Stroke Flashcards
Risk factors
Non-Modified: FAME MNEMONIC
Age, sex, race, previous vascular event and familial tendency. The incidence increases with age and is higher in men than in women.
Modified: systolic or diastolic hypertension, diabetes, hyperlipidaemia, heart disease, cigarette smoking, heavy alcohol consumption, and oral contraceptive use, obesity, elevated waist- to- hip ratio, diet, inactivity, stress/depression, cardiac disorders.
five of these factors being more important for hemorrhagic stroke:
Hypertension Smoking Waist-to-hip ratio Diet Alcohol
CT is usually preferred for initial diagnosis
widely available and rapid and
can readily make the critical distinction between ischemia and hemorrhage by detecting
the presence or absence of intracranial hemorrhage.
MRI is superior to CT scan for demonstrating
early ischemic infarcts, showing ischemic
strokes in the brainstem or cerebellum, and detecting thrombotic occlusion of venous
sinuses. Diffusion-weighted MRI can be helpful by proving that ischemia occurred, the
absence of a lesion does not rule out ischemia
The ischaemic penumbra is the target for therapeutic interventions
salvage is
associated with neurological improvement and recovery and better prognoses
Most deaths that occur within 1 week after massive cerebral
infarction are attributable to
cerebral edema, causing herniation and downward displacement of the brain through the tentorium.
Two pathological mechanisms can produce ischemic stroke:
1- Thrombosis produces stroke by occluding large cerebral arteries (especially the internal
carotid, middle cerebral, or basilar), small penetrating arteries (as in lacunar stroke),
cerebral veins, or venous sinuses.
2- Embolism produces stroke when cerebral arteries are occluded by the distal
passage of thrombus from the heart, aortic arch, or large cerebral arteries. Emboli in the
anterior cerebral circulation most often occlude the middle cerebral artery or its branches,
Hemorrhage may interfere with cerebral function through a variety of mechanisms
including destruction or compression of brain tissue and compression of vascular structures, leading to secondary ischemia and edema.
According to the duration of deficits, ischemic stroke can be classified as:
A. Transient ischemic attack (TIA) is a transient episode of neurologic dysfunction caused
by focal brain, spinal cord or retinal ischemia without acute infarction and 80% last less
than 30 minutes.
Immediate attention to TIA makes a huge difference in outcome as it can reduce risk for
stroke by 80 %. B. In contrast to TIA, acute ischemic stroke implies a persistent focal neurologic deficit,
which may be improving, stable, or worsening (stroke in evolution or progressing
stroke) when the patient is seen.
80 % of ischemic stroke are caused by
thrombosis or artery to artery embolism. Atherosclerosis affects large and medium-sized elastic and muscular arteries
Within the cerebral circulation, the sites of predilection are
the origin of the common carotid artery, the internal carotid artery just above the common carotid bifurcation and within the cavernous sinus, the origin of the middle cerebral artery, the vertebral artery at its origin and just above where it enters the skull, and the basilar artery.
Lacunar infarction of the brain results from
occlusion of small penetrating branches of the major cerebral arteries due to intrinsic disease of the vessels, especially those that supply the basal ganglia, thalamus, internal capsule, and pons. lacunar infarcts result from either atherosclerosis or degenerative changes in the arterial walls including lipohyalinosis and fibrinoid necrosis.
Cardioembolic stroke
Mural thrombus complicating myocardial infarction or cardiomyopathy is a recognized
source of cerebral embolism. The risk of stroke in the first weeks after
myocardial infarction is related to the size of the cardiac lesion. 2- Arrhythmias (e.g. atrial fibrillation) 3- Prosthetic heart valves 4- Endocarditis
Infective (bacterial or fungal) endocarditis is a cause of transient cerebral ischemia
and embolic cerebral infarction during the active phase of infection and during the first few months following antibiotic cure. The middle cerebral artery is the most
common site of cerebral embolization. Intracerebral or subarachnoid hemorrhage can also occur as a result of bleeding into an infarct or rupture of a mycotic aneurysm.
Nonbacterial (marantic) endocarditis is most frequent in patients with cancer most
often adenocarcinomas of the lung or gastrointestinal tract. Vegetations are present on the mitral or aortic valves.
5- Rheumatic heart disease
is the most
common site of cerebral embolization in Infective (bacterial or fungal) endocarditis
middle cerebral artery
Intracerebral or subarachnoid hemorrhage can also occur as a result of
bleeding into an infarct or rupture of a mycotic aneurysm.
Stroke of other determined cause
1- Hematological disorders
Thrombocytosis, thrombocytopenia
Polycythemia, anemia (including sickle cell disease)
Leukocytosis (e.g., leukemia).
Hypercoagulable states: Hyperviscosity of the serum from estrogen therapy, oral
contraceptive use, postpartum and postoperative states, hereditary coagulopathies and cancer may be accompanied by coagulopathies that lead to cerebral thrombosis or embolism. Antiphospholipid antibodies, including lupus anticoagulants and anticardiolipin antibodies, associated with an increased incidence of ischemic stroke.
2- Rare causes of stroke
a) Cervicocephalic arterial dissection
Idiopathic
traumatic
secondary to identifiable collagen disease
b) Vasculitis Inflammatory autoimmune vasculitis (primary and secondary) Infectious arteriopathy:
Associated with acute or chronic meningitis
Herpes Zoster Ophthalmicus Followed by Contralateral Hemiparesis due to
Granulomatous Arteritis with secondary infarction. Syphilis HIV infection
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c) Non-atherosclerotic vasculopathy Inherited vasculopathies, such as CADASIL, Fabry disease, mitochondrial disease,
moyamoya disease, Ehlers-Danlos syndrome, Marfan’s disease, Susac’s
syndrome. Cerebral amyloid angiopathy and polycystic kidney disease commonly cause
hemorrhage and rarely cause ischemia. Migraine-induced stroke Illicit-drug use (e.g., use of cocaine or amphetamines) Delayed radiation vasculopathy in a former cancer patients
d) Cerebral fat embolism as in hip fracture e) Cerebral air embolism as in central line removal f) posterior reversible encephalopathy syndrome and reversible cerebral
vasoconstriction syndrome
Hematological disorders those cause stroke
Thrombocytosis, thrombocytopenia
Polycythemia, anemia (including sickle cell disease)
Leukocytosis (e.g., leukemia).
Hypercoagulable states: Hyperviscosity of the serum from estrogen therapy, oral
contraceptive use, postpartum and postoperative states, hereditary coagulopathies and cancer may be accompanied by coagulopathies that lead to cerebral thrombosis or embolism. Antiphospholipid antibodies, including lupus anticoagulants and anticardiolipin antibodies, associated with an increased incidence of ischemic stroke
Infectious arteriopathy:
Associated with acute or chronic meningitis
Herpes Zoster Ophthalmicus Followed by Contralateral Hemiparesis due to
Granulomatous Arteritis with secondary infarction. Syphilis HIV infection
Non-atherosclerotic vasculopathy cause stroke such
Inherited vasculopathies, such as CADASIL, Fabry disease, mitochondrial disease,
moyamoya disease, Ehlers-Danlos syndrome, Marfan’s disease, Susac’s
syndrome. Cerebral amyloid angiopathy and polycystic kidney disease commonly cause
hemorrhage and rarely cause ischemia. Migraine-induced stroke Illicit-drug use (e.g., use of cocaine or amphetamines) Delayed radiation vasculopathy in a former cancer patients
General physical examination
1- The blood pressure 2- Examination of the neck may reveal the absence of carotid pulses or the presence of
carotid bruits. 3- Cardiac examination 4- peripheral pulses
underlying process other than focal cerebral ischemia should be suspected
resulting neurologic deficit does not conform to the distribution of any single cerebral artery. In addition, strokes do not typically impair consciousness in the absence of profound focal deficits, whereas other cerebral disorders may do so.
Differential Diagnosis of ischemic stroke:
Structural brain lesions such as tumor or abscess can also produce focal cerebral
symptoms. Metabolic disturbances, particularly hypoglycemia and hyperosmolar nonketotic
hyperglycemia, hepatic encephalopathy may present in stroke-like fashion. Todd’s paralysis, demyelination, hypertensive encephalopathy and encephalitis also can
mimic strokes.
When should TIA lead to emergency referral
Age > 60
Blood pressure > 140/90
Clinical such unilateral weakness or speach disturbance without weakness
Duration of symptoms more or less than 1 hr
Diabetes
All give 1 point except the unilateral and more than 1 hr give 2 points
Investigations
A. CT scan and/or MRI
B. Blood tests
C. Cerebral angiography
D. Cardiac investigations
E. Transcranial Doppler ultrasonography
Transcranial Doppler ultrasonography can detect
accelerated velocities consistent
with significant stenosis and can be used in patients unable to undergo CTA or MRA
Options for the treatment of this patient with stroke include:
antithrombotic therapy (antiplatelet and anticoagulation therapy), intravenous thrombolysis and endovascular treatment.
Transient ischemic attack: treatment
- Antiplatelet therapy
- Anticoagulation
patients with TIA or minor acute ischemic stroke treatment with anti platelet
21-day course of combination aspirin and clopidogrel followed
by monotherapy reduced the risk of subsequent stroke when administered within 24 hours
of onset.
Anticoagulation is indicated for patients with TIAs caused
by cardiac embolus and is
typically continued indefinitely or for as long as the cause of embolization (e.g., atrial
fibrillation or prosthetic heart valve) persists.
Intravenous Thrombolysis: IV thrombolysis with rtPA is proven to be effective in
improving functional outcomes after an ischemic stroke up to ………
to 4.5 hours after symptom
onset; however benefit from IV thrombolysis is much greater in the first 90 minutes from
symptom onset
only laboratory test absolutely required in ischemic stroke prior to initiation of IV
recombinant tissue plasminogen activator is
finger-stick blood glucose
Mechanical thrombectomy can be attempted when
IV thrombolysis does not result in rapid clinical improvement and also in patients who are ineligible for IV rtPA. For patients with ischaemic stroke caused by a large vessel occlusion in the internal carotid artery, proximal middle cerebral artery or with tandem occlusion of both the cervical carotid and intracranial arteries,
Candidates for endovascular stroke therapy are patients with:
severe neurologic symptoms no major ischemic changes on the baseline CT scan good prestroke functional status and early presentation.
Contraindicates to tPA
Sample stage mnemonic
Stroke or head trauma last 3 month
Anticoagulation with INR of > 1.7 or prolonged PTT
Mi last 3 months
Previous intracranial hemmorhge
Low platelets count
Elevated blood pressure
Surgery major in last 2weeks
TIA within 6 months
Git or urinary bleeding in the last 3 weeks
Elevated or decreased blood glucose
Anticoagulation is recommended for
at least 3 months in patients with
myocardial infarction and left ventricular thrombus because of high risk of embolization.
Patients with acute ischaemic stroke due to arterial dissection should be treated with
either antiplatelet or anticoagulant therapy for
3 to 6 months
Potential benefits of the novel oral anticoagulants over warfarin include
fixed dosing rapid onset of action fewer drug interactions no dietary restrictions lack of laboratory monitoring and lower rates of intracerebral hemorrhage.
Blood pressure should be lowered in stroke patients if there is:
extremely elevated values on repeated measurements (systolic pressure >220mmHg or
diastolic pressure >120mmHg) or concomitant myocardial ischemia, heart failure, or in patients with arterial dissection,
in which case cautious lowering <15% is appropriate.
Blood pressure should be less than
185/110 mm Hg before thrombolysis, which can be achieved with intravenous labetalol or nicardipine
Immediate initiation of statin treatment is not recommended in people with acute stroke.
It would be safe to start statins after
48 hours
Patients with ….. consideration of decompressive hemicraniectomy within ……
malignant middle cerebral artery territory infarction should undergo urgent
neurosurgical assessment
48 hours of stroke
onset.
……… should undergo urgent carotid
imaging
All TIA patients with anterior circulation symptoms should undergo
Patients with asymptomatic carotid stenosis should be prescribed a
daily aspirin and
statin and screened for other treatable risk factors with appropriate medical
therapies and lifestyle changes instituted.
General measures:
In stroke patients are
Prevention of deep venous thrombosis and pulmonary embolism starts with early
initiation of venous thromboembolism prophylaxis. All stroke patients should have their hydration status assessed, monitored, and
managed throughout their hospital admission. Where fluid support is required,
crystalloid solution should be used in favorite to colloid solutions as the first
option to treat or prevent dehydration All stroke patients should have their blood glucose level monitored for the first 72
hours following admission and appropriate glycaemic therapy instituted to treat
hyperglycaemia
Complete interruption of cerebral blood flow followed by reperfusion, such as occurs
in cardiac arrest with resuscitation, produces
damage that selectively affects
metabolically vulnerable neurons of the cerebral cortex, basal ganglia, and cerebellum.
With less profound hypotension for prolonged periods, the damage is concentrated in
the
anatomically vulnerable border zones between the territories supplied by the major
arteries of cerebral cortex, cerebellum, basal ganglia, and spinal cord. It is most severe in
the watershed region between the territories supplied by the anterior, middle, and
posterior cerebral arteries.
Unilateral watershed infarction occurs in
hemodynamic failure with underlying severe
arterial stenosis or occlusion and noncompetent circle of willis.
The result is that the damage caused by ICH is due the
mass effect of the hematoma as well as the toxic effects of the blood itself.
Most hypertensive hemorrhages originate in certain areas of predilection, corresponding
to
long, narrow, penetrating arterial branches lenticulostriate and
thalamostriate arteries that supply the basal ganglia and thalamus respectively along which Charcot-Bouchard aneurysms
are found.
intracerebral hemorrhage tends to cause
headache, vomiting and disturbance of consciousness as well as focal neurologic deficits.
Blood pressure is elevated after the hemorrhage has occurred. And so ….
normal or low blood pressure in a patient with stroke makes the diagnosis of hypertensive hemorrhage unlikely, as does onset before 50 years of age.
A fatal outcome is most often due to …… in stroke patients
herniation caused by the combined mass effect of the hematoma and the surrounding edema.
Other causes of intracerebral hemorrhage
- Cerebral amyloid angiopathy occurs in elderly patients causes both microhemorrhages
and macrohemorrhages, resulting in typical stroke symptoms and progressive dementia. 2. Trauma (e.g. epileptic seizures) 3. Vascular malformations 4. Aneurysms
Risk factors for symptomatic unruptured intracranial aneurysms include size and location
(posterior circulation, posterior communicating artery, anterior communicating artery). 5. Cavernous haemangiomas 6. Hemorrhage into cerebral infarcts 7. Anticoagulation
increase risk for developing spontaneous or traumatic intracerebral hemorrhage. 8. Coagulopathies
intracerebral hemorrhage is a complication of disorders of both clotting factors and
platelets, such as hemophilia (factor viii deficiency) and idiopathic thrombocytopenic
purpura. acute myelogenous leukemia with white blood cell counts greater than
150,000/ µl may also predispose to intracerebral hemorrhage. 9. Hemorrhage into a tumour 10. Venous thrombosis 11. Cerebral vasculitis 12. Disseminated intravascular coagulation (DIC). 13. Infective endocarditis 14. Malaria 15. Amphetamine/cocaine ingestion
In patients with intracerebral haemorrhage blood pressure may be acutely reduced to
target systolic blood pressure of around 140mmHg. Medications that can be titrated easily, such as nicardipine or labetalol, are preferred; nitrates should be avoided because of the potential for increasing intracranial pressure.
Statin in ICH is
Contraindicated
Surgical measures: in ICH
- Surgical measures: A. Cerebellar decompression: The most important therapeutic intervention in hypertensive
hemorrhage is surgical decompression for cerebellar hematomas. B. Cerebral decompression: Surgery can be useful when a superficial hemorrhage in the
cerebral white matter is large enough to cause a mass effect with shift of midline
structures and incipient herniation. C. Surgical clipping or endovascular coiling can be considered in patients with
aneurysms. D. Options for treating an arteriovenous malformation to reduce hemorrhage risk or
seizures include surgical excision or stereotactic radiosurgery. Endovascular
embolization is a common adjunctive procedure. E. In patients with hydrocephalus, external shunting of cerebrospinal fluid may be
required when clinical evidence of elevated intracranial pressure is detected;
osmotherapy with mannitol or hypertonic saline can be considered in patients with
elevated intracranial pressure as salvage therapy.
Vascular cognitive impairment may be subclassified as:
Poststroke vascular cognitive impairment, which refers to the direct immediate
consequence of clinical stroke.
Nonstroke vascular cognitive impairment, which is most commonly caused by cerebral
small vessel disease.
Features that suggest the diagnosis of multi-infarct dementia include:
The onset of cognitive deficits associated with a stroke
Abrupt onset of symptoms followed by stepwise deterioration
Findings on neurologic examination consistent with prior stroke(s)
Infarcts on cerebral imaging
Binswanger disease.
nonstroke vascular
cognitive impairment is caused by subcortical ischemic cerebral small vessel disease,
has some efficacy in patients with vascular dementia
……….drug
Memantine
The most common sinus involved in CVT is
sagittal sinus, followed by the lateral sinuses.
Etiology of CVT is
The most common are raised oestrogen levels in women, associated with pregnancy, the puerperium and the contraceptive pill. Other factors include dehydration and hypercoagulable states. In 20% of cases of venous thrombosis no etiology is uncovered.
Clinical features: of CVT
headaches, seizures, disturbance of consciousness, focal signs and optic disc swelling.
Cavernous sinus thrombosis (CVT) should be considered a separate entity as it
most commonly caused by local sepsis rather than primary or secondary non‐septic hypercoagulable states.
The accepted treatment of intracranial venous thrombosis is
anticoagulation, whether haemorrhage is present or not. The evidence for this is controversial. Anticoagulation for 6 months or for longer terms if a persisting reason for hypercoagulability persists.
with significant intracranial pressure will need ventilation and occasionally consideration for craniotomy.
suspected bacterial infection should receive appropriate antibiotics and surgical drainage of purulent collections of infectious sources associated with CVT when appropriate (i.e., subdural empyemas or purulent collections within the paranasal sinuses).
MCA stroke can cause CHANGes
Contra lateral paresis and sensory lose in face and arm
Hemiparrisis
Aphasiain dominant
Neglect in non dominant
Gaspze preference toward the side of lesion
Homonyms hemianopsia
ACA occlusion give
Contra lateral paresis and sensory loss in the leg
Personality change
Urinary incontinance
PCA occlusion give
Ipsilateral of the face and contra lateral of the limb loss of sensation
Ataxia of limbs
CNIX an X damage and vertigo also homonyms hemenoapsia
Lacunae stroke cause
Pure motor , pure sensory , ataxic hemiparesis
Disarthria and clumps hand thalami’s pain syndrome
Wallenberg syndrome / PICA and vertebral
Pain and temperature lose on ipsilateral face and contra lateral body
Ipsilateral bulbar weakness
Ipsilateral Horner syndrome
Vertigo and nystagmus
