Cerebrovascular Diseases

                                              Literary Review – Modern

Introduction-

Cerebrovascular diseases include some of the most common and devastating disorders ischemic stroke, hemorrhagic stroke, and cerebrovascular anomalies such as intracranial aneurysms and arteriovenous malformations (AVM). Most cerebrovascular diseases are manifest by the abrupt onset of a focal neurologic deficit, as if the patient was "struck by the hand of God." A stroke, or cerebrovascular accident, is defined by this abrupt onset of a neurologic deficit that is attributable to a focal vascular cause. Thus, the definition of stroke is clinical, and laboratory studies including brain imaging are used to support the diagnosis. The clinical manifestations of stroke are highly variable because of the complex anatomy of the brain and its vasculature. Neurologic symptoms are manifest within seconds because neurons lack glycogen, so energy failure is rapid. If the cessation of flow lasts for more than a few minutes, infarction or death of brain tissue results. When blood flow is quickly restored, brain tissue can recover fully and the patient's symptoms are only transient: This is called a transient ischemic attack (TIA). The standard definition of TIA requires that all neurologic signs and symptoms resolve within 24 hours regardless of whether there is imaging evidence of new permanent brain injury; stroke has occurred if the neurologic signs and symptoms last for >24 hours. However, a newly proposed definition classifies those with new brain infarction as ischemic strokes regardless of whether symptoms persist.

 

Epidemiology-

From e medicine                                                                                   

According to the World Health Organization (WHO), 15 million people suffer stroke worldwide each year. Of these, 5 million die and another 5 million are left permanently disabled.^[27]

The global incidence of stroke has at least a modest variation from nation to nation, suggesting the importance of genetics and environmental factors, such as disparities in access to health care in developing countries. The age-adjusted incidence of total strokes per 1000 person-years for people 55 years or older has been reported in the range of 4.2 to 6.5. The highest incidences have been reported in Russia, Ukraine, and Japan.

Overall, the incidence of acute stroke has demonstrated a constant decline over the past several decades, most notably during the 1970s-1990s, although in recent years the rate trend has begun to plateau. However, the increased survival among stroke victims will place an increased demand on health-care systems globally.^{[11, 29]}

Stroke is the leading cause of disability and the fourth leading cause of death in the United States.^{[47, 48]} Each year, approximately 795,000 people in the United States experience new (610,000 people) or recurrent (185,000 people) stroke.^[6]Epidemiologic studies indicate that 82-92% of strokes in the United States are ischemic.

Sex-, and age-related demographics

Global measurements undertaken by the WHO revealed an up to ten-fold difference in age-adjusted and sex-adjusted mortality rates and burden (measured in disability-adjusted life year loss rates among countries. Both were considerably higher in low-income countries (North Asia, Eastern Europe, Central Africa, and South Pacific) compared to high-income countries (Western Europe, North America).^1,2 

 

Prevalence- (http://www.strokeforum.com/stroke-background/epidemiology.html)

• One in every 10 deaths is caused by stroke; thus it is the third most common cause of death in developed countries, exceeded only by coronary heart disease and cancer.³

Incidence-

• Worldwide, 15 million people suffer a stroke each year; one-third die and one-third are left permanently disabled.³

Cost of stroke-

Burden of stroke-

• Stroke incidence has declined by over 40% in the past four decades in high-income countries, but over the same period, incidence has doubled in low- and middle-income countries.⁹

• Given that age is one of most substantiated risk factors for stroke, the ageing of the world population implies a growing number of persons at risk.¹⁰

• The World Health Organization (WHO) predicts that disability-adjusted life years (DALYs) lost to stroke (a measure of the burden of disease) will rise from 38 million in 1990 to 61 million in 2020.³

 

Classification of stroke-

Stroke is a heterogeneous disease with more than 150 known causes. Strokes can broadly be divided into:

• Ischaemic - restricted or interrupted blood and therefore oxygen supply to an area of the brain
• Haemorrhagic - bleeding into an area of the brain, due to rupture of a blood vessel or abnormal vascular structure in the brain

 

This distinction between haemorrhagic and ischaemic stroke is critical for stroke management and treatment decisions.

 

Haemorrhagic strokes can further be distinguished into intracerebral and subarachnoid strokes.

 

Of all strokes, 88% are ischaemic and 12% are haemorrhagic in nature. Of the haemorrhagic strokes, 9% are due to an intracerebral haemorrhage, and 3% are due to a subarachnoid haemorrhage.

Stroke subtypes-

There are various classification systems for the subtypes of ischaemic strokes, each with their own strengths and weaknesses.

Some of the most commonly used systems include:

1. Stroke Data Bank Subtype (NINDS) Classification-

Derived from the Harvard Stroke Registry classification, the National Institute of Neurological Disorders and Stroke (NINDS) Stroke Data Bank recognised 5 major groups

1. Infarction of unknown cause
2. Infarction with normal angiogram
3. Infarction in association with arterial pathology
4. Embolism from a cardiac source
5.  Infarction due to atherosclerosis
6. Lacune infarct
7. Parenchymatous or intracerebral haemorrhage
8. All other strokes

 

2. The Oxford Community Stroke Project classification (OCSP, also known as the Bamford or Oxford classification)-

Relies primarily on the initial symptoms; based on the extent of the symptoms, the stroke episode is classified as:

1. Total anterior circulation stroke (TAC)
2. Partial anterior circulation stroke (PAC)
3. Lacunar stroke (LAC)
4. Posterior circulation stroke (POC)

 

The type of stroke is then coded by adding a final letter to the above:

I – for infarct (e.g. TACI)

H – for haemorrhage (e.g. TACH)

S – for syndrome; intermediate pathogenesis, prior to imaging (e.g. TACS)

 

These four entities predict the extent of the stroke, the area of the brain affected, the underlying cause, and the prognosis.

 

3. The TOAST (Trial of Org 10172 in Acute Stroke Treatment) classification-

Is based on clinical symptoms as well as results of further investigations. Based on this, a stroke is classified as being due to:

1. Thrombosis or embolism due to atherosclerosis of a large artery
2. Embolism of cardiac origin
3. Occlusion of a small blood vessel
4. Other determined cause
5. Undetermined cause

            a. Two possible causes

            b. No cause identified

            c. Incomplete investigation

 

Determination of the subtype is important when:

• Classifying patients for therapeutic decision-making in daily practice
• Describing patients’ characteristics in a clinical trial
• Grouping patients in an epidemiological study.
• Careful phenotyping of patients in a genetic study.

 

Etiology-

1.     Causes Of Ischemic Stroke :

·       It results from several etiological factors out of which three are predominant:

      Thrombosis, embolism and lacunar disease.

 

Common causes

Uncommon causes

1.     Thrombosis ·       Lacunar stroke (small vessel) ·       Large vessel thrombosis ·       Dehydration 2.     Embolic occlusion     Artery-to-artery Ø  Carotid bifurcation Ø  Aortic arch Ø  Arterial dissection     Cardioembolic Ø  Atrial fibrillation Ø  Mural thrombus Ø  Myocardial infarction Ø  Dilated cardiomyopathy Ø  Valvular lesions o   Mitral stenosis o   Mechanical valve o   Bacterial endocarditis Ø  Paradoxical embolus ·       Atrial septal defect ·       Patent foramen ovale Ø  Atrial septal aneurysm Ø  Spontaneous echo contrast

·       Hypercoagulable disorders Ø  Protein C deficiency Ø  Protein S deficiency Ø  Antithrombin III deficiency Ø  Antiphospholipid syndrome Ø  Factor V Leiden mutationa Ø  Prothrombin G20210 mutationa Ø  Systemic malignancy Ø  Sickle cell anemia Ø  Thalassemia Ø  Polycythemia vera Ø  Systemic lupus erythematosus Ø  Homocysteinemia Ø  Dysproteinemias Ø  Nephrotic syndrome Ø  Inflammatory bowel disease Ø  Oral contraceptives ·       Venous sinus thrombosisb ·       Fibromuscular dysplasia ·       Vasculitis o   Systemic vasculitis] o   Primary CNS vasculitis o   Meningitis (syphilis, tuberculosis, fungal, bacterial, zoster) Cardiogenic Ø  Mitral valve calcification Ø  Atrial myxoma Ø  Intracardiac tumor Ø  Marantic endocarditis Ø  Libman-Sacks endocarditis Subarachnoid hemorrhage vasospasm Drugs: cocaine, amphetamine Moyamoya disease Eclampsia

 

 

II. Causes Of Intracranial Haemorrhage 

 

Cause	Location	Comments
Head trauma	Intraparenchymal: frontal lobes, anterior temporal lobes; subarachnoid	Coup and contrecoup injury during brain deceleration
Hypertensive hemorrhage	Putamen, globus pallidus, thalamus, cerebellar hemisphere, pons	Chronic hypertension produces haemorrhage from small(~100µm) vessels in these regions.
Transformation of prior ischemic infarction	Basal ganglion, subcortical regions, lobar	Occurs in 1–6% of ischemic strokes with predilection for large hemispheric infarctions
Metastatic brain tumor	Lobar	Lung, choriocarcinoma, melanoma, renal cell carcinoma, thyroid, atrial myxoma
Coagulopathy	Any	Uncommon cause; often associated with prior stroke or underlying vascular anomaly
Drug	Lobar, subarachnoid	Cocaine, amphetamine, phenylpropanolamine
Arteriovenous malformation	Lobar, intraventricular, subarachnoid	Risk is 2–4% per year for bleeding
Aneurysm	Subarachnoid, intraparenchymal, rarely subdural	Mycotic and nonmycotic forms of aneurysms
Amyloid angiopathy	Lobar	Degenerative disease of intracranial vessels; linkage to Alzheimer's disease, rare in patients <60 years
Cavernous angioma	Intraparenchymal	Multiple cavernous angiomas linked to mutations in KRIT1, CCM2, and PDCD10 genes
Dural arteriovenous fistula	Lobar, subarachnoid	Produces bleeding by venous hypertension
Capillary telangiectasias	Usually brainstem	Rare cause of hemorrhage

 

Risk factors

Risk factors for ischemic stroke include modifiable and nonmodifiable conditions. Identification of risk factors in each patient can uncover clues to the cause of the stroke and the most appropriate treatment and secondary prevention plan.

Nonmodifiable risk factors- include the following (although there are likely many others):

·       Age

·       Race

·       Sex

·       Ethnicity

·       History of migraine headaches^[21]

·       Fibromuscular dysplasia

·       Heredity: Family history of stroke or transient ischemic attacks (TIAs)

In a prospective study of 27,860 women aged 45 years or older who were participating in the Women's Health Study, Kurth et al found that migraine with aura was a strong risk factor for any type of stroke. The adjusted incidence of this risk factor per 1000 women per year was similar to those of other known risk factors, including systolic blood pressure 180 mm Hg or higher, body mass index 35 kg/m2 or greater, history of diabetes, family history of myocardial infarction, and smoking.^[22]

Modifiable risk factors -^[23] :

·       Hypertension (the most important)

·       Diabetes mellitus

·       Cardiac disease: Atrial fibrillation, valvular disease, heart failure, mitral stenosis, structural anomalies allowing right-to-left shunting (eg, patent foramen ovale), and atrial and ventricular enlargement

·       Hypercholesterolemia

·       TIAs

·       Carotid stenosis

·       Hyperhomocystinemia

·       Lifestyle issues: Excessive alcohol intake, tobacco use, illicit drug use, physical inactivity^[24]

·       Obesity

·       Oral contraceptive use/postmenopausal hormone use

·       Sickle cell disease

Large-artery occlusion

Large-artery occlusion typically results from embolization of atherosclerotic debris originating from the common or internal carotid arteries or from a cardiac source. A smaller number of large-artery occlusions may arise from plaque ulceration and in situ thrombosis. Large-vessel ischemic strokes more commonly affect the MCA territory, with the ACA territory affected to a lesser degree. (See the images below.)

Noncontrast computed tomography (CT) scan in a 52-year-old man with a history of worsening right-sided weakness and aphasia demonstrates diffuse hypodensity and sulcal effacement with mass effect involving the left anterior and middle cerebral artery territories consistent with acute infarction. There are scattered curvilinear areas of hyperdensity noted suggestive of developing petechial hemorrhage in this large area of infarction.Magnetic resonance angiogram (MRA) in a 52-year-old man demonstrates occlusion of the left precavernoussupraclinoid internal carotid artery (ICA, red circle), occlusion or high-grade stenosis of the distal middle cerebral artery (MCA) trunk and attenuation of multiple M2 branches. The diffusion-weighted image (right) demonstrates high signal confirmed to be true restricted diffusion on the apparent diffusion coefficient (ADC) map consistent with acute infarction.Maximum intensity projection (MIP) image from a computed tomography angiogram (CTA) demonstrates a filling defect or high-grade stenosis at the branching point of the right middle cerebral artery (MCA) trunk (red circle), suspicious for thrombus or embolus. CTA is highly accurate in detecting large- vessel stenosis and occlusions, which account for approximately one third of ischemic strokes.

Lacunar strokes

Lacunar strokes represent 13-20% of all ischemic strokes. They result from occlusion of the penetrating branches of the MCA, the lenticulostriate arteries, or the penetrating branches of the circle of Willis, vertebral artery, or basilar artery. The great majority of lacunar strokes are related to hypertension. (See the image below.)

Axial noncontrast computed tomography (CT) scan demonstrates a focal area of hypodensity in the left posterior limb of the internal capsule in a 60-year-old man with acute onset of right-sided weakness. The lesion demonstrates high signal on the fluid-attenuated inversion recovery (FLAIR) sequence (middle image) and diffusion-weighted magnetic resonance imaging (MRI) scan (right image), with low signal on the apparent diffusion coefficient (ADC) maps indicating an acute lacunar infarction. Lacunar infarcts are typically no more than 1.5 cm in size and can occur in the deep gray matter structures, corona radiata, brainstem, and cerebellum.

Causes of lacunar infarcts include the following:

·       Microatheroma

·       Lipohyalinosis

·       Fibrinoid necrosis secondary to hypertension or vasculitis

·       Hyaline arteriosclerosis

·       Amyloid angiopathy

·       Microemboli

Embolic strokes

Cardiogenic emboli may account for up to 20% of acute strokes. Emboli may arise from the heart, the extracranial arteries, including the aortic arch or, rarely, the right-sided circulation (paradoxical emboli) with subsequent passage through a patent foramen ovale.^[39] Sources of cardiogenic emboli include the following:

·       Valvular thrombi (eg, in mitral stenosis or endocarditis or from use of a prosthetic valve)

·       Mural thrombi (eg, in myocardial infarction, atrial fibrillation, dilated cardiomyopathy, or severe congestive heart failure)

·       Atrial myxoma

Acute myocardial infarction is associated with a 2-3% incidence of embolic strokes, of which 85% occur in the first month after the infarction.^[40] Embolic strokes tend to have a sudden onset, and neuroimaging may demonstrate previous infarcts in several vascular territories or may show calcific emboli.

Cardioembolic strokes may be isolated, multiple and in a single hemisphere, or scattered and bilateral; the latter 2 types indicate multiple vascular distributions and are more specific for cardioembolism. Multiple and bilateral infarcts can be the result of embolic showers or recurrent emboli. Other possibilities for single and bilateral hemispheric infarctions include emboli originating from the aortic arch and diffuse thrombotic or inflammatory processes that can lead to multiple small-vessel occlusions. (See the image below.)^{[41, 42]}

Cardioembolic stroke: Axial diffusion-weighted images demonstrate scattered foci of high signal in the subcortical and deep white matter bilaterally in a patient with a known cardiac source for embolization. An area of low signal in the left gangliocapsular region may be secondary to prior hemorrhage or subacute to chronic lacunar infarct. Recurrent strokes are most commonly secondary to cardioembolic phenomenon.

For more information, see Cardioembolic Stroke.

Thrombotic strokes

Thrombogenic factors may include injury to and loss of endothelial cells; this loss exposes the subendothelium and results in platelet activation by the subendothelium, activation of the clotting cascade, inhibition of fibrinolysis, and blood stasis. Thrombotic strokes are generally thought to originate on ruptured atherosclerotic plaques. Arterial stenosis can cause turbulent blood flow, which can promote thrombus formation; atherosclerosis (ie, ulcerated plaques); and platelet adherence. All cause the formation of blood clots that either embolize or occlude the artery.

Intracranial atherosclerosis may be the cause of thrombotic stroke in patients with widespread atherosclerosis. In other patients, especially younger patients, other causes should be considered, including the following^{[8, 43]} :

·       Hypercoagulable states (eg, antiphospholipid antibodies, protein C deficiency, protein S deficiency, pregnancy)

·       Sickle cell disease

·       Fibromuscular dysplasia

·       Arterial dissections

·       Vasoconstriction associated with substance abuse (eg, cocaine, amphetamines)

Watershed infarcts

Vascular watershed, or border-zone, infarctions occur at the most distal areas between arterial territories. They are believed to be secondary to embolic phenomenon or to severe hypoperfusion, as occurs, for example, in carotid occlusion or prolonged hypotension. (See the image below.)^{[44, 45, 46]}

Magnetic resonance imaging (MRI) scan was obtained in a 62-year-old man with hypertension and diabetes and a history of transient episodes of right-sided weakness and aphasia. The fluid-attenuated inversion recovery (FLAIR) image (left) demonstrates patchy areas of high signal arranged in a linear fashion in the deep white matter, bilaterally. This configuration is typical for deep border-zone, or watershed, infarction, in this case the anterior and posterior middle cerebral artery (MCA) watershed areas. The left-sided infarcts have corresponding low signal on the apparent diffusion coefficient (ADC) map (right), signifying acuity. An old left posterior parietal infarct is noted as well.

Flow disturbances

Stroke symptoms can result from inadequate cerebral blood flow because of decreased blood pressure (and specifically, decreased cerebral perfusion pressure) or as a result of hematologic hyperviscosity from sickle cell disease or other hematologic illnesses, such as multiple myeloma and polycythemiavera. In these instances, cerebral injury may occur in the presence of damage to other organ systems. For more information, see Blood Dyscrasias and Stroke.

Hemorrhagic Stroke –

The etiologies of stroke are varied, but they can be broadly categorized into ischemic or hemorrhagic. Approximately 80-87% of strokes are from ischemic infarction caused by thrombotic or embolic cerebrovascular occlusion. Intracerebralhemorrhages account for most of the remainder of strokes, with a smaller number resulting from aneurysmal subarachnoid hemorrhage.^{[8, 9, 10, 11]}

In 20-40% of patients with ischemic infarction, hemorrhagic transformation may occur within 1 week after ictus.^{[12, 13]}

Differentiating between the different types of stroke is an essential part of the initial workup of patients with stroke, as the subsequent management of each disorder will be vastly different.

Risk factors

The risk of hemorrhagic stroke is increased with the following factors:

• Advanced age
• Hypertension (up to 60% of cases)
• Previous history of stroke
• Alcohol abuse
• Use of illicit drugs (eg, cocaine, other sympathomimetic drugs)

Causes of hemorrhagic stroke include the following^{[11, 12, 14, 15, 16]} :

• Hypertension
• Cerebral amyloidosis
• Coagulopathies
• Anticoagulant therapy
• Thrombolytic therapy for acute myocardial infarction (MI) or acute ischemic stroke (can cause iatrogenic hemorrhagic transformation)
• Arteriovenous malformation (AVM), aneurysms, and other vascular malformations (venous and cavernous angiomas)
• Vasculitis
• Intracranial neoplasm

Hypertension

The most common etiology of primary hemorrhagic stroke (intracerebralhemorrhage) is hypertension. At least two thirds of patients with primary intraparenchymalhemorrhage are reported to have preexisting or newly diagnosed hypertension. Hypertensive small-vessel disease results from tiny lipohyalinotic aneurysms that subsequently rupture and result in intraparenchymalhemorrhage. Typical locations include the basal ganglia, thalami, cerebellum, and pons.

Aneurysms and subarachnoid hemorrhage

The most common cause of atraumatic hemorrhage into the subarachnoid space is rupture of an intracranial aneurysm. Aneurysms are focal dilatations of arteries, with the most frequently encountered intracranial type being the berry (saccular) aneurysm. Aneurysms may less commonly be related to altered hemodynamics associated with AVMs, collagen vascular disease, polycystic kidney disease, septic emboli, and neoplasms.

Nonaneurysmal perimesencephalic subarachnoid hemorrhage may also be seen. This phenomenon is thought to arise from capillary or venous rupture. It has a less severe clinical course and, in general, a better prognosis.

Berry aneurysms are most often isolated lesions whose formation results from a combination of hemodynamic stresses and acquired or congenital weakness in the vessel wall. Saccular aneurysms typically occur at vascular bifurcations, with more than 90% occurring in the anterior circulation. Common sites include the following:

• The junction of the anterior communicating arteries and anterior cerebral arteries—most commonly, the middle cerebral artery (MCA) bifurcation
• The supraclinoid internal carotid artery at the origin of the posterior communicating artery
• The bifurcation of the internal carotid artery (ICA)

Hemorrhagic transformation of ischemic stroke

Hemorrhagic transformation represents the conversion of a bland infarction into an area of hemorrhage. Proposed mechanisms for hemorrhagic transformation include reperfusion of ischemically injured tissue, either from recanalization of an occluded vessel or from collateral blood supply to the ischemic territory or disruption of the blood-brain barrier. With disruption of the blood-brain barrier, red blood cells extravasate from the weakened capillary bed, producing petechial hemorrhage or frank intraparenchymal hematoma.^{[11, 12, 20]} (For more information, seeReperfusion Injury in Stroke.)

Hemorrhagic transformation of an ischemic infarct occurs within 2-14 days postictus, usually within the first week. It is more commonly seen following cardioembolic strokes and is more likely with larger infarct size.^{[11, 13, 21]}Hemorrhagic transformation is also more likely following administration of tissue plasminogen activator (tPA) in patients whose noncontrast computed tomography (CT) scans demonstrate areas of hypodensity.^{[20, 22, 23]} See the image below.

Noncontrast computed tomography scan (left) obtained in a 75-year-old man who was admitted for stroke demonstrates a large right middle cerebral artery distribution infarction with linear areas of developing hemorrhage. These become more confluent on day 2 of hospitalization (middle image), with increased mass effect and midline shift. There is massive hemorrhagic transformation by day 6 (right), with increased leftward midline shift and subfalcine herniation. Obstructive hydrocephalus is also noted, with dilatation of the lateral ventricles, likely due to compression of the foramen of Monroe. Intraventricularhemorrhage is also noted layering in the left occipital horn. Larger infarctions are more likely to undergo hemorrhagic transformation and are one contraindication to thrombolytic therapy.

 

Pathophysiology-

A stroke occurs when the blood flow to an area of the brain is interrupted, resulting in some degree of permanent neurological damage. The two major categories of stroke are ischaemic (lack of blood and hence oxygen to an area of the brain) and haemorrhagic (bleeding from a burst or leaking blood vessel in the brain) stroke.

Pathophysiology of ischaemic stroke-

The common pathway of ischaemic stroke is lack of sufficient blood flow to perfuse cerebral tissue, due to narrowed or blocked arteries leading to or within the brain.

 

Ischaemic strokes can be broadly subdivided into thrombotic and embolic strokes.

 

Narrowing is commonly the result of atherosclerosis – the occurrence of fatty plaques lining the blood vessels. As the plaques grow in size, the blood vessel becomes narrowed and the blood flow to the area beyond is reduced.

 

Damaged areas of an atherosclerotic plaque can cause a blood clot to form, which blocks the blood vessel – a thrombotic stroke.

 

In an embolic stroke, blood clots or debris from elsewhere in the body, typically the heart valves, travel through the circulatory system and block narrower blood vessels.

 

Based on the aetiology of ischaemic stroke, a more accurate sub-classification is generally used:

• Large artery disease – atherosclerosis of large vessels, including the internal carotid artery, vertebral artery, basilar artery, and other major branches of the Circle of Willis.

• Small vessel disease – changes due to chronic disease, such as diabetes, hypertension, hyperlipidaemia, and smoking, that lead decreased compliance of the arterial walls and/or narrowing and occlusion of the lumen of smaller vessels.

• Embolic stroke – the most common cause of an embolic stroke is atrial fibrillation.

• Stroke of determined aetiology – such as inherited diseases, metabolic disorders, and coagulopathies.

• Stroke of undetermined aetiology – after exclusion of all of the above.

 

In the core area of a stroke, blood flow is so drastically reduced that cells usually cannot recover and subsequently undergo cellular death.

 

The tissue in the region bordering the infarct core, known as the ischaemic penumbra, is less severely affected. This region is rendered functionally silent by reduced blood flow but remains metabolically active. Cells in this area are endangered but not yet irreversibly damaged. They may undergo apoptosis after several hours or days but if blood flow and oxygen delivery is restored shortly after the onset of stroke, they are potentially recoverable (figure 1).

Figure 1: Ischaemic penumbra – Potential to reverse neurologic impairment with post-stroke therapy

The ischaemic cascade

After seconds to minutes of cerebral ischaemia, the ischaemic cascade is initiated. This is a series of biochemical reactions in the brain and other aerobic tissues, which usually goes on for two to three hours, but can last for days, even after normal blood flow returns.

The goal of acute stroke therapy is to normalise perfusion and intervene in the cascade of biochemical dysfunction to salvage the penumbra as much and as early as possible.

Although it is called a cascade, events are not always linear (figure 2).

Figure 2: The ischaemic cascade

(Source: http://neuro4students.wordpress.com/pathophysiology/)

Important steps of the ischaemic cascade

1. Without adequate blood supply and thus lack of oxygen, brain cells lose their ability to produce energy - particularly adenosine triphosphate (ATP).
2. Cells in the affected area switch to anaerobic metabolism, which leads to a lesser production of ATP but releases a by-product called lactic acid.
3.   Lactic acid is an irritant, which has the potential to destroy cells by disruption of the normal acid-base balance in the brain.
4. ATP-reliant ion transport pumps fail, causing the cell membrane to become depolarized; leading to a large influx of ions, including calcium (Ca++), and an efflux of potassium.
5. Intracellular calcium levels become too high and trigger the release of the excitatory amino acid neurotransmitter glutamate.
6. Glutamate stimulates AMPA receptors and Ca++-permeable NMDA receptors, which leads to even more calcium influx into cells.
7. Excess calcium entry overexcites cells and activates proteases (enzymes which digest cell proteins), lipases (enzymes which digest cell membranes) and free radicals formed as a result of the ischaemic cascade in a process called excitotoxicity.
8. As the cell's membrane is broken down by phospholipases, it becomes more permeable, and more ions and harmful chemicals enter the cell.
9. Mitochondria break down, releasing toxins and apoptotic factors into the cell.
10. Cells experience apoptosis.
11. If the cell dies through necrosis, it releases glutamate and toxic chemicals into the environment around it. Toxins poison nearby neurons, and glutamate can overexcite them.
12. The loss of vascular structural integrity results in a breakdown of the protective blood brain barrier and contributes to cerebral oedema, which can cause secondary progression of the brain injury.

Pathophysiology of haemorrhagic stroke-

Haemorrhagic strokes are due to the rupture of a blood vessels leading to compression of brain tissue from an expanding haematoma. This can distort and injure tissue. In addition, the pressure may lead to a loss of blood supply to affected tissue with resulting infarction, and the blood released by brain haemorrhage appears to have direct toxic effects on brain tissue and vasculature.

• Intracerebral haemorrhage – caused by rupture of a blood vessel and accumulation of blood within the brain. This is commonly the result of blood vessel damage from chronic hypertension, vascular malformations, or the use medications associated with increased bleeding rates, such as anticoagulants, thrombolytics, and antiplatelet agents.

• Subarachnoid haemorrhage is the gradual collection of blood in the subarachnoid space of the brain dura, typically caused by trauma to the head or rupture of a cerebral aneurysm.

 

Symptomatology-

The common mode of expression of CVD is the stroke, defined as a sudden nonconclusive, focal neurological deficit. Hemiplegia stands as a classical sign of CVD in which paralysis occurs of one side of the body affecting both arm and leg and sometimes face. Hemiplegia is most commonly seen in damage to the UMN above the level of the foramen magnum. A discrete lesion of the spinal cord in the upper cervical region may produce hemiplegia but this is rare.

 

 

Features of the major stroke subtypes-

 

Type and subtype	Clinical feature	Diagnosis
Ischaemic stroke
Lacunar infarct	Small (< 5 mm) lesions in the basal ganglia, pons, cerebellum, or internal capsule; less often in deep cerebral white matter; prognosis generally good; clinical features depend on location, but may worsen over first 24–36 hours.	MRI with diffusion-weighted sequences usually defines the area of infarction; CT is insensitive acutely but can be used to exclude hemorrhage.
Carotid- >Circulation >Obstruction	signs vary depending on occluded vessel.	Noncontrast CT to exclude hemorrhage but findings may be normal during first 6–24 hours of an ischemic stroke; diffusion-weighted MRI is gold standard for identifying acute stroke; electrocardiography, echocardiography, blood glucose, complete blood count, and tests for hypercoagulable states, hyperlipidemia are indicated; Holter monitoring in selected instances; carotid duplex studies, CTA, MRA, or conventional angiography in selected cases.
Vertebrobasilar Occlusion	signs vary based on location of occluded vessel.	As for carotid circulation obstruction.
Haemorrhagic stroke
Spontaneous intracerebral hemorrhage	Commonly associated with hypertension; also with bleeding disorders,amyloid angiopathy. Hypertensive hemorrhage is located commonly in the basal ganglia and less commonly in the pons, thalamus, cerebellum, or cerebral white matter.	Noncontrast CT is superior to MRI for detecting bleeds of < 48 hours duration; laboratory tests to identify bleeding disorder: angiography may be indicated to exclude aneurysm or AVM. Do not perform lumbar puncture.
Subarachoid hemorrhage	Present with sudden onset of worst headache of life, may lead rapidly to loss of consciousness; signs of meningeal irritation often present; etiology usually aneurysm or AVM, but 20% have no source identified.	CT to confirm diagnosis, but may be normal in rare instances; if CT negative and suspicion high, perform lumbar puncture to look for red blood cells or xanthochromia; angiography to determine source of bleed in candidates for treatment.
Intracranial aneurysm	Most located in the anterior circle of Willis and are typically asymptomatic until subarachnoid bleed occurs; 20% rebleed in first 2 weeks.	CT indicates subarachnoid hemorrhage, and angiography then demonstrates aneurysms; angiography may not reveal aneurysm if vasospasm present.
AVMs	Focal deficit from hematoma or AVM itself.	CT reveals bleed, and may reveal the AVM; may be seen by MRI. Angiography demonstrates feeding vessels and vascular anatomy.

 

AVMs, arteriovenous malformations; CTA, computed tomography angiography; MRA, magnetic resonance angiography.

 

CLINICAL FEATURES OF HEMIPLEGIA

 

1. STAGE OF ONSET :-

If the responsible cerebral lesion is acute the paralysis is at first flaccid (Shock effect).

In complete hemiplegia the arm is affected more than the leg and the distal

movements suffer more than proximal ones. The lower face is more affected than the

upper. The trunks muscular are weakened on the affected side but the ocular muscles

and those of mastication escape, as they have dual innervations from both

hemispheres.

Determination of the side of hemiplegia in an unconscious patient -

· Away from the paralysed side – A transient conjugate deviation of the head and

eyes towards the unparalysed side may be observed for a few days.

· On the hemiplegia side –

- Check puffs out during respiration.

- Nasolabial fold obliterated.

- Corneal reflex diminished

- Pain stimulation less effective

- More absolute flaccidity of limbs (dropping test)

- Paralysed leg extended and assumes position of external rotation while healthy

one tends to be semi flexed.

- Pupil large on the side of haemorrhage

- Eyelid release test: Eye-lid slides down slowly after both the eyelids are pulled up

and released simultaneously.

- Temperature of paralysed side usually higher.

In conscious patients – (On affected side)

- Weakness of closure of the eyes and the orbicularis muscle

- Weakness of the lower face when the patient is asked to show teeth with flattening

of the nasolabial fold and the base of the tongue may be higher.

- In slighter cases- weakness of dorsiflexion of the wrist and clumsiness of the fine

finger movements with the thumb-finger test, weakness of the extensors of the

fingers and elbow joint, and in the leg there is inability to dorsiflex the affected

foot as powerfully as that on the unaffected side, with weakness of the flexors of

the knee and hip.

- The tendon reflexes may be abolished for some hours.

2. Stage of Recovery (Residual Hemiplegia) :-

In chronic progressive lesion and in stage of recovery of acute lesions there is:

- Spasticity making its appearance of “Clasp-Knife” variety. Hence the tendon

reflexes return, become greatly exaggerated and may be accompanied by clonus.

- The abdominal and cremasteric reflexes on the affected side remain absent and the

planter response is clearly extensor.

- As the spasticity is greatest in the flexor muscles of the upper limb, the arm is

adducted at the shoulder, flexed at the elbow, wrist and fingers, with the forearm

slightly pronated.

- Spasticity being greater in the extensor muscles of lower limb, it is extended at the

hip and knee joints.

- The gait is characteristic, the paralysed leg being dragged round in semi circle

(circumduction), the toes scrapping the floor.

- Weakness of the affected side of face

- Tongue protruded to the affected side of face

- Certain involuntary associated movements in the affected limbs.

The spastic gait in hemiplegia

During the process of recovery, movement usually returns first at the proximal joints,

cruder movements are regained first while delicate activity of the fingers and toes is

the last to return. Power returns first, with hypertonus, to the flexor muscles of the

arm, in accordance with the physiological principle that primitive function is the last

to be destroyed and the first to recover. Thus patient may soon be able to elevate and

abduct the affected upper limb at the shoulder and to flex the elbow, fingers and wrist.

In the lower limb, power returns first to the extensors of the hip and knee, and to the

adductors. The upper abdominal reflex returns before the lower, the planter reflex

may become flexor. The recovery of aphasia usually precedes recovery of paralysis.

LOCALIZATION OF THE LESIONS PRODUCING HEMIPLEGIA

The following are some distinctive symptoms of lesions of the corticospinal tract at

different points in its course –

CORTICAL LESION:- Cortical corticospinal lesions produces monoplegia or

paralysis of even smaller muscle group, Aphasia (if dominant cortex is involved),

cortical sensory loss. Jacksonian fits may occur if the lesion is in or near the cortex.

SUBCORTICAL LESION:- Weakness predominates in one limb but the whole of the

opposite side is affected, impairment of postural sensibility and tactile discrimination

by involvement of thalamocortical sensory fibres; crossed homonymous hemianopia

by damage to optic radiation.

INTERNAL CAPSULE:- It is the commonest site and presents with a pure motor and

isolated hemiplegia, hemianesthesia if lesion in posterior one-third part. Sometimes

homonymous hemianopia on the same side may be present.

LESIONS IN THE MIDBRAIN :-

- Weber’s Syndrome: IIIrd nerve palsy with crossed hemiplegia.

- Benedikt’s Syndrome: IIIrd nerve affection on the side of lesion with tremors,

hypertonia and ataxy on opposite side.

- Facial diplegia of the supranuclear type.

Weber’s Syndrome

LESIONS IN THE PONS:

- Millard- Gubbler Syndrome: Paralysis of

lateral rectus, with or without LMN type

of facial paralysis on one side with

crossed hemiplegia.

- Foville’s Syndrome: Similar to

Millard-Gubbler syndrome except that

instead of lateral rectus paralysis, there is conjugate ocular deviation to side of

the lesion.

- Horner’s Syndrome: Paralysis of the ocular sympathetic may result from a

lesion in the tegmentum of the pons.

LESIONS IN THE MEDULLA :

- Many variety of crossed hemiplegia in unilateral medullary lesion.

- In midline lesion: Unilateral paralysis of half of the tongue, crossed

hemiplegia, loss of postural sensibility is found.

- Lesion in lateral part of medulla: Vocal cord paralysis, Horner’s syndrome,

trigeminal analgesia, thermo anesthesia, and some cerebellar deficiency - all

on the side of the lesion with loss of appreciation of pain, heat and cold in the

limbs and trunk on the opposite side.

LESION IN THALAMUS: Thalamic Syndrome:

- Fleeting hemiparesis or hemiplegia on the opposite side of the lesion.

- Impairment of superficial & loss of deep sensation on opposite side.

- Elevation of threshold to cutaneous, tactile, and painful stimuli.

- Intolerable, spontaneous pains & hyperpathia on the opposite side.

- Ataxia, tremor &/or choreoathetoid movements on the opposite side.

Spinal Cord Lesion: Unilateral lesion of the cortico-spinal tract below the medulla

and 5th cervical spine produces spinal hemiplegia with out paralysis of muscles

innervated by cranial nerves.

SYMPTOMS PRODUCED BY OCCLUSION OF VARIOUS

VESSELS

Obstruction of a cerebral artery gives a clinical picture, which depends upon loss of

function of the parts of the brain supplied by the vessel. This is influenced by the

point at which the obstruction occurs, since blockage at the origin of a vessel may

impair the function of a larger region than is the case when the block lies more

distally or involves only a single branch.

When an infarction lies in the territory of a carotid artery, unilateral signs

predominates as–hemiplegia, hemianesthesia, hemianopia, aphasia, etc. In the

territory of the basilar artery the signs of infarction are frequently bilateralquadriparesis,

bilateral sensory impairment, etc.

INTERNAL CAROTID ARTERY:- The symptoms of the blockage are

extraordinarily variable varying from no symptoms to a completed stroke.

- Progressive obliteration of lumen may cause TIAs (giving aphasia, confusion or

contralateral paraesthesiae or weakness) and stuttering hemiplegia.

- In complete occlusion there may be contralateral homonymous hemianopia,

hemiplegia, loss of spatial and discriminative sensibility on the opposite side,

aphasia of receptive, expressive or global type when the lesion is in the dominant

hemisphere.

- Occlusion of ophthalmic branch leads to unilateral blindness.

- Occlusion of the anterior choroidal artery may give contralateral hemiplegia and

hemianalgesia. It is often asymptomatic.

- Some signs of occlusion of carotid artery are recurrent loss of consciousness,

fainting on arising from horizontal position, headache, neck pain, paresthesia,

dimness of vision with exercise, abnormal facial pigmentation and loss of hair.

ANTERIOR CEREBRAL ARTERY:- It can be occluded at several different points

with varying clinical effects:

- Occlusion at its origin: Causes hemiplegia on the opposite side with sensory loss

of cortical type in lower limb, expressive aphasia and apraxia on left when lesion

is on the dominant side.

- Occlusion of Heubner’s artery: Leads to Paralysis of face, tongue and upper limb

on the opposite side, expressive aphasia (dominant hemisphere lesion).

- Occlusion distal to Heubner’s branch: Causes contralateral hemiplegia, weakness

more in lower limb. There is often forced grasping in the affected limb.

- Occlusion of the paracentral artery: The result is a spastic monoplegia on the

opposite side, with or without sensory loss of cortical type in affected lower limb.

- Occlusion of both anterior cerebral arteries: Characterized by profound dementia,

bilateral grasp reflexes may be present and akinetic mutism.

MIDDLE CEREBRAL ARTERY:-

- Obstruction at the origin causes hemiplegia with sensory loss on opposite side,

weakness most marked in the face, tongue and upper limb, Broca’s aphasia and/or

Wernicke’s aphasia if lesion in dominate hemisphere.

- Obstruction at frontal division causes a dense sensorimotor deficit in the face and

limbs with total aphasia.

- Obstruction at inferior division causes Wernicke’s dysphasia with or without

hemiparesis and hemianopia.

Above all, contralateral hemiplegia, hemianaesthasia, homonymous hemianopia and

global dysphasia are the classical features of middle cerebral artery occlusion.

THE POSTERIOR CEREBRAL ARTERY:-

- Its occlusion causes contralateral homonymous hemianopia. Visual agnosia may

result from ischemia of the left occipital lobe and impairment of memory from

damage to the medial aspect of temporal lobe.

- If anterior and proximal branches are occluded the transitory hemiparesis

accompanied by severe sensory loss of opposite side are produced.

- There may be distortion of taste. Occlusion of paramedian branches gives rise to

Weber’s syndrome.

THE BASILAR AND VERTEBRAL ARTERIES:- Incomplete obstruction in the

vertebro-basilar system leads to many transitory or permanent disorders of brainstem

function, including deafness, vertigo, drop attacks, ophthalmoplegia, ataxia,

 

nystagmus, and bilateral dysaesthesia over the body and bilateral cortisopinal tract

signs.

- Complete occlusion of the main trunk of the basilar artery is usually rapidly fatal

leading to impairment of consciousness, small fixed pupils, pseudobulbar palsy

and quadriplegia. A ‘locked in’ state of quadriplegia can also occur.

- A pure motor hemiplegia is caused by occlusion in single perforating branches of

basilar.

- Cerebellar symptoms may occur.

- Paroxysmal symptoms, which may be precipitated by head movements, include

vertigo, drop attacks and syncope.

- Symptoms of vertebro-basilar insufficiency may occur due to diversion of blood

from the vertebral artery to the brachial artery because of occlusion of subclavian

artery. This known as ‘Subclavian steal syndrome’.

- Many eponymous syndromes of brainstem infarction due to occlusion of branches

of the vertebral and basilar arteries have been described. These are – Weber’s

syndrome, Claude’s syndrome, Benedikt’s syndrome, Millard-Gubler syndrome,

Foville’s syndrome, Lateral medullary syndrome of Wallenberg.

The above descriptions apply particularly to infarction and ischemia due to embolism

and thrombosis. Although haemorrhage within a specific vascular territory may give

rise to many of the same effects, the total clinical picture is apt to differ because in its

deep extension the haemorrhage involves the territory of more than one artery and by

its mass effect may cause an increased intracranial pressure.

SIGNS AND SYMPTOMS PRODUCED BY CEREBRAL HAEMORRHAGE

AT VARIOUS SITES:

The neurological signs and symptoms produced depend on the situation and size of

the haemorrage.

INTERNAL CAPSULE OR PUTAMEN: The commonest site for haemorrahge is the

lenticulo-striate artery. The patient lapses almost immediately into a comatose state

with hemiplegia and his condition visibly deteriorate as the hours pass. In a few

minutes the face sags on one side, speech becomes slurred or aphasic, the arm and leg

gradually weaken and the eyes tend to deviate away from the side of the paretic limbs.

The pulse rate is slow. Gradually the paralysis worsens, the affected limbs become

flaccid, pinprick is not appreciated, Babinski sign appears, speaking becomes

impossible and confusion gives way to stupor. In worst cases, signs of upper brain

stem compression appear viz., coma, deep, irregular or intermittent respiration,

dilated pupils and occasionally rigidity occurs.

THALAMIC HAEMORRHAGE:– Produces contralateral hemiplegia due to pressure

on the adjacent internal capsule. The sensory deficit equals or outstrips the motor

weakness. There may be transient hemianopia and aphasia if the dominant hemispehe

is involved. There may be paralysis of the vertical gaze, skew deviation, ipsilateral

ptosis and miosis, hemibalismus, mutism. Apractagnosia is found if non-dominant

hemisphere involved.

PONTINE HAEMORRHAGE: If the patient is seen soon after the onset of a pontine

haemorrhage the signs may be those of a unilateral lesion of the pons, namely facial

paralysis on the side of the lesion with flaccid paralysis of the limbs. Paralysis of

conjugate ocular deviation and rotation of head to the side of the lesion is found.

Extension of the haemorrhage soon involves the opposite side and signs may be

bilateral from beginning. When both sides of the pons are thus affected there is

paralysis of the face and limbs on both sides with bilateral extensor planter reflexes.

The pupils are pin point (1 mm) due to bilateral destruction of the ocular sympathetic

fibres. There is often a terminal hyperpyrexia.

LOBAR HAEMORRHAGE: Occipital haemorrhage gives pain around the ipsilateral

eye and dense hemianopia. Haemorrhage into the dominant temporal lobe gives pain

in the region of the ear with fluent dysphasia and an incomplete contralateral

hemianopia. In frontal haemorrhage severe weakness of the contralateral arm and

minimal face and leg weakness with frontal headache is present. Parietal haemorrhage

gives rise to ipsilateral anterior temporal headache and contralateral hemisensory

deficit.

CEREBELLAR HAEMORRHAGE:- Cerebellar haemorrhage usually develops over a

period of several hours with loss of consciousness. Repeated vomiting is a hallmark of

cerebellar haemorrhage along with inability to walk or stand, occipital headache and

vertigo. The ocular signs include “ocular bobbing”, blepharospasm, involuntary

closure of one eye, skew deviation, dysarthria and dysphagia may be prominent.

Ocular signs as a tool of differentiating among the type of haemorrhage :-

- Putaminal Haemorrhage – Eyes deviated to opposite side

- Thalamic Haemorrhage – Downwards deviation of eye, pupil unreaction

- Pontine Haemorrhage – Eyes fixed

- Cerebellar Haemorrhage – Eyes deviate laterally.

SMALL VESSEL “LACUNAR” STROKE:-

Clinical Manifestation: The most common lacunar syndromes are-

- Pure motor hemiparesis from an infarct in the posterior limb of the internal

capsule or basis pontis, the face, arm and leg are almost always involved.

- Pure sensory stroke from an infarct in the ventrolateral thalamus.

- Ataxic hemiparesis from an infarct in the base of the pons.

- Dysarthria and a clumsy hand or arm due to infarction in the base of the pons or in

genu of the internal capsule.

- Pure motor hemiparesis with motor aphasia due to thrombotic occlusion of a

lenticulostriate, anterior limb of the internal capsule.

SUBARACHNOID HAEMORHAGE:

- The main feature of the headache due to SAH from an intracranial aneurysm is its

suddenness and its severity.

- At one extreme SAH may lead to immediate coma, profound shock and death in

few hours, while at other extreme it may cause a headache.

- Loss of consciousness occurs rapidly when the leakage is considerable, vomiting

not uncommon at onset.

- In less severe cases the patient may pass into a semi-stupor state and confused and

irritable when roused.

- Headache is severe and the presence of blood in subarachnoid space produces

signs of meningeal irritation; moderate pyrexia may be present.

- Changes are most likely to be seen in the fundi when SAH is near optic nerve.

- Other signs – loss of tendon reflexes and of the abdominal reflexes and extensor

plantar responses.

- Focal symptoms are due to compression of neighboring cranial nerves by blood

clot or to invasion of the cerebral hemisphere by the haemorrhage. The latter is

likely to produce a crossed hemiplegia.

 

 

Investigation-

Investigations are necessary for identifying the type of stroke and management.

 

Cerebral Thrombosis:-

·       Blood Tests-

Hb

Haematocrit

Platelet count

ESR

Blood glucose

Lipid profile

Serum uric acid is often raised

Serum electrolytes, blood urea nitrogen, prothrombin time, partial thromboplastin time should be evaluated.

·       Urinanalysis should be done to rule out renal pathology.

·       CSF Test – Raised protein levels is seen. There may be pleocytosis including a moderate excess of polymorphonuclear cells. CSF pressure is normal.

·       Moderate increase in serum and CSF creatine kinase, aldolase and lactic dehydrogenase occurs.

·       ECG – Usually shows marked abnormalities after infarction or haemorrhage.

·       CT Scan is almost certain to show the site of lesion though possibly not within 24 hours. Contrast enhanced CT Scans (CT angiograms) are useful in acute stroke management to reveal the presence or absence of large vessel pathology.

·       Magnetic resonance imaging can demonstrate lesions in the posterior fossa not visible by CT and demonstrates ischemic zones within few hours after stroke. MRA (magnetic resonance angiography) is highly sensitive for extracranial internal carotid plaques as well as intracarnial stenosis of large vessels.

·       Computerized Cranial Tomography (CCT) is the single most important non-invasive investigation to distinguish an infarction from cerebral haematoma.

·       Cerebral Angiography:- Conventional x-ray cerebral Angiography is useful for identifying and quantifying atherosclerotic stenosis of cerebral arteries and other pathologies including aneurysm, intra-luminal thrombi, collateral blood flow, etc. Use of cerebral Angiography coupled with endovascular techniques for cerebral revascularization may become routine in near future. Aortic arch catheterization, digital subtractions angiography are also helpful tests.

·       Ultrasound Techniques:- Carotid Doppler (Duplex Ultrasound) is useful in identifying and quantifying stenosis of carotids and blood flowing in some cerebral arteries. Trans-cranial Doppler (TCD) is used to detect stenotic lesions of cerebral arteries and assess collateral flow across anterior and posterior circle of Willis.

·       Other techniques:- Both Xenon-CT and position emission tomography (PET) can quantify CBF(collateral blood flow). They can be useful for determining the significance of arterial stenosis and planning for revascularization surgery. Single positron emission computed tomography (SPECT), CT-Perfusion and MR-perfusion techniques report relative CBF.

Cerebral Embolism:

In general, the findings are similar to those outlined under cerebral thrombosis.

·       In septic infarct the WBC count may be very high.

·       CSF – In haemorrhagic cerebral infarction the CSF is often bloodstained. The

      protein values are elevated, but the glucose content is within normal limits.

·       ECG – Atrial fibrillation, tachyarrhythmia and other ECG abnormalities are

      frequently documented.

      Echocardiography determines whether a cardiac thrombus was the source of

      embolism, by imaging the ventricular chambers.

·       Arterial imaging (CT or MRA or TCD) performed is characteristic and show

      migratory occlusive lesion of isolated branches in early stages. A repeat

      arteriography after a few days may be entirely normal, this suggests vanishing

      emboli.

·       2 D echo helps to define intracardiac and valvular emboli.

·       MRI better documents the extent and location of the embolic infarction. When

      coupled with MRA can help identify arterial source of emboli.

      Embolic infarction may appear as a single low-density area on CT imaging.

Intracerebral Haemorrhage-

·       There is often leucocytosis – with WBC 15,000 to 20,000/cu mm, a higher figure

      than thrombosis.

·       Serum and CSF creatine kinase, aldolase and lactic dehydrogenase are increased;

      they are more striking than thrombosis.

·       Transient glycosuria or albuminuria are common.

·       Skull x-ray, echo-encephalogram and cerebral angiography rarely help in the

      diagnosis of an infratentorial haematoma, but they may show signs of midline

      displacement in supratentorial lesions.

·       CSF – It confirms the diagnosis. Fluid is uniformly bloodstained,

      does not clot on standing, shows xanthochromia, WBC count may be

      elevated. RBCs appear within 2 hours and usually clear up in about 4 weeks. With

      conversion of oxyhaemoglobin to bilirubin in the first 72 hours an indirect van

      den Bergh test may show a positive reaction.

·       EEG – High voltage, focal or diffuse slow waves are often seen on EEG.

·       CT scan is highly diagnostic defining the anatomical location as wall as dimension

      of the cerebral haemorrhage. A heamorrhage up to half a centimeter in diameter

      will be apparent immediately. Coexisting cerebral swelling and displacement of

      intracranial contents are readily appreciated.

·       Conventional x-ray angiography is indicated to rule out middle cerebral artery

      aneurysm and before surgical intervention in case of AVM.

Subarachnoid Haemorrhage:

·       CSF under raised pressure and containing about a million RBCs/cubic mm tends to confirm the diagnosis of SAH. CSF pleocytosis is present.

·       Cerebral Angiography or DSA is valuable in arriving at a diagnosis. It not only outlines the aneurysm, but also shows coincident vasospasm or a subdural clot.

·       Acute subarachnoid haemorrhage may be associated with ECG abnormalities suggestive of MI.

·       EEG and skull films are of little help.

·       CT scan is of diagnostic and prognostic help.

·       MRI scan can often image an aneurysm better than a CT scan.

  Diagnosis-

 

 

Complications-

Stroke like many other serious medical illnesses can be followed by a host of otherproblems. These complications can sometimes cause neurological deterioration.

Complications of Stroke:

I. Cerebrovascular System

· Cerebral Oedema: It represents the major cause of death. Cerebral oedema maybegin within hours but usually doesn’t become clinically obvious until 1 to 4 daysafter stroke. The two main components of oedema are intracellular cytotoxicoedema and extracellular vasogenic oedema. Cerebral oedema impairs theneuronal function over a wide area and increases the risk of transtentorialherniation and secondary brain stem haemorrhage.· Seizures: Seizures may also follow stroke. While they might not be a cause ofmortality, seizures complicate the care of the patient. Patient with cortical infarcts,especially large ones, with persistent hemiplegia are most susceptible to postinfarction epilepsy. Patients with subcortical slit haemorrhage are also prone toearly seizures.

II. Respiratory System

·       Aspiration: In patients with brainstem stroke, combined cerebral and brain stemstrokes and bilateral cerebral lesions are susceptible to aspiration.

·       Dysphagia: Noted in brainstem and hemispheral stroke.

·       Pulmonary embolism: The true frequency of pulmonary emboli is probablyunknown because many are silent. Pulmonary emboli can be a cause of death inpatients who die during the first week following stroke. Patients who have sudden shortness of breath, chest pain, hypotension, haemoptysis, change in respiratorypattern, agitation, confusion or other worsening are suspected of having apulmonary embolism.

·       Pneumonia

III. Cardiovascular system

·       Myocardial Infarction

·       Cardiac failure

·       Cardiac arrhythmia.

Cardiac dysfunction is another frequent accompaniment of stroke. Patients with bothischemic and haemorrhagic stroke have been demonstrated at necropsy to havesubendocardial haemorrhages and focal regions of necrosis of cardiac muscle cells.ECG changes consistent with ischemia, elevated creatine-phosphokinase – myoglobinand various cardiac arrhythmias are found in stroke patients, even without previouheart disease. Stroke causes an increase in sympathetic tone, elevating levels ofcatecholamines, which in turn causes focal myocardial damage and subsequentarrhythmias.

IV. Infections

·       Urinary tract Infections: Indwelling catheter placed to empty urinary bladderallows the introduction and growth of bacteria. Functioning of the urinary bladderand the external sphincter can be altered by stroke. Urinary symptoms arecommon even in uninfected bladders and they include urinary urgency, frequencyand retention. Tsuchidaet. al. documented these symptoms and attempted toestablish their relationship to brain lesion.

·       Frontal and internal capsular lesions – hyperactive bladder or inhibited sphincterrelaxation, with urinary frequency and incontinence.

·       Putaminal lesions – hyperactive bladders, with normal sphincter functions.

·       In few lesions – hypoactive or inactive bladder, urinary retention and normalsphincter.

·       Septicemia

·       Skin infections.

V. Metabolic and Nutritional Disorders

Fluid, electrolyte and nutritional abnormalities may occur during the recovery period.Post stroke hyponatremia is usually related to inappropriate secretion of ADH. (Joyntet al.). Prolonged under nutrition is an important but seldom recognized complicationof stroke, especially in elderly patients whose nutritional intake is poor or marginalbefore their stroke.Vomiting, dehydration, hyperglycemia and renal failure are other complications.

VI. Mechanical

Spasticity, Pseudo-contractures (contractures) of muscles, Periarthritis at shoulder,elbow, wrist, knuckles, knee and ankle; Ankle swelling, Osteoporosis, Fractures,Pressure sores, sublaxation of shoulders, Reflex sympathetic dystrophy syndrome(RSDS) - characterized by severe shoulder pain, swelling, burning pain,hyperaesthesia and dystrophic changes. -Peripheral nerve compression: Peroneal nerve compression – foot drop; Compressionof nerve at elbow – Ulnar palsy.

VII. Psychological Effects- Depression, Anxiety, Apathy.

A rare complication of SAH is haemosiderosis of the Nervous system causing deafness, dementia, cerebellar ataxia and other progressive neurological signs.

Prognostic factors in stroke-(e medicine)-

Ischemic Stroke-

In the Framingham and Rochester stroke studies, the overall mortality rate at 30 days after stroke was 28%, the mortality rate at 30 days after ischemic stroke was 19%, and the 1-year survival rate for patients with ischemic stroke was 77%. However, the prognosis after acute ischemic stroke varies greatly in individual patients, depending on the stroke severity and on the patient’s premorbid condition, age, and poststroke complications.^[4]

A study utilizing the large national Get With The Guidelines - Stroke registry found that the baseline National Institutes of Health Stroke Scale (NIHSS) score was the strongest predictor of early mortality risk, even more so than currently used mortality prediction models incorporating multiple clinical data.^[51] Cardiogenic emboli are associated with the highest 1-month mortality in patients with acute stroke.

The presence of computed tomography (CT) scan evidence of infarction early in presentation has been associated with poor outcome and with an increased propensity for hemorrhagic transformation after fibrinolytic therapy (see Pathophysiology).^{[5, 52, 53]} Hemorrhagic transformation is estimated to occur in 5% of uncomplicated ischemic strokes in the absence of fibrinolytic therapy, although it is not always associated with neurologic decline. Indeed, hemorrhagic transformation ranges from the development of small petechial hemorrhages to the formation of hematomas requiring evacuation.

Acute ischemic stroke has been associated with acute cardiac dysfunction and arrhythmia, which then correlate with worse functional outcome and morbidity at 3 months. Data suggest that severe hyperglycemia is independently associated with poor outcome and reduced reperfusion in fibrinolysis, as well as extension of the infarcted territory.^{[54, 55, 56]}

In stroke survivors from the Framingham Heart Study, 31% needed help caring for themselves, 20% needed help when walking, and 71% had impaired vocational capacity in long-term follow-up. For more information, see the Medscape Reference article Motor Recovery in Stroke.

Hemorrhagic Stroke 

The prognosis in patients with hemorrhagic stroke varies depending on the severity of stroke and the location and the size of the hemorrhage. Lower Glasgow Coma Scale (GCS) scores are associated with poorer prognosis and higher mortality rates. A larger volume of blood at presentation is also associated with a poorer prognosis. Growth of the hematoma volume is associated with a poorer functional outcome and increased mortality rate.

The intracerebralhemorrhage score is the most commonly used instrument for predicting outcome in hemorrhagic stroke. The score is calculated as follows:

• GCS score 3-4: 2 points
• GCS score 5-12: 1 point
• GCS score 13-15: 0 points
• Age ≥80 years: Yes, 1 point; no, 0 points
• Infratentorial origin: Yes, 1 point; no, 0 points
• Intracerebralhemorrhage volume ≥30 cm³: 1 point
• Intracerebralhemorrhage volume < 30 cm³: 0 points
• Intraventricularhemorrhage: Yes, 1 point; no, 0 points

In a study by Hemphill et al, all patients with an IntracerebralHemorrhage Score of 0 survived, and all of those with a score of 5 died; 30-day mortality increased steadily with the Score.^[30]

Other prognostic factors include the following:

• Nonaneurysmalperimesencephalic stroke has a less severe clinical course and, in general, a better prognosis
• The presence of blood in the ventricles is associated with a higher mortality rate; in one study, the presence of intraventricular blood at presentation was associated with a mortality increase of more than 2-fold
• Patients with oral anticoagulation-associated intracerebralhemorrhage have higher mortality rates and poorer functional outcomes

In studies, withdrawal of medical support or issuance of Do Not Resuscitate (DNR) orders within the first day of hospitalization predict poor outcome independent of clinical factors. Because limiting care may adversely impact outcome, American Heart Association/American Stroke Association (AHA/ASA) guidelines suggest that new DNR orders should probably be postponed until at least the second full day of hospitalization. Patients with DNRs should be given all other medical and surgical treatment, unless the DNR explicitly says otherwise.^[3]

 

Prognostic scales in stroke-

Stroke scales are used in clinical researchto summarize the deficits found in groups ofpatients. In individual patients, stroke scales areuseful to document and communicate baselinedeficits, as well as changes over time, with othermembers of the health care team, and to provideprognostic information. Scales are even moreuseful for research to assure that stroke severity isbalanced between groups and to provide an outcomemeasure of disability. The ideal clinicalstroke scale, which does not yet exist, would besimple, easy, and quick to administer; have highreproducibility by one observer and betweenobservers, and give useful prognostic information.The ideal outcome scale would have all ofthese features, and measure disability in a waythat is important to patients and their quality oflife. Stroke scales should avoid visual analoguescales, whose use in stroke patients has been

shown to be problematic. Most recent studies used the NationalInstitutes of Health Stroke Scale (NIHSS) to assessbaseline stroke severity. The Canadian Stroke Scale (CSS) and theScandinavian Stroke Scale (SSS) also have beenused in many trials and share some features with the NIHSS. The Oxfordshire Classification is thesimplest scale, and also is used in research toboth classify stroke and approximate its severity.The Mathew Scale, the Orgogozo Scale, and theHemispheric Stroke Scale are older tools thathave fallen out of use and will not be described inthis review. The Glasgow Coma Scale (GCS) isused occasionally to assess ischemic stroke, but ismore appropriate in the setting of head injury andsubarachnoid hemorrhage.

In addition to deficit scales, there are severalvalidated outcome scales to assess disabilityfollowing stroke; the most commonly used are themodified Rankin Scale (mRS), the Barthel Index(BI), and the Glasgow Outcome Scale (GOS).

Stroke Assessment Scales-

Prehospital Stroke Assessment Scales-

·       Cincinnati Stroke Scale

·       Los Angeles Prehospital Stroke Scale (LAPSS)

·       ABCD Score

Acute Assessment Scales

·       Canadian Neurological Scale (CNS)

·       European Stroke Scale

·       Glasgow Coma Scale (GCS)

·       Hemispheric Stroke Scale

·       Hunt & Hess Scale

·       Mathew Stroke Scale

·       NIH Stroke Scale (NIHSS)

·       Orgogozo Stroke Scale

·       Oxfordshire Community Stroke Project Classification (Bamford)

·       Scandinavian Stroke Scale

·       World Federation of Neurological Surgeons Grading System for Subarachnoid Hemorrhage Scale

Functional Assessment Scales

·       Berg Balance Scale

·       Lawton IADL Scale

·       Modified Rankin Scale

·       Stroke Specific Quality of Life Measure (SS-QOL)

Outcome Assessment Scales

·       Barthel Index

·       Functional Independence Measurement (FIM™)

·       Glasgow Outcome Scale (GOS)

·       Health Survey SF-36™

·       Health Survey SF-12™

·       Community Integration Questionnaire

Other Diagnostic & Screening Tests

·       Action Research Arm Test

·       Blessed-Dementia Scale

·       Blessed-Dementia Information-Memory-Concentration Test

·       DSM-IV criteria for the diagnosis of vascular dementia

·       HachinskiIschaemia Score

·       Hamilton Rating Scale for Depression

·       NINDS – AIREN criteria for the diagnosis of vascular dementia

·       Orpington Prognostic Scale

·       Short Orientation-Memory-Concentration Test

There exist several stroke scales with some degree of validation, however de facto consensus at this time suggests using the NIHSS to rate clinical severity, and the mRS to assess for disability following stroke. These scales all have different strengths and weaknesses, and perhaps further modification, or entirely new scales, may improve the usefulness of stroke scales in the future.

Out come Scales

The Rankin Scale (RS) was developed in 1957 to assess the extent of disability after a stroke43; it was later modified (mRS) to a 6-pointscale from 0 to 5 (Table 5).44 Patients with noimpairment or symptoms receive the best score of 0, while patients with severe disability who are bedridden, incontinent, and require constant nursing care and attention receive the worst score of 5; death can be rated 6 in the mRS. The modified scale has moderate to excellent inter-rater reliability. 45,46 The mRS has been shown to be valid ,47 and is considered more powerful than the BarthelIndex (BI) as a primary endpoint in clinical trials of stroke therapy.48,49,50 The Barthel Index51,52 measures the patient’s degree of independence in performing activities of daily living (ADL), and is the most frequently

used measure of ADL competence in clinical stroke trials (Table 6).53 It also is widely used

to assess stroke-related disability outside the context of clinical trials.54,55 The BI consists of 10 items assessing feeding, chair/bed transfer, grooming, toileting, bathing, ambulation, stair

climbing, dressing, bowel control, and bladder control. Patients with higher scores are more likely to be able to live outside of an assisted living environment, although a patient with a perfect score is not necessarily able to live independently.56,57 The BI has been exhaustively studied, and concurrent validation has been reported by many groups.58 The Glasgow Outcome Scale (GOS)59 was developed to rank outcomes after head injury, but has been used in stroke studies (Table 7).60,61,62 It is a single-item scale with the following categories: (1) no or minimal disability or handicap, 2) moderate disability, (3) severe disability, (4) persistent vegetative state, and (5) death.

 

 

 

1a. Level of Consciousness: The investigator must choose a response if a full evaluation is prevented by such obstacles as an endotracheal tube, language barrier, orotracheal trauma/bandages. A 3 is scored only if the patient makes no movement (other than reflexive posturing) in response to noxious stimulation.	0 = Alert; keenly responsive. 1 = Not alert; but arousable by minor stimulation to obey, answer, or respond. 2 = Not alert; requires repeated stimulation to attend, or is obtunded and requires strong or painful stimulation to make movements (not stereotyped). 3 = Responds only with reflex motor or autonomic effects or totally unresponsive, flaccid, and areflexic.
1b. LOC Questions: The patient is asked the month and his/her age. The answer must be correct - there is no partial credit for being close. Aphasic and stuporous patients who do not comprehend the questions will score 2. Patients unable to speak because of endotracheal intubation, orotracheal trauma, severe dysarthria from any cause, language barrier, or any other problem not secondary to aphasia are given a 1. It is important that only the initial answer be graded and that the examiner not "help" the patient with verbal or non-verbal cues.	0 = Answers both questions correctly. 1 = Answers one question correctly. 2 = Answers neither question correctly.
1c. LOC Commands: The patient is asked to open and close the eyes and then to grip and release the non-paretic hand. Substitute another one step command if the hands cannot be used. Credit is given if an unequivocal attempt is made but not completed due to weakness. If the patient does not respond to command, the task should be demonstrated to him or her (pantomime), and the result scored (i.e., follows none, one or two commands). Patients with trauma, amputation, or other physical impediments should be given suitable one-step commands. Only the first attempt is scored	0 = Performs both tasks correctly. 1 = Performs one task correctly. 2 = Performs neither task correctly
2. Best Gaze: Only horizontal eye movements will be tested. Voluntary or reflexive (oculocephalic) eye movements will be scored, but caloric testing is not done. If the patient has a conjugate deviation of the eyes that can be overcome by voluntary or reflexive activity, the score will be 1. If a patient has an isolated peripheral nerve paresis (CN III, IV or VI), score a 1. Gaze is testable in all aphasic patients. Patients with ocular trauma, bandages, pre-existing blindness, or other disorder of visual acuity or fields should be tested with reflexive movements, and a choice made by the investigator. Establishing eye contact and then moving about the patient from side to side will occasionally clarify the presence of a partial gaze palsy.	0 = Normal. 1 = Partial gaze palsy; gaze is abnormal in one or both eyes, but forced deviation or total gaze paresis is not present. 2 = Forced deviation, or total gaze paresis not overcome by the oculocephalicmaneuver.
3. Visual: Visual fields (upper and lower quadrants) are tested by confrontation, using finger counting or visual threat, as appropriate. Patients may be encouraged, but if they look at the side of the moving fingers appropriately, this can be scored as normal. If there is unilateral blindness or enucleation, visual fields in the remaining eye are scored. Score 1 only if a clear-cut asymmetry, including quadrantanopia, is found. If patient is blind from any cause, score 3. Double simultaneous stimulation is performed at this point. If there is extinction, patient receives a 1, and the results are used to respond to item 11	0 = No visual loss. 1 = Partial hemianopia. 2 = Complete hemianopia. 3 = Bilateral hemianopia (blind including cortical blindness).
4. Facial Palsy: Ask – or use pantomime to encourage – the patient to show teeth or raise eyebrows and close eyes. Score symmetry of grimace in response to noxious stimuli in the poorly responsive or non-comprehending patient. If facial trauma/bandages, orotracheal tube, tape or other physical barriers obscure the face, these should be removed to the extent possible.	0 = Normal symmetrical movements. 1 = Minor paralysis (flattened nasolabial fold, asymmetry on smiling). 2 = Partial paralysis (total or near-total paralysis of lower face). 3 = Complete paralysis of one or both sides (absence of facial movement in the upper and lower face).
5. Motor Arm: The limb is placed in the appropriate position: extend the arms (palms down) 90 degrees (if sitting) or 45 degrees (if supine). Drift is scored if the arm falls before 10 seconds. The aphasic patient is encouraged using urgency in the voice and pantomime, but not noxious stimulation. Each limb is tested in turn, beginning with the non-paretic arm. Only in the case of amputation or joint fusion at the shoulder, the examiner should record the score as untestable (UN), and clearly write the explanation for this choice.	0 = No drift; limb holds 90 (or 45) degrees for full 10 seconds. 1 = Drift; limb holds 90 (or 45) degrees, but drifts down before full 10 seconds; does not hit bed or other support. 2 = Some effort against gravity; limb cannot get to or maintain (if cued) 90 (or 45) degrees, drifts down to bed, but has some effort against gravity. 3 = No effort against gravity; limb falls. 4 = No movement. UN = Amputation or joint fusion, explain: _____________________ 5a. Left Arm 5b. Right Arm
6. Motor Leg: The limb is placed in the appropriate position: hold the leg at 30 degrees (always tested supine). Drift is scored if the leg falls before 5 seconds. The aphasic patient is encouraged using urgency in the voice and pantomime, but not noxious stimulation. Each limb is tested in turn, beginning with the non-paretic leg. Only in the case of amputation or joint fusion at the hip, the examiner should record the score as untestable (UN), and clearly write the explanation for this choice	0 = No drift; leg holds 30-degree position for full 5 seconds. 1 = Drift; leg falls by the end of the 5-second period but does not hit bed. 2 = Some effort against gravity; leg falls to bed by 5 seconds, but has some effort against gravity. 3 = No effort against gravity; leg falls to bed immediately. 4 = No movement. UN = Amputation or joint fusion, explain: ________________ 6a. Left Leg 6b. Right Leg ______ Rev 10/
7. Limb Ataxia: This item is aimed at finding evidence of a unilateral cerebellar lesion. Test with eyes open. In case of visual defect, ensure testing is done in intact visual field. The finger-nose-finger and heel-shin tests are performed on both sides, and ataxia is scored only if present out of proportion to weakness. Ataxia is absent in the patient who cannot understand or is paralyzed. Only in the case of amputation or joint fusion, the examiner should record the score as untestable (UN), and clearly write the explanation for this choice. In case of blindness, test by having the patient touch nose from extended arm position.	0 = Absent. 1 = Present in one limb. 2 = Present in two limbs. UN = Amputation or joint fusion, explain:
8. Sensory: Sensation or grimace to pinprick when tested, or withdrawal from noxious stimulus in the obtunded or aphasic patient. Only sensory loss attributed to stroke is scored as abnormal and the examiner should test as many body areas (arms [not hands], legs, trunk, face) as needed to accurately check for hemisensory loss. A score of 2, “severe or total sensory loss,” should only be given when a severe or total loss of sensation can be clearly demonstrated. Stuporous and aphasic patients will, therefore, probably score 1 or 0. The patient with brainstem stroke who has bilateral loss of sensation is scored 2. If the patient does not respond and is quadriplegic, score 2. Patients in a coma (item 1a=3) are automatically given a 2 on this item.	0 = Normal; no sensory loss. 1 = Mild-to-moderate sensory loss; patient feels pinprick is less sharp or is dull on the affected side; or there is a loss of superficial pain with pinprick, but patient is aware of being touched. 2 = Severe to total sensory loss; patient is not aware of being touched in the face, arm, and leg.
9. Best Language: A great deal of information about comprehension will be obtained during the preceding sections of the examination. For this scale item, the patient is asked to describe what is happening in the attached picture, to name the items on the attached naming sheet and to read from the attached list of sentences. Comprehension is judged from responses here, as well as to all of the commands in the preceding general neurological exam. If visual loss interferes with the tests, ask the patient to identify objects placed in the hand, repeat, and produce speech. The intubated patient should be asked to write. The patient in a coma (item 1a=3) will automatically score 3 on this item. The examiner must choose a score for the patient with stupor or limited cooperation, but a score of 3 should be used only if the patient is mute and follows no one-step commands.	0 = No aphasia; normal. 1 = Mild-to-moderate aphasia; some obvious loss of fluency or facility of comprehension, without significant limitation on ideas expressed or form of expression. Reduction of speech and/or comprehension, however, makes conversation about provided materials difficult or impossible. For example, in conversation about provided materials, examiner can identify picture or naming card content from patient’s response. 2 = Severe aphasia; all communication is through fragmentary expression; great need for inference, questioning, and guessing by the listener. Range of information that can be exchanged is limited; listener carries burden of communication. Examiner cannot identify materials provided from patient response. 3 = Mute, global aphasia; no usable speech or auditory comprehension
10. Dysarthria: If patient is thought to be normal, an adequate sample of speech must be obtained by asking patient to read or repeat words from the attached list. If the patient has severe aphasia, the clarity of articulation of spontaneous speech can be rated. Only if the patient is intubated or has other physical barriers to producing speech, the examiner should record the score as untestable (UN), and clearly write an explanation for this choice. Do not tell the patient why he or she is being tested.	0 = Normal. 1 = Mild-to-moderate dysarthria; patient slurs at least some words and, at worst, can be understood with some difficulty. 2 = Severe dysarthria; patient's speech is so slurred as to be unintelligible in the absence of or out of proportion to any dysphasia, or is mute/anarthric. UN = Intubated or other physical barrier, explain:
11. Extinction and Inattention (formerly Neglect): Sufficient information to identify neglect may be obtained during the prior testing. If the patient has a severe visual loss preventing visual double simultaneous stimulation, and the cutaneous stimuli are normal, the score is normal. If the patient has aphasia but does appear to attend to both sides, the score is normal. The presence of visual spatial neglect or anosagnosia may also be taken as evidence of abnormality. Since the abnormality is scored only if present, the item is never untestable.	0 = No abnormality. 1 = Visual, tactile, auditory, spatial, or personal inattention or extinction to bilateral simultaneous stimulation in one of the sensory modalities. 2 = Profound hemi-inattention or extinction to more than one modality; does not recognize own hand or orients to only one side of space.

 

 

 

 

 

 

 

GLASGOW OUTCOME SCALE

 

 

 

 

Score Description

1             DEATH

2             PERSISTENT VEGETATIVE STATE

Patient exhibits no obvious cortical function.

3             SEVERE DISABILITY

(Conscious but disabled). Patient depends upon others for daily support due to mental or physical disability or both.

4             MODERATE DISABILITY

(Disabled but independent). Patient is independent as far as daily life is concerned. The disabilities found include varying degrees of dysphasia, hemiparesis, or ataxia, as well as intellectual and memory deficits and personality changes.

5             GOOD RECOVERY

Resumption of normal activities even though there may be minor neurological or psychological

 

References

Jennett B, Bond - M. “Assessment of outcome after severe brain damage.” Lancet 1975 Mar 1;1(7905):480-4+