STROKE AND STROKE MANAGEMENT
Aung Tha Tun
Owner, self employment at Private Clinic and making clinical research for stroke rehabilitation.
Stroke
A stroke is the rapidly developing loss of brain functions because of disturbance in the blood supply to brain. It can be due to ischemia caused by thrombosis or embolism or due to hemorrhage. 85% will have sustained a cerebral infarction due to inadequate blood flow to part of the brain. The remainder will have had an intracerebral hemorrhage. Sometimes stroke symptoms are resolved completely within 24 hours because of the reversibility of tissue damage from ischemic attack that is called transient ischemic attack (TIA). If affected area of the brain that is large, neurological deficient of cerebrovascular cause that persists beyond 24 hours or is interrupted by death within 24 hours.
An ischaemic stroke is occasionally treated with thrombolysis, but usually with supported care (physiotherapy, speech and language therapy and occupational therapy) in a ”stroke unit” and secondary prevention with antiplatelet drugs (aspirin and often dipyridamole), blood pressure control, statins and selected patient with carotid endarterectomy and anticoagulation. [1] [2]
Various systems have been proposed to increase recognition of stroke. Sudden onset face weakness, arm drift (i.e. if a person, when asked to raise both arms, involuntarily lets one arm drift downward), and abnormal speech are the findings most likely to lead to the correct identification of a case of stroke increasing the likelihood by 5.5 when at least one of these is present). All of these are absent, the likelihood of stroke is significantly decreased (likelihood ratio of 0.39). [1]
Propose systems include FAST (face, arm, speech, and time) as advocated by the Department of Health (UK) and the Stroke Association, the American Stroke Association, the National Stroke Association (US), Los Angeles Prehospital Stroke Screen (LAPSS) and Cincinnati Prehospital Stroke Scale (CPSS). Use of these scales is recommended by professional guidelines. [1]
For the people referred to emergency room, early recognition of stroke, a scoring system is called ROSIER (recognition of stroke in the emergency room), it is based on features from the medical history and physical examination.[1] [2]
Epidemiology
Stroke could soon be the most common cause of death worldwide. Stroke is currently the second leading cause of death in the Western world, ranking after heart disease and before cancer, and causes 10% of death worldwide.
Geographic disparities in stroke incidence have been observed, including the existence of a “Stroke belt” in the Southeastern United states, but causes of these disparities have not been reported.
The incidence of stroke increases exponentially from 30 years of age, and etiology varies by age. Advanced age is one of the most significant stroke risk factors. 95% of strokes occur in people age 45 and older, and two-thirds of strokes occur in those over the age of 65. A person’s risk of dying if he or she does have a stroke also increases with age. However, stroke can occur at any age, including fetuses.
Family members may have a genetic tendency for stroke or share a lifestyle that contributes to stroke. Higher levels of Von Willebrand factor are more common amongst people who have had ischaemic stroke for first time. The results of this study found that the only significant genetic factor was the person’s blood type.
Having had a stroke in the past greatly increases one’s risk of future stroke.
Men are 25% more likely to suffer strokes than women, yet 60% of deaths from stroke occur in women. Since women live longer, they are older on average when they have their strokes and thus more often killed. Some risk factors for stroke apply only to women. Primary among those are pregnancy, childbirth, menopause, and treatment thereof. [1]
Clinical classification of stroke
Transient ischaemic stroke (TIA)
This describes strokes in which symptoms resolved within 24 hours-an arbitrary cut off which has little value in practice apart from perhaps indicating that underlying cerebral hemorrhage or extensive cerebral infarction is extremely unlikely. [2]
The term TIA traditionally also includes patient with transient monocular blindness (amaurosis fugax), usually due to a vascular occlusion in retina. Transient symptoms such as syncope, amnesia, confusion, and dizziness, which do not reflect focal cerebral dysfunction, are often mistakenly attributed to TIA. [2]
Stroke
In epidemiological studies, the term stroke is reserved for those events in which symptoms last more than 24 hours.
Progressive stroke (or stroke in evolution)
This describes a stroke in which the focal neurological deficit worsens after the patient first presents. Such worsening may be due to increasing volume of infarction, hemorrhage or related oedema.
Completed stroke
This describes a stroke in which the focal deficit persists and is not progressing.
Differential diagnosis of Stroke and TIA
Primary cerebral tumours
Metastatic cerebral tumours
Subdural hematoma
Peripheral nerve lesions (vascular or compressive)
Cerebral abscess
Todd’s paresis (after epileptic seizure)
Demyelination
Hypoglycaemia
Encephalitis
Conversion disorder
Migrainous aura (with or with headache)
Focal seizure [2]
Clinical features
The clinical assessment provides an estimate of the site of lesion (i.e. which arterial territory is involved) and its size, both of which will have a bearing on management, such as suitability for carotid endarterectomy. The neurological deficits can be identified from the patient’s history and, if these are persistent, from the neurological examination.
In most case, the symptoms affected only one side of the body (unilateral). The effect in the brain is usually on the opposite side of the body. [1] [2]
If the area of brain affected contains one of the three prominent central nervous system pathways-the spinothalamic tract, corticospinal tract and dorsal column (medial lemniscus), (see figures 1.),symptoms include:
-Hemiplegia and muscle weakness of face
-Numbness and
-Reduction in sensory or vibratory sensation.
Figure 1. (A) The motor System
(B) The main somatic sensory pathway
Credit from Davidson’s principle and practice of medicine
However, the presence of any one of these symptoms does not necessarily suggest a stroke, since these
Pathways also travel in spinal cord and any lesion there can also produce these symptoms.
In addition to the above CNS pathways, the brainstem also consists of the 12 cranial nerves. A stroke affecting the brain stem therefore can produce symptoms relating in these cranial nerves. (see fig.2)
Figure 2. Anatomy of brain stem
Credit from Davidson’s principle and practice of medicine
-altered smell, taste, hearing, or vision (total or partial)
-dropping of eyelid (ptosis) and weakness of ocular muscles
-decreased reflexes: gag, swallow, pupil light reactivity
-decreased sensation and muscle weakness of the face
-balance problems and nystagmus
-altered breathing and heart rate
-weakness in sternocleidomastoid muscle with inability to turn head to one side
-weakness in tongue (inability to protrude and/or move from side to side)
If the cerebral cortex is involved, the CNS pathway is again be affected, but also can produced the following symptoms. (see fig.3)
-Aphasia (inability to speak or understand language from involvement of Broca’s or Wernicke’s areas)
-Apraxia (altered voluntary movements)
-Visual field defect
-Memory deficit (involvement of temporal lobe)
-Hemineglect (involvement of parietal lobe)
-Disorganized thinking, confusion, hypersexual gesture (with involvement of frontal lobe)
-Anosognosia (persistent denial of the existence of a, usually stroke -related, deficit)
Figure 3. (A) Classification of aphasia
Credit from Davidson’s principle and practice of medicine
(A) All have naming difficulty (anomia). Fluent aphasias arise from lesionsposterior to the central fissure, repetition is affected by lesion around the slyvian fissure. (1) Wernicke’s aphasia, (2) Conduction aphasia, (3) Broca’s aphasia, (4) Transcortical sensory aphasia, (5) Transcortical motor aphasia. N.B. Large lesions affecting all regions 1-5 cause global aphasia.
(B) The anatomy of cerebral cortex
If the cerebellum is involved, the patient may have the following:
-trouble walking
-altered movement coordination
-vertigo and or disequilibrium
Different combinations of these deficits can defined several stroke syndromes which reflect the site and size of lesion and may provide clues to underlying pathology.
Reduced conscious level usually indicates a large volume lesion in the cerebral hemisphere but may result from a lesion in the brainstem or complications as obstructive hydrocephalous, hypoxia or severe systemic infection.
Clinical assessment of the patient with a stroke should also include general examination (see below) since this may provide clues to the causes of stroke, and identify important comorbidities and complications of stroke.
Loss of consciousness, headache, and vomiting usually occurs more often in hemorrhagic stroke than in thrombosis because of the increased intracranial pressure from the leaking blood compressing on the brain. [1] [2]
Causes of stroke
Thrombotic stroke;
In thrombotic stroke a thrombus usually forms around atherosclerotic plaques. Since blockage of the artery is gradual, onset of symptomatic thrombotic strokes is slower. A thrombus itself can lead to an embolic stroke if the thrombus breaks off, at which point it is called an “embolus”. Two type of thrombosis can cause stroke:
-Large vessel disease involves the common internal carotids, vertebral and Circle of Willis. Diseases that may form thrombi in the large vessels included: atherosclerosis, vasoconstriction, aortic, carotid or vertebral artery dissection, various inflammatory diseases of the blood vessel wall ( Takayasu areritis, giant cell arteritis, vasculitis), noninflammatory vasculopathy,Moyamoya disease and fibromuscular dysplasia.
-Small vessel disease involves the smaller arteries inside the brain: branches of Circle of Willis, middle cerebral artery, stem, and arteries arising from the distal vertebral and basilar artery. Diseases that may form thrombi in the small vessels include: Lipohyalinosis(build up of fatty hyaline matter in the blood vessel as a result of high blood pressure and aging) and fibrinoid degeneration and microarthroma.
-Sickle cell anemia which can cause blood cell to clump up and block blood vessels can also lead to stroke. [1]
Embolic stroke
An embolic stroke refers to the blockage of an artery by an embolus, a travelling particle or debris in the arterial blood stream originating from elsewhere. An embolus is most frequently a thrombus, but it can also be a number of other substances including fats (e.g. from bone marrow in a broken bone), air, cancer cells or clumps of bacteria (usually from infectious endocarditis)
Because an embolus arises from elsewhere, local therapy only solves the problem temporally. Thus the source of embolus must be identified. Because the emboli blockage is sudden onset, symptoms usually
are maximal at start. Also symptoms may be transient as the embolus is partially resorbed and moves to a different location or dissipates altogether.
Emboli most commonly arise from the heart (especially in atrial fibrillation) but may originate from elsewhere arterial tree. In paradoxical embolism, deep vein thrombosis embolises hrough an atrial or ventricular septal defect in the heart into the brain.
Cardiac causes can be distinguished between high and low risk: [1]
Systemic hypoperfusion
Systemic hypoperfusion is the reduction of blood flow to all parts of body. It is most commonly due to cardiac pump failure from cardiac arrest or arrhythmias, from reduced cardiac output as a result of myocardial infarction, pulmonary embolism, pericardial effusion, or bleeding. Hypoximia may precipitate the hypoperfusion. Because reduction in blood flow is global, all parts of brain may be affected, especially ”watershed” areas-border zone regions supplied by the major cerebral arteries. The blood flow to these areas does not necessarily stop, but instead it may lessen to the point where brain damage can occur. This phenomenon is also referred to as “last meadow” to point to the fact that in irrigation the last meadow receives least amount of water. [1]
Venous thrombosis
Cerebral venous sinus thrombosis leads to stroke due to locally increased venous pressure, which exceeds the pressure generated by the arteries. Infarcts are more likely to undergo hemorrhagic transformation (leaking of blood into the damage area) than other types of ischaemic stroke. [1]
Intracerebral hemorrhage
It generally occurs in small arteries or arterioles and it is commonly due to hypertension, intracranial vascular malformation (including cavernous angiomas or arteriovenous malformations), cerebral amyloid angiopathy, or infarcts into which secondry hemorrhage has occurred. Other potential causes are trauma, bleeding disorders, amyloid angiopathy, illicit drug use (e.g. amphetamines or cocaine).The hematoma enlarges until pressure from surrounding tissue limits its growth, or until it decompresses by emptying into the ventricular system, CSF or pial surface. A third of intracerebral bleed is into the brain’s ventricules. ICH has a mortality rate of 44 percent after 30 days, may higher than ischemic stroke or even deadly subarachnoid hemorrhage. [1]
Silent stroke
A silent stroke is a stroke that does not have any outward symptoms, and the patients are typically unaware they have had a stroke. Despite not causing identifiable symptoms, a silent stroke still damages the brain, and places the patient at increased risk of both transient ischemic attack and major stroke in the future. Conversely those who have had a major stroke are also at risk of having silent strokes. [1]
General examination of stroke patients
Skin
Xanthelasma
Rashes (arteritis, splinter hemorrhage, livedo reticularis)
Limb ischemia/deep venous thrombosis
Eyes
Diabetic changes
Retinal emboli
Hypertensive changes
Arcus senilis
Cardiovascular system
Blood pressure (hypertension, hypotension)
Heart rhythm (atrial fibrillation)
Murmurs (sources of embolism)
Jugular venous pressure (heart failure, hypovolaemia)
Peripheral pulse and bruits (generalized arteriopathy)
Respiratory system
Pulmonary oedema
Respiratory infection
Abdomen
Urinary retention
Locomotor
Injuries sustained during collapse with stroke
Co-morbidities which influence functional abilities [2]
Neurological Examination
Motor System
The upper motor neuron (UMN) lesion weakness, increased tone, increased reflexes, pyramidal pattern of weakness (weak extensors in the arm, weak flexors in leg).
Te level of nervous system affected can be determined by the distribution and pattern of the weakness and by associated findings.
Tone
Testing muscle tone is very important indicator of the presence and site of pathology. Before examination, ensure the patient is relaxed, or at least distracted by conversation. Repeat each movement at different speeds. [3]
Grading of tones
Normal: Slight resistance through whole range of movement
Spasticity (increased tone): Resistance increases suddenly (‘the catch’); upper motor lesion.
Other grading of tones:
(Rigidity and cogwheel rigidity (increased tone): Resistance increases the whole range, as if bending a lead pipe (lead pipe rigidity) and regular intermittent break in tone through whole range; extrapyramidal syndrome. Causes: Parkinson’s disease, phenothiazines.
Flaccidity (reduced tone): loss of resistance through movement: lower motor neurone or cerebellar lesion.
Gegenhalten or paratonia (increased tone): Patient apparently opposes your attempts to move his limb; bilateral frontal lobe damage; causes: cerebrovascular disease, dementia.
Myotonia (rare): slow relaxation following action; causes: myotonic dystrophy and myotonica congenita)
Arms
Tone at the wrist
Tone at the elbow
Legs
Tone at the hip
Tone at the knee
Tone at the ankle
Power
Power when tested is graded conventionally using the Medical Research Council scale (MRC).
This is usually amended to divided 4 into 4+, 4 and 4- , as below: [3]
5 = normal power
4+ = submaximal movement against resistance
4 = moderate movement against resistance
4- = slight movement against resistance
3 = moves against gravity but not resistance
2 = moves with gravity eliminated
1 = flicker
0 = no movement
Power should be graded according to the maximum power attained, no matter how briefly this is maintained.
Arms
Basic screening examination:
A simple screening procedure is outlined below. Perform each test on one side then compare to the other side.
Shoulder abduction
Elbow flexion
Elbow extension
Finger extension
Finger flexion
Finger abduction
Finger adduction
Thumb abduction
Upper motor neuron or pyramidal weakness predominantly affects finger extension, elbow extension, and shoulder abduction. (N.B. Elbow flexion and grip are relatively preserved.)
Legs
Compare the left with right.
Hip flexion
Hip extension
Knee extension
Knee flexion
Foot dorsiflexion
Plantar flexion of the foot
Upper motor neuron or pyramidal weakness predominantly affects hip flexion, knee flexion, and foot dorsiflexion.
Notes: Look for the muscle wasting and fasciculation and for the position and contractures of limbs before Motor power examination.
Reflexes
Tendon reflexes are increased in upper motor neurone lesions and decrease in lower motor neurone lesions and muscle abnormalities. [3]
Reflexes can be graded
0 = absent
+ = present only with reinforcement
+ = present but depressed
++ = normal
+++ = increased
++++ = clonus
What to do
Biceps
Supinator
Triceps
Finger reflex
Knee reflex
Ankle reflex
Further manoeuvres
Demonstration of clonus
At the ankle
At the knee
Plantar response (Babinski’s sign)
Sensation
Vibration sense on toes and finger (use 128 HZ tuning fork)
Joint position sense in toes and fingers
Light touch in hand and feet (use a piece of cotton wool)
Pin prick in hand and feet (use a pin, disposable neurological pin; dispose after used)
Temperature (need cold and warm water tubes for formal test)
Vibration, joint position and temperature senses are often lost without prominent symptoms.
Light touch and pin prick loss is usually symptomatic. (3)
Brain stem (rare): loss of pain and temperature on the face and on the opposite side of the body.
Thalamic sensory loss: hemisensory loss of all modalities.
Cortical loss: parietal lobe; the patient is able to recognize all sensations but localizes them poorly; loss of two-point discrimination, astereognosis, sensory inattention.
Gait
If the patient can walk, test the gait.
Ask the patient to walk.
Symmetrical or not
Paces (small or normal)
Look at the posture and arm swing.
Look at the lateral distance between the feet (feet separation)
Look at the knees
Look at the pelvis and shoulder
Look at the whole movement
Look at one leg swing out to the side
Asymmetrical gait (hemiplegic gait); stroke, multiple sclerosis
Coordination
Arms
Finger-nose test
Legs
Heel-shin test
Speech
Aphasia
*All disorders of understanding or thought and word finding
Discover the patient’s first language
Assess understanding
Assess word-finding ability and naming
Assess repetition
Assess severity of impairment of speech
Dysphonia
*If the patient is unable to produce normal volume of sound or speaks in whisper, this is dysphonia.
Ask to cough
Dysarthria
*If the patient is able to give his name and address but the words are not formed properly, he has dysarthria.
Ask to patient to repeat difficult phrase.
Mental State and Higher Function
Mental state
Mental state relates to the mood and thoughts of a patient.
What to do and what you find?
Appearance and behavior
Watch the patient and ask questions yourself.
Are the signs of self neglect? (dirty or unkempt: depression, dementia)
Does the patient appear depressed? (furrowed brow, immobile, downcast facies, slow monotonous speech)
Does the patient appear anxious? (fidgety, restless)
Does the patient behave appropriately? (overfamiliar, disinhibited, or aggressive: frontalism Unresponsive, with little emotional response: flat effect)
Does the patient’s mood change rapidly? (crying or laughing easily: emotional lability) [3]
Mood
Ask the patient about mood (How are your spirits at the moment? How would you describe your mood?)
If you consider the patient may be depressed, ask those. (Are you ever able to cheer up?
Do you see any hope in the future?)
Patients with depression say they find it difficult to cheer up and see little hope in the future.
Patients with schizophrenia often have an apparent lack of mood: blunt affect
or inappropriate mood, smiling when you expect them to be sad: incongruous affect [3]
In mania, patients are euphoric.
Vegetative symptoms:
Ask the patient about vegetative symptoms ( weight loss or gain, sleep disturbance (waking early or difficulty getting to sleep), appetite (loss or increased), constipation, libido (loss or increased)) [3]
Symptoms of anxiety:
Look for symptoms of anxiety (palpation, sweating, hyperventilation (tingling in fingers, toes and around the mouth, dry mouth, dizziness and often a feeling of breathlessness). [3]
Organic psychosis:
A neurological deficit is producing an altered mental state; suggested by: altered consciousness, fluctuation level of consciousness, disturbed memory, visual, olfactory, somatic and gustatory hallucinations and sphincter disturbance. [3] [4]
Proceed to test higher function for localizing signs.
Three major syndromes:
1. Acute confusional state: (Delirium)
Clouded consciousness (neglect the surrounding, unresponsive, with little emotional response),
More than two following symptoms:
(Delusion, illusions, hallucinations, misinterpretation, incoherent speech, sleeping disturbances,)
Recent memory impairment and disorientation in time and place
Fluctuation of clinical features
(*Delusion; It is a firmly held belief, not altered by rational argument, and not a conventional belief within the culture and society of the patient.
*Illusion; a misinterpretation of external stimuli and it is particularly common in patient with altered consciousness. (e.g. a confused patient says he can see a giant fist shaking outside the window, which is in fact a tree is blowing in the wind outside)
*Hallucination; it is a perception experience without external stimuli that is indistinguishable from the perception of a real external stimuli.
(e.g. smell (olfactory), taste(gustatory), and sight(visual) are usually organic,
touch (somatic) and hearing (auditory) are usually psychiatric)) [3] [4]
2. Dysmnesic syndromes:
Prominent loss of short term memory
3. Dementia:
Clear consciousness
Poor memory (but can remember past events properly)
Behavior changes (restlessness, agitation, overfamiliar, disinhibited, sometimes apathetic and disinterested ,rigid and stereotyped routines, self-neglect, increased libido, aggressive, rudely talking and improper manner (e.g. stolen)),
Intellectual impairment (concrete thinking, impaired abstract thinking, reduced problem solving mind and ability, unable to do new task base on previous experiences and skill),
Emotional disturbance (anxiety and panic attack, irritability, suspiciousness, depression and suicidal tendency, emotional lability, an apparent lack of mood),
Disorientation for time, place and person
Problems increased in occupation and social functioning
Diagnosis criteria for the dementia:
1. Intellectual impairment and interfered with social or occupational functioning
2. Impaired memory
3. More than following two symptoms:
Impaired abstract thinking
Impaired social judgment
Altered personality
Aphasia, agnosia, aprexia
4. Underlying course (stroke) [3] [4]
Higher function
Higher function is a term used to encompass thought, memory, understanding, perception and intellect.
When should you test higher function?
Obviously, if the patient complains of loss of memory or of any alteration in higher function, you should test it formally. In other patients the clues that should lead you to test come from the history. Patients are often adept at covering their loss of memory: Vague answers to specific questions, inconsistencies given without apparent concern, may suggest the need for testing. If in doubt, test. History from the relatives and friends is essential. [3]
Attention and orientation: (diffuse disturbance of cerebral function; if acute often associated with disturbance of consciousness, if chronic limit ability for further testing, suggestive of dementia) [3]
Memory: (short term memory bilateral limbic system disturbance, bilateral temporal lesion, loss of long term memory with preserved short term memory: functional memory loss) [3]
Calculation: (a dominant parietal lobe syndrome) [3]
Abstract thought: (Test for frontal lobe function) [3]
Spatial: (Test for occipital lobe function) [3]
(It is difficult to assess in the presence of weakness)
Visual and body perception: (Test for parietal and occipital lesions) [3]
Apraxia: (Test for dominant parietal and premotor cortex of frontal lobe function) [3]
Examination of Cranial Nerves
The Eye (II, III)
General: Ptosis, exopthalmos, enopthalmos.
Pupils: size, regular in outline, any holes in the iris or foreign bodies (lens implants)
The direct reflex
The consensual reflex
Reaction to accommodation
Acuity: (test using bedside newspaper, count fingers, hand movement, perceive light)
Fields: to hand movements
Fundi:
You need an ophthalmoscope for the examination of fundus.
Optic disc: (papilloedema, optic atrophy, glaucoma)
Hypertensive retinopathy: (Mild_ A.V nipping, variable caliber;
Severe_ flame haemorhage, hard exudates, cotton wool spots)
Diabetic retinopathy: (blot-, dot-haemorhage, hard exudates, neo-vascularization, cotton wool spots)
Cholesterol emboli:
(Ophthalmoscope examination: Ophthalmologist opinion required)[3]
Cranial Nerves III, IV, VI:
Eye movements
Test the eye movements to pursuit
-Watch the movements of the eyes on upgaze and lateral gaze
-Check the double vision of patient’s report at any stage
Test saccadic eye movement
-Observe eye movements
-Look particularly at the speed of adduction
Test convergence
-Observe the limit of convergence of the eyes. (These are rarely affected in clinical practice.)
Vestibuol-ocular reflex (doll’s eye maneuver)
-The eyes should move within the orbit, maintaining forward gaze.
Nystagmus: It is a slow drift in one direction with a fast correction in the opposite direction.
Types: Physiological, Central, peripheral, retinal nystagmus [3]
Cranial Nerves V AND VII
The Face
Facial nerve VII: (Face, ear, taste, tear)
Face muscle of facial expression,
Ear: stapedius,
Taste: anterior two-third of tongue,
Tear: parasympathetic supply to lacrimal gland
Look at the symmetry of the face
-Note nasolabial folds, forehead wrinkles.
-Watch spontaneous movements: smiling, blinking.
Ask the patient to:
-show you his teeth (demonstrate)
-whistle
-close his eyes tightly as he had a soap in them (demonstrate)
-Look up at the ceiling
With lower motor neurone facial weakness all muscles are affected.
With upper motor neurone facial weakness the forehead is relatively preserved. [3]
Trigeminal Nerve V:
Motor (rare deficit)
Look at the side of the face
Ask the patient to clench his teeth.
Ask the patient to push his mouth open against your hand.
Jaw jerk
Ask the patient to let his mouth hang loosely open. Place your finger on his chin. Percuss your finger with patella hammer. Feel and observe the jaw movement.
Sensory
Test facial sensation
Test light touch and pin prick in each division on both sides:
V1: forehead (ophthalmic), V2: cheek (maxillary), V3: lower lip (mandibular).
N.B. Angle of jaw is not supplied by the trigeminal nerve but by the greater auricular (C2)
Trigeminal nerve innervates the scalp to the vertex not just to the hair line.
Trigger area: trigeminal neuralgia [3]
Cranial Nerves IX, X, XII
Mouth and tongue:
Ask the patient to open his mouth.
Look at the tongue: Size, rippling movements (fasciculations), colour and texture
Ask him to put his tongue.
Does it move straight out or deviate to one side?
Test speech (See dysarthria):
Pharynx:
Look at the position of uvula.
(Use tongue depressor if you cannot see the uvula)
Ask the patient to say ‘Ahh’
Look at the uvula movement.
Ask the patient to swallow (provide a glass of water)
Watch for smooth coordination of action
Note if there are two phases or any aspiration
Gag reflex:
Afferent glossopharyngeal and efferent Vagus
Touch the pharyngeal wall behind the pillar of fauces
Watch the uvula
Ask the patient to compare the sensation between two sides
*Uvula moved to one side (upper motor or lower motor lesion of vagus on the other side)
*Uvula does not move on saying ahh or gag (bilateral palatal muscle paresis)
*Uvula moved on saying ahh but not gag with reduced sensation of pharynx: IX palsy (rare).
Larynx:
Ask the patient to cough. [3]
Gradual-onset-cough; bovine cough: suggests vocal cord palsy
Bubbly voice and cough; suggests combine cord palsy and pharyngeal pooling due to 10th nerve lesion
Give the patient a glass of water to swallow [3]
Swallow followed by coughing indicate aspiration due to poor air way protection: suggests 10th nerve lesion
Unilateral cord palsy; recurrent laryngeal palsy or vagal lesion
(laryngoscopy and ENT opinion required)
Cranial Nerve XI (Accessory Nerve)
Look at the neck.
Look at the shoulders.
Sternocleidomastoid
Ask the patient to lift his head forward. (Neck flexion)
Ask the patient to turn his head to side.
Trapezius
Ask the patient to shrug his shoulders. [3]
Cranial Nerve VIII (Auditory Nerve)
Auditory
Test the hearing:
Rinne’s test: (use 516 HZ tuning fork)
Wiber’s test: (use 516 HZ tuning fork)
Vestibular
Gait (see above)
Nystagmus [3]
Cranial Nerve I (Olfactory Nerve)
This is rarely tested in clinical practice.
Pathology
Of patient presenting a stroke, 85% will have sustained a cerebral infection due to inadequate blood flow to part of the brain. The remainder will have had an intracerebral haemorrhage. [2]
Cerebral Infarction
Cerebral infarction is mostly due to thromboembolic disease secondary to atherosclerosis in the major extracranial arteries (carotid artery and aortic arch). About 20% of infarctions are due to embolism from the heart, and further 20% are due to intrinsic disease of small perforating vessels (lenticulostriate arteries), producing so- called ‘lacunar’ infarctions. The risk factors for ischaemic stroke reflect the risk factors for the underlying vascular disease (See below). Perhaps 5% are due to the rare causes, including vasculitis, endocarditis and cerebral venous diseases. [1] [2]
Figure 4. (A)
(B)
CT scans of peripheral and lacunar infarction. (A) Peripheral infarction from occlusion of a middle cerebral artery. (B) Lacunar infarction caused by occlusion of a deep perforating artery.
Credit from Davidson’s principle and practice of medicine
Stroke risk factors
Fixed
-Age
-Gender (male>female, except in the very young and very old)
-Race (Afro-Caribbean>Asian>European)
-Heredity
-Previous vascular event, e.g. myocardial infarction, stroke or peripheral embolism
-High fibrinogen
Modifiable
-High blood pressure
-Heart disease (atrial fibrillation, heart failure, endocarditis)
-Diabetes mellitus
-Hyperlipidaemia
-Smoking
-Excess alcohol consumption
-Polycythemia
-Oral contraceptives
-Social deprivation
-Lack of physical activity
-Obesity
-Processed red meat consumption
-Unhealthy diet
-Drugs (amphetamine and cocaine) [1] [2]
Pathophysiology
Cerebral infarction is a process which takes some hours to complete, even though the patient’s deficit may be maximal close to the onset of the vascular occlusion. After the occlusion of a cerebral artery, the opening of the anastomotic channels from other arterial territories may restore perfusion to its territory. Similarly, a reduction in perfusion pressure leads to compensatory homeostatic changes to maintain oxygenation. These changes can sometimes prevent even occlusion of a carotid artery from having any clinically apparent effect.
However, if and when these homeostatic mechanisms fail, the process of ischaemia starts and ultimately leads to infarction. As the cerebral blood flow declines, different neuronal functions fail at various thresholds.
Once blood flow falls below the threshold for the maintenance of the electrical activity, neurological deficit appears. At this level of blood flow, the neurons are still viable; if blood flow is increase again, function returns and the patient will have had a transient ischaemic attack.
However, if the blood flow falls further, a level is reached at which the process of cell death starts. Hypoxia leads to inadequate supply of adenosine triphosphate (ATP), which in turn leads to failure of
membrane pumps, thereby allowing influx of sodium and into the cell (cytotoxic oedema) and the release of the excitatory neurotransmitter glutamate into the extracellular fluid. Glutamate opens membrane channels, allowing the influx of calcium and more sodium into the neurons.
Calcium entering the neurons activates intracellular enzymes that complete the destructive process.
The release of inflammatory mediators by microglia and astrocytes produces death of all cell types in the area of maximum ischaemia.
The infarction process is worsened by the anaerobic production of lactic acid and consequent fall in tissue PH.
Attempts to produce ‘neuroprotective drugs’ to slow down the processes, leading to irreversible cell death have so far been largely disappointing.
The final result of the occlusion of a cerebral blood vessel therefore depends up on the competence of the circulatory homeostatic mechanisms, and the severity and duration of the reduction in blood flow.
Higher brain temperature, as might occur in fever, and higher blood sugar have both been associated with greater volume of infarction for a given reduction in cerebral blood flow.
If ischaemic damage has occurred to the endothelium, subsequent restoration of blood flow may cause haemorrhage into the infarcted area (so-called haemorrhagic transformation).This is particularly like to occur in large infarcts, in patients given antithrombotic and thrombolytic drugs, and the possibly following embolic occlusion when the embolus is lysed by the blood’s intrinsic thrombolytic mechanisms.
In addition to injurious effects on brain cells, ischaemia and infarction can result in loss of structural integrity of brain tissue and blood vessels, partly through the release of matrix metalloproteases, which are zinc- and calcium-dependent enzymes that breakdown collagen, hyaluronic acid, and other elements of connective tissues. Other proteases also contribute to this process. The loss of vascular structural integrity results in a breakdown of the protective blood brain barrier that contributes to cerebral oedema, which can cause secondary progression of the brain injury.
Radiologically, a cerebral infarct can be seen as a lesion which comprises brain tissue that is ischaemic and swollen but recoverable (the ischaemic pneumbra), as well as dead brain tissue that is already undergoing autolysis.
The infarct swells with time and is at its maximal size a couple of days after the stroke onset. At this stage it may be big enough to exert some mass effect both clinically and radiologically. As the weeks go by, the oedema subsides and the infracted area is replaced by a sharply defined fluid-filled cavity. [1] [2]
Intracerebral Haemorrhage
This is usually results from rupture of blood vessel within the brain parenchyma: a primary intracerebral haemorrhage. It may also occur in a patient with a subarachnoid haemorrhage if the artery ruptures into the brain substance as well as into the subarachnoid space.
Haemorrhage frequently occurs into an area of brain infarction; if the volume of haemorrhage is large, this may be difficult to distinguish from intracerebral haemorrhage both clinically and radiologically. The risk factors and underlying causes of intracerebral haemorrhage are listed below. [1] [2]
Figure 5. (A)
(B)
CT scans of intracerebral hemorrhage (A) Acute intracerebral hemorrhage (arrows), (B) Resolved lesion leaving a silt-shaped defect
Credit from Davidson’s clinical principal and practice of medicine
Causes of intracerebral haemorrhage and associated risk factors
Diseases Risk factors
Complex and small vessel disease Age
with disruption of vessel wall Hypertension
Amyloid angipoathy familial (rare)
Age
Impaired blood clothing Anticoagulant therapy
Blood dyscrasia
Thrombotic therapy
Vascular anomaly Arteriovenous malformation
Cavernous haemangioma
Substance misuse Alcohol
Amphetamines
Cocaine
Pathophysiology
The explosive entry of blood into the brain parenchyma causes immediate cessation of functions in that area as neurons are structurally disrupted and white matter fibre tracts are split apart. The haemorrhage itself may expand over the first minutes or hours or it may be associated with a rim of cerebral oedema, which, along with the haematoma, acts like a mass lesion to cause progression of the neurological deficits. If big enough, this can cause shift of the intracranial contents, producing transtentorial coning and sometimes rapid death. If the patient survives, the haematoma is gradually absorbed, leaving a haemosiderin-lined clift in the brain parenchyma. [1] [2]
Risk factors for a stroke in people under 55
-Premature atherosclerosis
-Trauma
-Migraine
-vasculitis
-Systemic lupus erythematosus (SLE)
-Embolism from heart (atrial fibrillation (AF), Post myocardial infarction)
-Hyperlipidaemia
-Carotid dissection
-Thrombophilia (Protein C and S deficiency, antithrombin III deficiency)
-Homocystinuria
-Anticardiolipin syndrome
-Mitochondrial cytopathy
-Primary intracerebral haemorrhage ( Arteriovenous malformation(AVM), Coagulopathy, drug abuse)
-Subarachnoid haemorrhage ( Saccular ‘Berry’ aneurysm, AVM, Carotid dissection)
-Severe anaemia
-Alcoholic binge drinking
-pregnancy
-Sickle-cell anaemia
-Illegal recreational drugs (Cocaine)
-neurovascular syphilis
-CADASIL(Cerebral Autosomal Dominant Ateriopathy with Subcortical Infarct and Leucoencephalopathy)
-Antiphospolipid antibody syndrome [2]
Investigation of Acute Stroke
Investigation of a patient presenting with an acute stroke aims to confirm the vascular nature of lesion, distinguish cerebral infarction from haemorrhage and identify the underlying vascular disease and risk factors.
Stroke is diagnosed through several techniques: neurological examination, CT scans (most often without contrast enhancements) or MRI scans, Doppler ultrasound, and arteriography. The diagnosis of stroke itself is clinical, with assistance from the imaging techniques. Imaging techniques also assist in determining the subtypes and causes of stroke.
There is yet no commonly used blood test for stroke diagnosis itself, though blood test may be help to detect common vascular risk factors and markers of rare causes.
Moreover, electrocardiogram and echocardiogram are used to identify arrhythmia and resultant clots in the heart which may spread to the brain vessels through the blood stream.
Angiogram of cerebral vasculature can be used to detect, if a bleed is thought to have originated from an aneurysm or arteriovenous malformation.
Where there is uncertainty about the nature of stroke, further investigations are usually indicated. This is especially applies to younger patients who are less likely to have atherosclerotic disease. (See below) [1] [2]
Imaging the brain
Brain imaging with either CT or MRI should be performed in all patients with stroke. Exceptions to this include patients in whom the brain scan results would not influence management, such as the patient who has stroke in the latter stage of a terminal illness.
CT scan
CT is the most practical and widely available method of imaging the brain. It will usually exclude non-stroke lesions, including subdural haematoma and brain tumours. It will demonstrate intracerebral haemorrhage within minutes of stroke onset.
However, especially within the first few hours after symptom onset, CT changes in cerebral infarction may completely absent or very subtle, though change usually evolve over time. The CT scan performed within the first day for most purpose, or so is adequate for clinical care, but there are certain circumstances in which an immediate CT scan is essential. (See below)
Even in the absence of the changes suggesting infarction, abnormal perfusion of brain tissue can be imaged with CT after injection of contrast media (e.g. perfusion scanning). This can be useful in guiding hyper-acute treatment of ischaemic stroke. [1]
Indications for an immediate CT/MRI in acute stroke patient
-Patient on anticoagulants or with abnormal coagulation
-Plan to give thrombolysis or immediate anticoagulants
-Deteriorating conscious level or rapidly progressing deficits
-Suspected cerebellar haematoma, to exclude hydrocephalus
For diagnosing ischaemic stroke in the emergency setting:
CT scans without contrast enhancements
Sensitivity = 16%
Specificity = 96%
For diagnosing haemorrhagic stroke in the emergency setting:
CT scans without contrast enhancements
Sensitivity = 89%
Specificity = 100%
MRI scan
MRI is not widely available as CT, Scanning times are longer and it cannot be used some individuals with contraindications (e.g. Scanners claustrophobic and Pacemaker). However, MRI diffusion weighted imaging (DWI) can detect ischaemia earlier than CT, and other MRI sequences can also be used to demonstrate abnormal perfusion.
MRI is more sensitive than CT in detecting stroke affecting the brain-stem and cerebellum and unlike CT, can rapidly distinguish haemorrhage from ischaemia stroke even several weeks after onset. [1]
For diagnosing ischaemic stroke in the emergency setting:
MRI scans
Sensitivity = 83%
Specificity = 98%
For diagnosing haemorrhage stroke in the emergency setting:
MRI scans
Sensitivity = 81%
Specificity = 100%
For detecting chronic haemorrhages, MRI scan is more sensitive
Imaging blood vessels
Many ischaemic strokes are caused by atherosclerotic thromboembolic diseases of the major extracranial vessels. Those can be detected non-invasively indentified with duplex ultrasound, MR angiography (MRA), or CT angiography.
Because of the significant risk of complications intra-arterial contrast angiography is reserved for patients in whom non-invasive methods have provided contradictory or incomplete information, or in whom it is necessary to image the intracranial circulation in detail: for example, to delineate a saccular aneurysm, an arteriovenous malformation or vasculitis. [1] [2]
Detecting a cardiac source of embolism
Approximately 20% of ischaemic strokes are thought to be due to embolism from the heart. The most common causes of cardiac embolism are atiral fibrillation, prosthetic heart valves, other vascular abnormalities and recent myocardial infarction. These can also be identified by clinical examination and ECG.
However, cardiac sources of embolism can exist without obvious clinical or ECG signs. A transthoracic or transoesophageal echocardiogram can be useful, either to confirm the presence of a clinically apparent cardiac source or to identify an unsuspected source such as endocarditis, atrial myxoma, intracardiac thrombus or patent foramen ovale. Such findings may lead on to specific treatment. [2]
Investigation of a patient with an acute stroke
Diagnostic question Investigation
Is it vascular lesion? CT/MRI
Is it ischaemic or haemorrhagic? CT/MRI
Is it a subarachnoid haemorrhage? CT, lumbar puncture
Is there any cardiac source of embolism? Electrocardiogram (ECG), echocardiogram
What is the underlying vascular disease? Duplex ultrasound of carotids,
Magnetic resonance angiography (MRA),
CT angiography (CTA), Contrast angiography
What are the risk factors? Full blood count, Cholesterol, Blood glucose
Is there are unusual cause? ESR, Clotting/thrombophilia screen
A Holter monitor study to identify intermittent abnormal heart symptoms;
Causes and investigation of acute stroke in young patients
Cause Investigation
Cardiac embolism Echocardiography (including transoesophageal)
Premature atherosclerosis Serum lipids
Arterial dissections MRI, Angiography
Thrombophilia Protein C, Protein S, Antithrombin III
Homocystinuria Urinary amino acid, Methionine loading test
Antiphospolipid antibody syndrome Anticardiolipin antibodies/lupus anticoagulant
Systemic lupus erythematous Anti nuclear antibodies
Vasculitis ESR, CRP, Antineutrophil cytoplasmic antibody (ANCA)
CADASIL (Cerebral Autosomal MRI brain, Genetic analysis, Skin biopsy
Dominant Ateriopathy with Subcortical
Infarcts and Leucoencephalopathy)
Mitochondrial cytopathy Serum lactate, Muscle biopsy
Neurovascular syphilis Syphilis serology
Primary intracerebral haemorrhage
-Artreiovenous malformation (AVM) Delay MRI, Contrast angiography
-Drug misuse Drug screen (amphetamine, cocaine)
-Coagulopathy Prothrombin time (PT), and activated partial
thromboplastin time (APTT), Platelet count
Subarachnoid haemorrhage
-Saccular (‘berry’) aneurysm MRI/angiography
-AVM MRI/angiography
-Vertebral dissection MRI/angiography
General management of patients with acute stroke
Management is aimed to minimizing the volume of brain that is irreversibly damaged, preventing complications, reducing the patient’s disability and handicap through rehabilitation, and reducing the risk of recurrent attacks.
Early admission of patients to a special stroke unit facilitates coordinated care from a specialized multidisciplinary team and has been shown to reduce both mortality and residual disability amongst survivors.
Consideration of patient’s rehabilitation needs should commence at the same time as acute medical management.
Dysphagia is common after stroke and can be detected by an early bedside test of swallowing, which allows hydration, feeding and medication to given safely, if necessary by nasogastric tube or intravenously. In the acute phase it may be useful to refer to a checklist (see below) to ensure that all the factors which might influence the patient’s outcome have been addressed. [2]
Acute stroke management admission checklist
Airway
-Is the patient able to protect his/her airway?
-Can the patient swallow without evidence of aspiration?
-Perform a swallow screen and keep the patient nil by mouth if swallowing unsafe.
Breathing
-Is the patient breathing adequately?
-Check oxygen saturation and give supplementary oxygen if oxygen saturation < 95%
Circulation
-Are peripheral perfusion, pulse and blood pressure adequate?
-Treat with fluid replacement, anti-arrhythmics and inotropic drugs as appropriate.
Hydration
-Is the patient dehydrated or unable to swallow?
-Give fluid replacement parenterally or by nasogastric tube if swallow is unsafe.
Nutrition
-Assess nutritional status.
-Consider nutritional supplements.
-If dysphagia persists for a day or two, start feeding via a nasogastric tube.
Medication
-If patient is dysphagic, consider alternative routes for essential medications.
Blood pressure
-Unless there is heart failure or renal failure, evidence of hypertensive encephalopathy or aortic dissection, do not lower the blood pressure in the first week since it will often return toward the patient’s normal level within first few days.
-Early blood pressure reduction may decrease cerebral perfusion and increase infarction to offset potential benefits. Trials of early blood pressure lowering are ongoing.
Blood glucose
-Is the blood glucose> 11.1 mmol/l (200 mg/dl)?
-Hyperglycaemia may increase infarct volume, therefore use insulin (via infusion or glucose/ potassium/ insulin (GKI)) to normalize levels but monitor closely to avoid hypoglycaemia.
-Trials of more rigorous glycaemic control are ongoing.
Temperature
-Is the patient pyrexia?
-Raise brain temperature may increase infarct volume.
-Investigate and treat any cause but give antipyretics early.
Pressure areas
-These should be formally assessed and measures taken to reduce the risk.
-Treat infection, maintain nutrition, provide a pressure-relieving mattress and turn immobile patients regularly.
Incontinence
-Ensure the patient is not to constipated or urinary retention
-Avoid urinary catheterization unless the patient is in acute urinary retention or incontinence is threatening pressure areas.
The deteriorating stroke patient
The patient’s neurological deficits may worsen during the hours or days after their onset. This is probably most common amongst those with lacunar infarction but may occur in other patients, due to extension of the area of infarction, haemorrhage into it or the development of oedema with consequent mass effect.
It is important to distinguish such patients from those who deteriorating as a result of complications such as hypoxia, sepsis, epileptic seizure or metabolic abnormalities which may be more easily reversed.
Patients with cerebellar haematomas or infarcts with mass effect may develop obstructive hydrocephalus and some will benefit from insertion of a ventricular drain and/or decompressive surgery.
Some patients with large haematomas or infarction with massive oedema in the cerebral hemispheres may benefit from anti-oedema agents such as mannitol, artificial ventilation and/or surgical decompression to reduce intracranial pressure, although evidence for the effectiveness of these interventions is still incomplete. [2]
Complications of acute stroke
Complication Prevention Treatment
-Chest infections Nurse semi-erect Antibiotics
Avoid aspiration Physiotherapy
-Epileptic seizure Maintain cerebral oxygenation Anticonvulsants
Avoid metabolic disturbance
-Deep venous thrombosis/ Maintain hydration Anticoagulants (exclude
Pulmonary embolism Early mobilization haemorrhagic stroke first)
Anti-embolism stocking
Heparin (for high-risk patient only)
-Painful shoulder Avoid traction injury Physiotherapy
Shoulder/arm supports Local corticostreroid
Physiotherapy injections
-Pressure sores Frequent turning Nursing care
Monitor pressure area Pressure-relieving mattress
Avoid urinary damage skin
-Urinary infection Avoid catheterization if possible Antibiotics
Use penile sheath
-Constipation Appropriate aperients and diets Appropriate aperients
-Depression and anxiety Maintain positive attitude and Antidepressants
provide information
Specific treatment for stroke
Treatment varies according to the underlying cause of stroke, thromboembolic (ischaemic) or haemorrhagic. A non contrast head CT scan can rapidly identified a haemorrhagic stroke by imaging bleeding in or around the brain. If no bleeding is seen, a presumptive diagnosis of ischaemic stroke is made. (1) (2)
Treatment of ischaemic stroke
Ischaemic stroke is caused by a thrombus (Blood clot) occluding blood flow to artery supplying the brain. Definitive therapy is aimed at removing the blockage by breaking the clot down (thrmbolysis), or by removing it mechanically (thrombectomy). The more rapidly blood flow is restored to the brain, the fewer brain cells die.
Other medical therapies are aimed at minimizing clot enlargement or preventing new clot formation. To this end, treatment with medications such as aspirin, clopidogrel and dipyridamole may be given to prevent platelets aggregation.
In addition to definite therapies, management of acute stroke includes control of blood sugars, ensuring the patient has adequate oxygenation and adequate fluids (intravenous or nasogastric tube). Patients may be positioned with their heads flat on the stretcher, rather than sitting up, to increase blood flow to the brain. It is common for elevation of the blood pressure immediately following a stroke. Although high blood pressure may cause some stoke, hypertension during acute stroke is desirable to allow adequate blood flow to the brain. [1] [2]
Thrombolysis
Pharmacologic thrombolysis with the drug recombinant tissue plasminogen activator (rt-PA) is used to dissolve the clot and un-clot artery. However, the use of rt-PA in acute stroke is controversial, because of increasing the risk of hemorrhage transformation of cerebral infarct with potentially fatal results.
On the other hand, it is endorsed by the American Heart Association and American Academy of Neurology as recommended treatment for acute stroke within 3 hours of onset of symptoms as long as there are not other contraindications (such as abnormal lab values, high blood pressure, or recent surgery).
This position for rt-PA is based upon the finding of two studies by one group of investigators which showed that rt-PA improves the chances for a good neurological outcome. When administered within the first 3 hours 39% of all patients who were treated with rt-PA had a good outcome at three months, only 26% of placebo controlled patients had a good functional outcome. [1]
A recent study using alteplase for thrombolysis in ischaemic stroke suggests clinical benefit with administration 3 to 4.5 hours after stroke onset. [1] [2]
Mechanical Thrombectomy
Another intervention for acute ischaemic stroke is removal of the offending thrombus directly. This is accomplished by inserting a catheter into the femoral artery, directing it into the cerebral circulation, and deploying a corkscrew-like device to ensnare the clot, which is then withdraw from the body.
Mechanical embolectomy devices have been demonstrated effective at restoring blood flow in patients who were unable to receive thrombotic drugs or for whom the drugs were ineffective. The devices have only been tested on patient treated with mechanical colt embolectomy within 8 hours of onset of symptoms. [1] [2]
Angioplasty and stenting
Angioplasty and stenting have begun to be been looked at as possible viable options in treatment of acute ischaemic stroke. In a systemic review of six uncontrolled, single centre trials, involving a total of 300 patients, of intracranial stenting in symptomatic antracranial arterial stenosis, the rate of technical success (reduction to stenosis of < 50%) range from 90-98 %, and the rate of major peri-procedural complications ranged from 4-10 %. The rates of restenosis and/or stroke following the treatment were also favorable. This data suggests that a large, randomized controlled trial is needed to more completely evaluate the possible therapeutic advantage of the treatment. [1] [2]
Therapeutic Hypothermia
Most of the data concerning therapeutic hypothermia’s effectiveness in treating ischaemic stroke is limited to animal studies. These studies have focused primarily on ischaemic as oppose to hemorrhagic stroke,as hypothermia has been associate with a lower clotting threshold. In these animal studies investigating the effect of temperature decline following ischaemic stroke, hypothermia has been shown to be an effective all-purpose neuroprotectant. This promising data has led to the initiation of a variety of human studies.
At the time of this article’s publishing, this research has yet to return results. However, in terms of feasibility, the use of hypothermia to control intracranial pressure after an ischemic stroke was found to be both safe and practical. The device used in this study was called the Arctic Sun. [1]
Aspirin
Aspirin (300 mg daily) should be started immediately after an ischaemic stroke unless rt-PA has been given, in which case it should be withheld for at least 24 hours. Aspirin reduces the risk of early recurrence and had a small but clinically worthwhile effect on long-term outcome; it may be given by rectal suppository or by nasogastric tube in dysphagic patients. (In acute stroke as in myocardial infarction, given aspirin alone reduces mortality rate from 13 to 10 %.) [1] [2]
Heparin
Formal anticoagulation with heparin has been widely used in treating acute ischaemic stroke in past. Whilst this does reduce the risk of early ischaemic recurrences and venous thromembolism, these benefits are offset by definite increase in the risk of both intracranial and extracranial haemorrhage.
Furthermore, routine use of heparin does not result in better long-term outcomes, and therefore it should not be used in the routine management of acute stroke.
It is unclear whether anticoagulation with heparin might provide benefit in selected patients, such as those with recent myocardial infarction, arterial dissection or progressing strokes.
Intracranial haemorrhage must be excluded on brain imaging before considering anticoagulation. [1] [2]
Corticosteroids, haemodilution, vasodilators and ‘neuroprotective’ agents
Routine use of these agents should be avoided since they may all have adverse effects and none has shown to improve patient outcomes. [2]
Treatment of haemorrhagic stroke
Patients with intracerebral haemorrhage require neurosurgical evaluation to detect and treat the cause of the bleeding, although many may not need surgery. Anticoagulant and antithrombotic can make bleeding worse and cannot be used in intracranial haemorrhage. Patients are monitored and their blood pressure, blood sugar, and oxygenation are kept at optimum levels.
Coagulation abnormalities, most commonly due to oral anticoagulants, should be reversed as quickly as possible to reduce the likelihood of haematoma enlarging.
Promising research suggests that, in highly selected patients, haematoma enlargement may be reduced by the early administration of recombinant factor VII even in patient without clotting problem. [1] [2]
Prevention of stroke
Given disease burden of stroke, prevention is an important public health concern. Primary prevention is less effective than secondary prevention (as judged by the number need to treat to prevent one stroke per year). Because stroke may indicate underlying atherosclerosis, it is important to determine the patient’s risk for other cardiovascular diseases such as coronary heart disease. Conversely, aspirin prevents against the first stroke in patient who have suffered a myocardial infarction.
The most important modifiable risk factors for stroke are high blood pressure and atrial fibrillation. Other modifiable risk factors include high blood cholesterol levels, diabetes, smoking, heavy alcohol consumption and drug abuse, lack of physical activity, obesity and unhealthy diet.
No high quality studies have shown the effectiveness of interventions aimed at weight reduction, promotion of regular exercise, reducing alcohol consumption or smoking cessation. Nevertheless, given the large body of circumstantial evidence best medical management for stroke includes advised on diet, exercise, smoking and alcohol use.
Medication or drug therapy is the most common method of stroke prevention, and carotid endarterectomy can be useful surgical method of preventing stroke. [1] [2]
Primary prevention
Blood pressure reduction in primary prevention of stroke
Hypertension accounts for 35-40 % of stroke risk. Epidemiological studies suggest that even a small blood pressure reduction (5 to 6 mmHg systolic, 2 to 3 mmHg diastolic) would result in 40% fewer stroke. Lowering blood pressure has been conclusively shown to prevent both ischaemic and haemorrhagic stroke. Studies show that intensive antihypertensive therapy results in a greater risk reduction.
Atrial fibrillation control in primary prevention of stroke
Patient with atrial fibrillation have a risk of 5 % each year to develop stroke, and this risk even higher in those with valvular atrial fibrillation. Depending on the stroke risk, anticoagulation with medication as coumarins or aspirin is warranted for stroke prevention.
Blood lipid lowering drugs in primary prevention of stroke
High cholesterol levels have been consistently associated with (ischaemic) stroke. Statins have been shown to reduce the risk of stroke by about 15 %. But other lipid lowering drugs did not show a decrease risk, statins might exert their effect though mechanisms other than their lipid lowering effects.
Diabetes mellitus control in primary prevention of stroke
Patient with diabetes mellitus are 2 to 3 times more likely to develop stroke, and they commonly have hypertension and hyperlipidaemia. Intensive diabetes control has been shown to reduced microvascular complications such as nephropathy but not macrovascular complications such as stroke.
Antiplatelet drugs and anticoagulants in primary prevention of stroke
In primary prevention however, antiplatelet drugs did not reduce the risk of ischaemic stroke while increasing the risk of major bleeding. Though, low-dose aspirin is effective for stroke prevention after sustaining a myocardial infarction. Oral anticoagulants are not advised for stroke prevention because any benefit is offset by bleeding. [1] [2]
Secondary prevention
The average risk of a further stroke is 5 to 10 % within the first week of stroke or TIA, perhaps 15 % in the first year and 5 % per year thereafter. The risks are not clearly different for intracerebral haemorrhage.
Patients with ischaemic events should be put on long term antiplatelet drug and statins to lower cholesterol. For patients in atrial fibrillation the risk can be reduced by about 60% by oral anticoagulation to achieve an INR of 2-3. The risk of recurrence after both ischaemic and haemorrhagic strokes can be reduced by blood pressure reduction, even for those with blood pressure in the normal range. [1] [2]
Antiplatelet drugs in secondary prevention of ischaemic stroke
‘Ongoing treatment with either aspirin 75-300 mg daily, clopidogrel 75 mg daily or a combination of asprin and dipyradamole modified release 200 mg 12-hourly reduces the risk of recurrent stroke, myocardial infarction and vascular deaths. Treating 1000 patients for a year prevents about 10 strokes.’
*Antithrombotic trials’ Collaboration. BMJ 2002; 324:72-86.*Hankey G.J, et al. Stroke 2000; 31:1779-1784
Statins in secondary prevention of stroke
‘Ongoing treatment with simvastatin 40 mg daily reduces the risk of recurrent stroke, myocardial infarction and vascular deaths. Treating 1000 patients for a year prevents about 17 strokes.’
*Heart protection study Collaborative Groups. Lancet 2002; 360:7-22
Anticoagulants in secondary prevention of ischaemic stroke
‘There is no net benefit to be gained in the routine use of anticoagulants after acute stroke except in the presence of atrial fibrillation, when treating 1000 patients for a year prevents about 80% strokes.’
*Hart RG, et al. Ann Intern Med 1999; 131:492-501
Blood pressure lowering in secondary prevention of stroke
‘Lowering blood pressure even in the ‘normal range’ reduces the risk of recurrent stroke, myocardial infarction and vascular deaths. Treating 1000 patients for a year prevents about 22 strokes.’
*PROGRES Collaboration Group. Lancet 2001; 358:1033-1041
For further information: www.cochrane.org
Carotid endarterectomy and angioplasty
A small proportion of patients with a carotid territory ischaemic stroke or TIA will have a greater than 70% stenosis of the carotid artery on the side of brain lesion. Such patients have a greater than average risk of stroke recurrence. For those without major residual disability, removal of stenosis has been shown to reduce the overall risk of recurrence, although the operation itself carries a 5% risk of stroke.
Carotid angioplasty and stenting are technically feasible but long-term effects on risk of stroke are unclear. [1] [2]
‘After a stroke with good functional recovery in the carotid territory and in the presence of an ipsilateral severe stenosis (70%), carotid endarterectomy reduces the risk of subsequent stroke. Operation on 1000 patients prevents about 40 strokes over the next year.
In asymptomatic carotid stenosis, endarterectomy has a smaller benefit. Operation on 1000 patients prevents about 13 strokes over the next year.’
*Rothwell PM, et al. Lancet 2003; 361:107-16
*Executive Committee for the Asymptomatic Carotid Atherosclerosis Study. JAMA 1995; 273:1421-1428
For further information: www.cochrane.org
Nutritional and metabolic interventions
Nutrition, specifically the Mediterranean-style diet, has the potential of more than having risk.
With regards to lowering homocysteine, a meta-analysis of previous trial has concluded that lowering homocysteine with folic acid and other supplements may reduce stroke risk. However, the two large randomized controlled trials included in the meta-analysis have conflicting results. One reported positive results; whereas the other was negative.
The European Society of Cardiology and European Association for Cardiovascular Prevention and Rehabilitation have developed an interactive tool for prediction and managing the risk of heart attack
and stroke in Europe. Heart Score is aimed at supporting clinicians in optimising individual cardiovascular risk reduction. Heart Score Programme is available in twelve languages and offers web based or PC version. [1] [2]
Care and Rehabilitation
Stroke rehabilitation is the process by which patients with disabling strokes undergo treatment to help them return to normal life as much as possible by regaining and relearning the skills of everyday living. It also aims to help the survivor understand and adapt to difficulties, prevent secondary complications and educate family members to play a supporting role.
A rehabilitation team is usually multidisciplinary as it involves staffs with different skills working together to help the patient. These include nursing staff, physiotherapy, occupational therapy, speech and language therapy, and usually a physician trained in rehabilitation medicine. Some teams may also include psychologist, social workers, and pharmacists since at least one third of the patients manifest post stroke depression.
Patient may have particular problems, such as complete or partial inability to swallow, which can cause swallowed material to pass into the lungs and cause aspiration pneumonia. The condition may improve with time, but in the interim, a nasogastic tube may be inserted, enabling liquid food to be given directly into the stomach. If swallowing is still unsafe after a week, then a percutaneous endoscopic gastrostomy (PEG) tube is passed and this can remain indefinitely.
Stroke rehabilitation should be started as immediately as possible and can last anywhere from few days to over a year. Most return of function is seen in the first few days and weeks, then improvement falls off with the “window” considered officially by U.S. state rehabilitation units and others to be closed after six months, with little chance of further improvement. However, patients have been known to continue to improve for years, regaining and strengthening abilities like writing, walking, running, and talking. Daily rehabilitation exercises should continue to be part of the stroke patient’s routine. Complete recovery is unusual but not impossible and most patients will improve some extent: a correct diet and exercise are known to help the brain to self-recover.
Some current and future therapy methods include the use of virtual reality and video games for rehabilitation.
Other non invasive rehabilitation methods are currently developed to augment physical therapy to improve motor function of stroke patient, such as transcranial magnetic stimulation (TMS) and transcranial direct-current stimulation (tDCS) and robotic therapies. [1] [2]
Prognosis
Disability affects 75% of stroke survivors enough to decrease their employability. Stroke can affect patient’s physically, mentally, emotionally, or a combination of the three. The results of stroke vary widely depending on size and location of lesion. Dysfunctions correspond to areas in the brain that have been damage.
Some of the physical disabilities that can result from stroke include paralysis, numbness, pressure sores, pneumonia, incontinence, apraxia (inability to perform learned movement), difficulties carrying out daily activities, appetite loss, speech loss, vision loss, and pains. If the stroke is severe enough, or in a certain a location such as parts of brain-stem, that can result coma or death.
Emotional problems resulting from stroke can result from direct damage to emotional centres in the brain or from frustration and difficulty adapting to new limitations. Post-stroke emotional difficulties include anxiety, panic attack, flat affect (failure to express emotion), mania, apathy, and psychosis.
30-50% of stroke survivors suffer post stroke depression, which is characterized by lethargy, irritability,
Sleep disturbance, lower self esteem, and withdrawal .Depression can reduce motivation and worsen outcome, but can be treated with antidepressants.
Emotional labiality, another consequence of stroke, causes the patient to switch quickly between emotional highs and lows and to express emotion inappropriately, for instance with an excess of laughing or crying with little or no provocation. While these expressions of emotion usually correspond to the patient’s actual emotion, a more severe form of emotion lability causes patients to laugh and cry pathologically, without regard to content or emotion. Some patients show the opposite of what they feel, for example crying when they are happy. Emotional lability occurs in about 20% of stroke patients.
Cognitive deficits resulting from stroke include perceptual disorders, speech problems, dementia, and problems with attention and memory. A stroke sufferer may be unaware of his or her own disabilities, a condition called anosognosia. In a condition called hemispatial neglect, a patient is unable to attend to anything on the side of space opposite to the damage hemisphere.
Up to 10% of all stroke patients develop seizures, most commonly in the week subsequent to the event; the severity of the stroke increases the likelihood of seizures. [1]
References
1. Stroke page from internet webs Wikipedia free encyclopedia
2. Davidson’s principle & practice of medicine 20th edition, Nicholas A. Boon, Nicki R. Coledge and Brian R. Walker, ISBN -13 978-0-443-10057-4
3. Neurological Examination Made Easy third edition, Geraint Fuller, Churchill Livingstone, ISBN 0-443-07421-6
4. Psychiatry for doctors by Professor U Thane Htay Pe and Dr San Yaung Nyunt