear stress and turbulence causing endothelial trauma and stagnation of blood, promoting thrombus formation.

The various vascular risk factors (eg., hypertension) and genetic predisposition determines individual susceptibility to atheroma development, whereas the anatomy of the arteries determines its site of occurrence.

ATHEROMA FORMATION :

Intimal fatty streaks form first. It is then invaded by circulating monocyte derived macrophages, eliciting an inflammatory response and lipid deposition , leading to formation of foam cells, proliferation of smooth muscle cells and fibrosis occurs, with necrosis and calcification complicating advanced lesions. The atheromatous plaques are further complicated by rupture, followed by the platelet adhesion and activation,which initiates coagulation and thrombus formation. The formed thrombus might get incorporated into the atheromatous plaque and can then re-endothelialise, leading to its propagation even till the next branching point.

The fate of thrombus complicating an atheromatous plaque, that is, its growth or lysis or its incorporation into the vessel wall, is determined by the balance of the pro and antithrombotic factors.

An atheromatous plaque is a highly dynamic lession. It may suddenly become unstable, as a result of cracking of the fibrous cap covering it, leading to the exposure to blood of the highly thrombogenic necrotic core, leading to thrombus formation and/or embolisation.

Hence, Atherothromboembolism could be regarded as an acute on chronic disease, where the plaque could be either quiescent with a thick fibrous cap or active with ongoing thrombus or embolus formation.

ATHEROMATOUS PLAQUE

- Cholesteral embolisation more often occurs as a complication of

instrumentation /surgery of large vessels or of anticoagulation or

thrombolysis.

- Fibromuscular dysplasia affects people of any age and females more

than males. The most commonly affected artery to the brain being the

midcervical portion of the ICA. There is a ‘string of beads’

appearance in histology, characterised by fibrosis and thickening of

the arterial wall alternating with atrophy.

- Intracranial small vessel disease:

 lenticulostriate branches of MCA, thalamo perforating branches of

PCA and perforating arteries to the brainstem, are the small

penetrating arteries, which are not supported by good collaterals .

 They seem to be least affected by emboli from extracranial sites

including heart .

 They are usually occluded by thrombus complicating small

vessel arteriopathy, called ‘lipohyalinosis’, wherein muscle and

elastin in the arterial wall are replaced by collagen, causing

thickening and tortuosity of the vessels.

- Others among arterial wall diseases include arterial dissection,

embolisation from aneurysms, inflammatory vascular diseases,

irradiation etc.

EMBOLISM FROM THE HEART28 :

About 1/5 of the ischemic strokes in developed nations are due to embolus from heart, among which non rheumatic AF being the most common etiology. The composition of the embolus varies from fibrin rich

(AF) to platelet rich (MVP) to calcium (mitral annular calcification), tumour (atrial myxoma) or vegetations (infective endocarditis).

The size of the embolus also varies, which decides its site of impaction. Some emboli might be more threatening (eg.rheumatic atrial fibrillation, prosthetic valve), when compared to others (eg., patent foramen ovale, MVP). Post MI strokes can be both ischemic and haemorhagic, as a result of thrombolytic usage. MVP, valvular calcification, paradoxical embolism, prosthetic valves, septal aneurysm etc., might contribute.

The cause of cerebral ichemia is mostly due to emboli from heart,

 When there is no competing cause of brain ischemia

 No general vascular disease like angina , claudication , arterial

bruits

 Ischemia involving > 1 arterial territory

 Patient is < 40 years29.

HAEMATOLOGICAL DISORDERS:

Hematological disorders including polycythemia, essential thrombocythemia , leukemia ,paraproteinemia ,sickle cell disease ,PNH,

TTP, DIVC etc., could cause ischemic stroke.

OTHER RARE CAUSES :

Rarely stroke might complicate pregnancy , puerperium , IBD , snake bite , Fabry’s disease , homocystinuria etc.,

CAUSES OF ICH :

Primary ICH is most commonly caused by ,

 Intracranial small vessel disease associated with hyprtension

 Cerebral amyloid angiopathy.

 Intracranial vascular malformations30 (including saccular

aneurysms, AVMs, telangiectasias, cavernous malformations etc.,)

 Or a combination of above.

Chronic hypertension leads to thickening and disruption of the walls of the small arteries perforating the base of the brain, particularly basal

34 ganglia, whose rupture causes hypertensive PICH. The clinical diagnosis of hypertensive PICH is considered, when there is no alternative explanation in an already known hypertension case or when there is an evidence of hypertensive organ damage including retinopathy, left ventricular hypertrophy, etc.,

From the site of PICH on CT brain, some clue to the cause could be made eg., Hypertensive ICH usually occurs in the basal ganglia, while lobar hemorrhages are more often caused by cerebral amyloid angiopathy, vascular malformations, etc.,

Early deterioration in hemorrhage could be because of the ischemia and edema around the hematoma31, causing brain shift, increased ICT, transtentorial herniation etc.,

STROKE SYNDROMES :

Here, stroke patients are divided under four main clinical syndromes, namely,

 TACS (Total anterior circulation syndrome )

 PACS (Partial anterior circulation syndrome )

 LACS (Lacunar syndrome )

 POCS (Posterior circulation syndrome ).

This categorisation depends entirely on the symptoms and signs, provide prognostic information regarding survival ,residual disability and recurrence.

TACS :

This syndrome is characterised by,

 Contralateral hemiparesis with or without sensory deficit involving

atleast 2/3 body areas (face, upper limb, lower limb )

 Homonymous visual field defect

 New cortical dysfunction

This is usually due to an acute atherothrombotic occlusion of the ICA or embolic occlusion of MCA from cardiac /arterial source 32.The cortex is sometimes relatively spared, with the infarction being largely subcortical

( striatocapsular infarction ), due to a good pial collaterals or because of rapid recanalisation.

PACS :

PACS or cortical infarcts consists of only 2/3 components of TACS.

They are caused due to occlusion of a branch of MCA / rarely the ACA trunk, as a result of embolism from heart or a proximal atherothrombus. Left

36 anterior cerebral infarcts are prone to cause a curious dyspraxia of the left upper limb, due to the infarction of the corpus callosum, thereby disconnecting the right motor centres from the left language centres.

LACS :

These are defined much clinically and characterised by small deep lesions in the corona radiata, internal capsule ,thalamus ,cerebral peduncle and pons, due to occlusion of a small perforating artery . Usually in LACS, there is no visual field defect, no new cortical defect, no impairement in consciousness and no features suggestive of brainstem syndrome.

4 main LACS are

1. Pure motor stroke

2. Pure sensory stroke

3. Sensorimotor stroke

4. Ataxic hemiparesis

POCS :

POCS indicates infarction in the vertebrobasilar circulation, the causes of which being rather heterogenous, is characterised by brainstem, cerebellar, thalamic or occipital lobe signs.

BOUNDARY ZONE / WATERSHED INFARCTS :

There are mainly three border zones between arterial territories and the infarcts involving these zones are called watershed infarcts.

1. Anterior boundary zone - Frontal parasagittal region between

superficial territories of MCA and ACA.

2. Posterior boundary zone - Parieto occipital region between

superficial territories of MCA and PCA .

3. Subcortical boundary zone - Paraventricular white matter of corona

radiata, between superficial and deep branches of MCA .

They are caused mainly in two main situations of hypotension :

1. Sudden cardiac arrest, causing profound hypotension.

2. ICA occlusion /extreme stenosis .

WATERSHED INFARCTS - BRAIN

ADVERSE PROGNOSTIC FACTORS FOR STROKE :

Hemorrhagic stroke has higher mortality than ischemic stroke. Among ischemic strokes, TACS carries almost equal poor outcome as PICH.

The best single predictor being impaired consciousness.Others include stroke severity, midline shift, high and low BP, fever, Atrial fibrillation, high blood glucose, premorbid state of the patient etc.,

Death in first few days is often due to either ICH / large infarct with edema,causing shift or herniation or due to direct disruption of vital centres.

Death after the first week is mainly because of indirect effects like pneumonia, pulmonary embolism or coexisting cardiac disease .

EVOLUTION OF THE STROKE IN CT SCAN OF BRAIN :

ISCHEMIC STROKE :

A diffuse low density area appears due to increasing water content, within a few hours. It might be accompanied by a subtle effacement of sulci and loss of the normal grey-white matter differentiation, loss of the insular ribbon, loss of lentiform nucleus outline and ventricular compression 33. In some cases, there may be ‘dense artery sign’. Infarct might become isodense in the II and III weeks and reappears as a well demarcated low density area

40 later34.Ipsilateral ventricular dilatation due to brain substance loss might occur later.

CT scan might be normal, immediately after onset, if the lesion is small (< 0.5 cm in diameter) or in the posterior fossa lesions.

PICH :

It appears at once as a well demarcated high density area. Even lesions of 0.5 cm diameter can be picked up in CT. Mixed density hemorrhages (blood of different ages ) indicates Amyloid angiopathy and a blood fluid level might suggest a hemostatic defect 35. In a day or two, a low density halo appears indicating edema, ischemic necrosis or clot retraction .

As the blood gets absorbed and the hemoglobin broken down, the high intensity area reduces and the density also reduces becoming isodense with the surrounding brain and finally in some, it becomes even hypodense .

CT BRAIN - ISCHEMIC STROKE

CT BRAIN – HAEMORRHAGIC STROKE

STUDY AIMS AND OBJECTIVES

AIMS AND OBJECTIVES

 To compare the clinical stroke scores (Siriraj score and Allen

score)

 To compare the results of clinical scores with CT Brain and

 To assess the predictive accuracy and validity of the clinical stroke

scores (Siriraj score and Allen score).

MATERIALS AND METHODS

PLACE OF STUDY :

MAHATMA GANDHI MEMORIAL GOVERNMENT

HOSPITAL, attached to KAP VISWANATHAM GOVERNMENT

MEDICAL COLLEGE, TIRUCHIRAPPALLI in southern region of India.

DEPARTMENT IN WHICH STUDY WAS CONDUCTED :

Department of General Medicine

PERIOD OF STUDY :

FROM JANUARY 2015 TO AUGUST 2015

STUDY DESIGN :

UNICENTRIC PROSPECTIVE OBSERVATIONAL STUDY

ETHICAL COMMITTEE :

Institutional Ethical committee approval obtained. The study population was clearly explained about the study, in local language.

Informed and written consent obtained from the study population.

STUDY GROUP :

Patients admitted in Department of General Medicine, MAHATMA

GANDHI MEMORIAL GOVERNMENT HOSPITAL, attached to KAP

VISWANATHAM GOVERNMENT MEDICAL COLLEGE,

TIRUCHIRAPPALLI in southern region of India.

SAMPLE SIZE :

100 , with the male and female in unequal proportion.

STATISTICAL ANALYSIS :

SPSS software

INCLUSION CRITERIA :

 Those with neurological deficit lasting for more than 24 hours and

CT showing Cerebral Haemorrhage or Infarction.

 Those presenting within 7 days of onset of stroke .

EXCLUSION CRITERIA :

 Trauma related stroke

 Those with insufficient data to calculate scores

 Patients with subarachnoid haemorrhage

 CT scan not done due to any reason

 Patients dying or leaving the hospital within 24 hours of admission

MATERIALS :

Two clinical scoring systems developed to differentiate the subtypes of Stroke, are used in this study, namely Siriraj score4 and Allen score5.

Allen score5 / Guy’s hospital score , developed at Guys hospital,

London, analyses thirteen clinical variables and scores obtained are interpreted as ,

>+24 - ICH (Intracerebral haemorrhage)

< +4 - IS (Ischemic stroke)

+ 4 to + 24 - Uncertain

Siriraj score4 , developed at Siriraj hospital, Mahidol University,

Bangkok , analyses five clinical variables and the scores obtained are interpreted as ,

>+1 - ICH (Intracerebral haemorrhage)

<-1 - IS (Ischemic stroke)

-1 to + 1 - Uncertain

SIRIRAJ SCORE FOR STROKE

VARIABLE CLINICAL FEATURES SCORE

-Consciousness Alert +0*2.5

Drowsy/Stupor +1*2.5

Semicoma/Coma +2*2.5

-Vomiting No +0*2

Yes +1*2

-Headache(within 2 hrs) No +0*2

Yes +1*2

-Diastolic BP ------mmHg +(-----*0.1)

-Atheroma markers None -0*3

( DM, Angina, Intermittent

Claudication) One or more -1*3

Constant ------12

ALLEN SCORE FOR STROKE

CLINICAL VARIABLE SCORE FEATURES -Apoplectic onset ( loss of consciousness, None or one 0 vomiting, headache within 2 hrs, Two or more +21.9 neck stiffness ) -Level of consciousness Alert 0 (24 hrs after admission) Drowsy +7.3 Unconscious +14.6 -Plantar response -Both flexors/single 0 extensor -Both extensor +7.1 -Diastolic BP (24 hrs after admission) ------+(-----*0.17) -Atheroma markers ( DM, Angina, None 0 Intermittent Claudication) One or more -3.7 -H/O Hypertension Not present 0 Present -4.1 -Previous Event None 0 (TIA / Stroke) Any number -6.7 -Heart Diseases -None 0 -Aortic/Mitral murmur -4.3 -Cardiac failure -4.3 -Cardiomyopathy -4.3 -AF -4.3 -Cardiomegaly -4.3 -MI within 6 months -4.3

Constant ------12.6

The details of each clinical variable was obtained. Incase of the patient being unconscious , details were obtained from a valid attendant, who is either his / her spouse or a first degree relative , staying with him/her in the same home and knows very well of his /her medical history and therapies . The level of conciousness and blood pressure was recorded on admission and at 24 hours of admission. Systolic blood pressure was considered as the first korotkoff and diastolic blood pressure as the V korotkoff sound .

For the history of hypertension, the use of antihypertensives/old records of BP more than 140/90 mmHg was looked for. History of diabetes mellitus considered, when there is a history of the use of oral hypoglycemics/insulin .

For intermittent claudication, h/o consistent calf pain induced by exercise and getting relieved by rest within about 10 minutes was enquired for. Atrial fibrillation was detected by ECG and cardiomegaly by chest X- ray [CardioThoracic ratio > 0.5 ].

CT Brain was used as the confirmatory tool for the diagnosis of

ICH/IS. It was reported by a consultant radiologist at our hospital.

METHODOLOGY :

From every patient , admitted with the clinical suspicion of acute stroke , detailed history was obtained and general, neurological and systemic examination done and needed information were recorded at the admission .

At 24 hours of admission patient was then reassessed and needed information recorded. Patients were done CT Brain preferably within 24 to

72 hours of admission and reported by a consultant radiologist. Other relevant investigations like complete blood count including ESR and platelet count, urea , creatinine , random blood sugar , Lipid profile ,ECG , Chest X ray , ECHO were performed.

Both Allen and Siriraj Scores were calculated and results interpreted in terms of ICH and IS and compared with the CT results , using SPSS software. The scores were assessed for their comparability (using kappa statistics) ,validity (sensitivity, specificity, positive predictive value and negative predictive value) and predictive accuracy.

RESULTS

FIGURE 1

MALE/FEMALE RATIO

Female 42%

Male 58%

FIGURE 2

CT BRAIN -ICH AND IS

ICH 33%

IS 67%

FIGURE 3 A

ASS - CERTAIN AND UNCERTAIN RESULTS

UNCERTAIN 30%

CERTAIN 70%

FIGURE 3 B

SSS - CERTAIN AND UNCERTAIN RESULTS

UNCERTAIN 21%

CERTAIN 79%

FIGURE 4 A

ASS- RESULTS

ICH 17% UC 30%

IS 53%

FIGURE 4 B

SSS RESULTS

UC ICH 21% 23%

IS 56%

FIGURE 5

COMMON DIAGNOSIS BY ASS/SSS

ICH 15%

Different Results 27%

UC 13% IS 45%

RESULTS

TABLE 1 :

ASS / SSS – INTERNAL COMPARISON

SSS

ICH IS UC

ICH 15 1 1

ASS IS 1 45 7

UC 7 10 13

Kappa = 0.551

TABLE 2 :

CERTAIN AND UNCERTAIN RESULTS

-ASS/ SSS COMPARISON

ASS

Certain Uncertain Total

Certain 62 17 79

SSS

Uncertain 8 13 21

Total 70 30 100

Kappa = 0.349

TABLE 3 :

SIMILARITY OF ASS / SSS IN THEIR RESULTS

ASS

ICH IS

ICH 15 1

SSS IS 1 45

Total certain results = 62.

Kappa = 0.916

TABLE 4 :

CT BRAIN AND ASS / SSS COMPARISON

CT BRAIN

ICH IS

ICH 13 4

ASS IS 8 45

UC 12 18

ICH 20 3

SSS IS 5 51

UC 8 13

TABLE 5 :

ICH PREDICTION WITH ASS

CT BRAIN

ICH NOT ICH

ICH 13 4

ASS NOT ICH 20 63

Sensitivity : 39.39%

Specificity : 94%

PPV : 76.47%

NPV : 75.9%

TABLE 6 :

IS PREDICTION WITH ASS

CT BRAIN

IS NOT IS

IS 45 8 ASS NOT IS 22 25

Sensitivity : 67.16%

Specificity : 75.75%

PPV : 84.9%

NPV : 53.19%

TABLE 7 :

ICH PREDICTION WITH SSS

CT BRAIN

ICH NOT ICH

ICH 20 3

SSS NOT ICH 13 64

Sensitivity : 60.60%

Specificity : 95.5%

PPV : 86.9%

NPV : 83.1%

TABLE 8 :

IS PREDICTION WITH SSS

CT BRAIN

IS NOT IS

IS 51 5 SSS NOT IS 16 28

Sensitivity : 76.1%

Specificity : 84.84%

PPV : 91%

NPV : 63.63%

SUMMARY OF RESULTS

FIGURE 1.

The sample size of this study is 100 .Among them, there were 58 males with age ranging between 48 to 80 years and 42 females with age ranging between 50 to 68 years. The average age being 62 years .

FIGURE 2.

Among the 100 patients, 67 had actual ischemic stroke by CT Brain and 33 had hemorrhagic stroke by CT Brain.

By Allen score5,

<+ 4 was considered to have ischemic infarction ,

>+ 24 as hemorrhagic stroke and

+ 4 to + 24 was considered uncertain .

By using Siriraj score4,

< -1 was considered ischemic infarction

> + 1 as hemorrhagic stroke and

– 1 to + 1 was considered uncertain .

FIGURE 3A, 3B :

Allen score gave certain results in 70 cases and uncertain results in

30, whereas Siriraj score gave certain results in 79 and uncertain results in

21 cases.

FIGURE 4A, 4B :

Within the certain results, 17 were shown as ICH, 53 were shown as

IS by Allen score and 23 as ICH, 56 as IS by Siriraj score respectively .

FIGURE 5 :

Common diagnosis by both scores as ICH was in 15 cases, IS in 45 cases, uncertain in 13 cases. Both scores gave different results in 27 cases.

TABLE 1 :

Both the scores were compared by kappa statistics by using SPSS software .

( 1 - Ideal agreement

> 0.75 - excellent agreement

0 .4 to 0.75 - Intermediate to good agreement

< 0.4 - poor agreement )

The comparability between the two scores came as fair [ kappa = 0.551 ].

TABLE 2

On comparing the certain and uncertain results of both scores ,the comparability came as poor in terms of certain results .[ kappa = 0.349]

TABLE 3

But the comparison of the certain results by both the scores showed an excellent agreement.[ kappa = 0.916]

TABLE 4

Compares both the scores with CT Brain. Of the 33 cases of ICH by

CT Brain, Allen score diagnosed 13 cases as ICH, 8 cases were misdiagnosed as ischemic infarction and 12 cases as uncertain .

Likewise, among 33 cases of ICH, Siriraj score correctly diagnosed 20 cases as ICH, 5 were misdiagnosed as IS and 8 cases as uncertain.

Among 67 cases of ischemic infarction, Allen score correctly diagnosed 45 cases ,misdiagnosed 4 cases as ICH , 18 cases as uncertain .

Among 67 cases of ischemic infarction, Siriraj score correctly diagnosed 51 cases , 3 cases were misdiagnosed as ICH and 13 cases as uncertain .

TABLE 5 :

The Allen score has 39.39% sensitivity , 94 % specificity, 76.47%

PPV, 75.9% NPV for ICH, on comparing with CT scan .

TABLE 6 :

The Allen score has 67.16 % sensitivity, 75.75% specificity, 84.9%

PPV, 53.19% NPV for IS , by comparison with CT scan.

TABLE 7

Siriraj score has 60.60% sensitivity, 95.5% specificity , 86.9 % PPV and 83.1 % NPV for ICH, when compared with CT scan.

TABLE 8 :

Siriraj score has 76 % sensitivity, 84.84% specificity, 91 % PPV,

63.63 % NPV for IS, on comparing with CT scan.

The predictive accuracy overall by this study for ,

Allen score = 58 %

Siriraj score = 71 % .

DISCUSSION

The acute brain attack/stroke, a life threatening condition, the management of which is mainly dependent on its subtype, that is,

Ischemic/hemorrhagic stroke. The stroke scores led to great hopes of the differentiation at bedside between ICH and IS, thus helping in their management.

The actual utilisation of these scores as the initial screening tests, would be to conclusively exclude the hemorrhage, so that thrombolytic / antithrombotic therapy could be offered to patients, in places where CT is not available . For this purpose the sensitivityof these scores should be much higher for ICH.

In our study, the Allen score showed only 39.39 % sensitivity, which would not be sufficient enough for one to exclude ICH, before thrombolytic/antithrombotic therapy. Other studies which showed similar results were Celani MG et al36 (38%) , Hawkins GC et al37 (31%) , Connor

MD et al38 (34%). But, Badam P et al39 showed a sensitivity of about 81% for ICH by ASS.

The specificity for ICH was 94 % by ASS, which was in agreement with other studies like Hawkins GC et al37 , Soman et al40 , Connor MD et al38, which showed specificity between 90 – 100 % .

PPV for ICH by Allen score was 76.4% by our study. By other studies like Celani MG et al36, it was 71% and Hawkins GC et al37, it was

73%. NPV by our study was 75.9%, which matches with 71% by Salawu F et al41 and 78% by Soman A et al40.

By Siriraj score in our study, the sensitivity for ICH was 60.6%, which was matching with other studies like Connor MD et al38 (60%),

Celani MG et al36 (61%), Shah FU et al42 (73%), Ogan S et al43 (50%),

Badam P et al39 (78%), wherein the sensitivity was <80%. Hence 60.6% sensitivity would not allow us to use Siriraj score as a screening test for ruling out ICH.

The original study by Pongvarin et al4, showed 80-90% sensitivity for

ICH by Siriraj score. This difference could be attributed to the difference in the number of ICH patients.(42 in Pongvarin et al; 33 in our study).

Specificity for ICH by Siriraj score was 95.5% in our study, agreeing with 94% in Celani MG et al36 and 90% in Shah FU et al42 and Hui ACF et al44.

PPV was 86.9% and NPV 83% for ICH by Siriraj score in our study, favouring Kocher et al45 (PPV 70% ; NPV 85% ) and Celani MG et al36

(PPV 70% ; NPV 93% ).

For Ischemic stroke, the sensitivity by Allen score in our study was

67%, which matches with other studies showing <80% sensitivity for IS by

Allen score.(Hawkins et al37, Connor et al38, Salawu et al41).

Specificity in our study came as 75% for IS by Allen score, which was nearer to 74% by Connor MD et al38. PPV was 84% and NPV 53% by our study. PPV was found as 91% by Celani et al36 and NPV as 55% by Akhtar sherin et al46.

By Siriraj score, the sensitivity for IS by our study was 76%. ( similar results: Kochar et al45 73%, Shah FU et al42 71%). But the original study by

Pongvarin for SSS showed 93% sensitivity for IS.

Specificity was 84% for our study for IS by Siriraj, which is favoured by 85% in Hung LY et al47. PPV 91%, NPV 63% in our study for IS by

Siriraj, which was consistent with PPV 93% in Nyandaiti YW et al48 and

NPV 71% by Kochar et al45.

On comparing ASS and SSS, both do not diagnose the same cases as

ICH or IS. Of the 100 cases, 15 were diagnosed as ICH, 45 as IS and 13 as uncertain by both the scores, whereas 27 cases showed different results.

The overall comparability of the two scores was fair ( kappa 0.551), similar to k=0.51 by Badam P et al39. Our study with a poor comparability in terms of certain results with kappa 0.349, was matching with k=0.23 by

Celani MG et al36.

The comparability, which was markedly increased by considering the results within the certainity range (62 cases), with the kappa showing excellent agreement(0.916), was also matching with other studies like 0.93 for Salawu F et al41.

The predictive accuracy overall was 71% for Siriraj and 58% for

Allen score. Studies have shown that the accuracy in diagnosis can be increased by combining both scores (Celani et al36, Illic T et al49), but there exists some limitations in the simultaneous application of both scores.

The clinical variables utilised for Siriraj scoring are all used in Allen score also. So it might seem like a waste of time in making double calculations. Allen score can be calculated only at the end of 24 hours.

Hence for any case dying within 24 hours of admission, Allen score couldn’t be calculated. When compared with Allen score, Siriraj score is much simple and requires only less information.

But as far as both scores are concerned, they both have only a vague definition for clinical variables including level of consciousness, which results in subjective error in the calculation of scores. Hawkins et al37 used

GCS for assessing level of consciousness, which with those of expressive aphasia and those with high GCS and mild drowsiness, gave underscores.

Both scores have some patients under the uncertain category. For them, CT has to be done to arrive at a diagnosis.

CONCLUSION

 Both the scoring systems have only insufficient statistical power in the

differentiation of ICH and IS, for making therapeutic decisions like

thrombolytic / antithrombotic therapy.

 Hence for epidemiological utilisation, more studies on larger basis are

needed.

 Until then, Neuroimaging is definitely needed for the acute stroke

patients, for making therapeutic decisions, aiming at salvaging the

ischemic penumbra.

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MASTER CHART

PROFORMA

NAME : AGE: SEX:

Sample number : Address :

H/O loss of consciousness: H/o HT: Vomiting : H/o DM: Headache(within 2 hrs): H/o Angina : H/o intermittent claudication: Level of consciousness H/o previous TIA/Stroke : On admission : H/o Heart disease : 24 hrs after admission: Diastolic BP On admission : 24 hrs after admission: Neck stiffness : Plantar response :

ALLEN SCORE : CT BRAIN : SIRIRAJ SCORE :

ABBREVIATIONS

ACA – Anterior cerebral artery

ACoA – Anterior communicating artery

AF – Atrial fibrillation

ASS – Allen stroke score

ATP – Adenosine triphosphate

AVM – Arterio-venous malformation

BP – Blood pressure

C – Certain

CBF – Cerebral blood flow

CBV – Cerebral blood volume

CMRO2 – Cerebral metabolic rate of oxygen

CPP – Cerebral perfusion pressure

CT – Computed tomography

DIVC – Disseminated intravascular coagulation

DM – Diabetes mellitus

ECA – External carotid artery

ECF – Extracellular fluid

ECG – Electrocardiogram

ECHO – Echocardiogram

ESR – Erythrocyte sedimentation rate

GCS – Glascow coma scale

HT – Hypertension

IBD – Inflammatory bowel disease

ICA – Internal carotid artery

ICH – Intracerebral haemorrhage

ICT – Intracranial tension

IS – Ischemic stroke

LACS – Lacunar syndrome

MCA – Middle cerebral artery

MI – Myocardial infarction

MVP – Mitral valve prolapse

NPV – Negative predictive value

OEF – Oxygen extraction fraction

PACS – Partial anterior circulation syndrome

PaCO2 – Partial pressure of carbondioxide

PaO2 – Partial pressure of oxygen

PCA – Posterior cerebral artery

PCoA – Posterior communicating artery

PICH – Primary intracerebral haemorrhage

PNH – Paroxysmal nocturnal haemoglobinuria

POCS – Posterior circulation syndrome

PPV – Positive predictive value

SSS – Siriraj stroke score

TACS – Total anterior circulation syndrome

TIA – Transient ischemic attack

TTP – Thrombotic thrombocytopenic purpura

UC – Uncertain

US – United states

WHO – World health organisation

100

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