This document discusses the evaluation of stroke. It begins by classifying the pathophysiologic processes that can cause stroke into four categories: those intrinsic to the vessel, those originating remotely as an embolism, those resulting from inadequate cerebral blood flow, and those from rupture of vessels in the brain. It then describes transient ischemic attacks, intracerebral hemorrhage, subarachnoid hemorrhage, and the three main subtypes of brain ischemia. The document outlines the initial assessment, history, physical exam, tests to confirm diagnosis including vascular studies, cardiac evaluation, and blood tests. It provides details on the appropriate cardiac and hypercoagulable testing based on a patient's history and symptoms.

1. Evaluation of Stroke
http://crisbertcualteros.page.tl

2. Stroke
• Result from ischemic infarction or bleeding
into part of the brain manifest by rapid onset
(seconds to mnutes) of CNS focal neurologic
deficits

3. Classification of pathophysiologic
processes:
A. Intrinsic to the vessel:
1) Atherosclerosis
2) Lipohyalinosis
3) Inflammation
4) Amyloid deposition
5) Arterial dissection
6) Developmental malformation
7) Aneurysmal dilatation
8) Venous thrombosis

4. Classification of pathophysiologic
processes:
B. Originate remotely - Embolus from
heart/extracrainal circulation
C. Inadequate cerebral blood flow – decreased
perfusion pressure/ increased blood viscosity
The first three cause: TIA/ ischemic stroke
D. Rupture of vessel in subarachnoid space or
intracerebral tissue
- SAH/ ICH

5. TIA
• Transient episode of neurologic dysfunction
caused by focal brain, spinal cord, or retinal
ischemia WITHOUT acute infarction
• Relies on the absence of end organ injury
based on imaging or other tests
• Temporary occlusion of part of cerebral
circulation by emboli
• Sx <24hours

6. Intracerebral hemorrhage
• Bleeding from small arteries/arterioles
• Bleeding directly into the brain  localized
hematoma  hematoma gradually enlarges
• Cause: HTN, trauma, bleeding
diathesis, amyloid angiopathy, illicit drug use
and vascular malformations
• less common: bleeding tumors, aneurysmal
rupture & vasculitis

7. SAH
• Spontaneous bleeding into subarachnoid space
• Aneurysmal rupture (saccular)  blood in
subarachnoid space  CSF rapidly increasing ICP
• Other causes: vascular malformation, bleeding
diathesis, trauma, amyloid angiopathy & illicit
drug use
• Sx: severe headache, pain lateralised to the side
of the aneurysm +/- brief LOC, seizure, N/V, focal
neuro deficit, stiffneck, kernig’s sign, retinal or
subhyaloid hemorrhages

8. Subtypes of Brain Ischemia
1) Thrombotic stroke:
- Thrombus formation in an artery produces a
stroke by reduced bld flow distally (low flow) or
embolic fragment that breaks off and travels to a
more distant vessel (artery to artery embolism)
a) Large vessel disease – atherothrombosis
- extra/intracranial arterial system
a) Small vessel disease – penetrating arteries
arising from the distal vertebral artery, basilar
artery, MCA stem & arteries of COW

9. Subtypes of Brain Ischemia
2) Embolic stroke- particle of debris originating
elsewhere that block particular access to the
brain regon
Causes: a) known sourcem- cardiac
b) ? Cardiac/ aortic – based on
Echocardiographic findings
c) arterial source
d) unknown source

10. Subtypes of Brain Ischemia
3) Systemic Hypoperfusion – reduced perfusion
due to cardiac pump failure by cardiac
arrest, arrythmia or reduced cardiac output 
AMI, Pericardial effusion or bleeding

11. Initial General Assesment
• A, B, C
• BP: usually elevated in stroke
• Breathing: pt with ICP  decreased respi drive
or muscular airway obstruction
• Fever: can worsen brain ischemia
• Hx & PE: DDX: seizures, syncope, migraine &
hypoglycemia

12. Initial General Assesment
• Non-contrast CT brain
– widespread acces and speed of acquisition
- highly sensitive for the diagnosis of bleeding in
acute cases
- focal white hyperdense lesionwithin the brain
parenchyma

13. Initial General Assesment
• MRI brain:
- Can show old hemorrhages since sensitive to
hemosiderin
- More sensitive than CT inearly detection of
infarction
• LP:
- Needed to make diagnosis for SAH

14. Initial General Assesment
• ? Thrombolytic Therapy – rt-PA
- Extracranial & intracranial US, CTA, MRA-show
occlusive thromboembolus
- Most severe complication: intracranial
hemorrhage (6%)

15. history
• Clinical course:
- Embolic stroke: occurs suddenly, focal loss of
brain function that is usually maximal, rapid
recovery
- Thrombosis – normal or abnormal or
progressing in a stepwise fashion with some
periods of improvements
- Penetrating artery occlusion- sx develop in
hours or a few days

16. history
- Intracerebral hemorrhage: does not improve
during the early period, progresses gradually
during minutes or few hours
- Aneurysmal SAH: develops instantly, focal brain
dysfunction is less common

17. history
• Ecology – age, sex and race
- Thrombotic and embolic strokes related to
atherosclerosis – occur in older patients
- Rare in <40yo, unless:
DM, HTN, HLD, smoker, strong Family Hx
- Cardiac origin embolism – common in young
pt with heart disease

18. history
- HTN ICH – common: blacks, in asians
• Previous TIA: strongly favors the presence of a
local vascular lesion (thrombosis)
• Activity at the onset or just before the stroke: a)
hemorrhages can be precipitated by physical
activities
b) trauma before stroke: traumatic dissection/
occlusion of arteries/traumatic brain hemorrhages

19. history
• Associated symptoms:
- Fever – endocarditis  embolic stroke
- Infections  activate acute phase reactants 
predisposing to thrombosis
- Headache: fx of hmg stroke, prodromal period
before thrombotic strokes
- Seizures: seen in lobar ICH or brain embolism
- Reduced alertness: indicates hemorrhage and:
(+) neurologic signs ICH
(-) neurologic signs SAH

20. PE:
• Absent of pulses: atherosclerosis with
thrombosis
• Unpalpable ICA (neck): occlusion of CCA
• Cardiac findings: AF, mumur, cardiac
enlargement cardiac origin embolism

21. Neurologic exam
• Weakness of face, arm, leg on one side
without sensory/visual/cognitive
abnormalities (pure motor stroke) 
thrombotic stroke in penetrating arteries /
small ICH
• Large focal neurlo deficits that begin abruptly/
progresses quicklyembolism / ICH
• Language abno, motor and sensory signs same
side of body anterior circulation disease

22. Confirm the diagnosis
• Vascular Studies:
1) Anterior circulation – exracranial and intracranial
carotid arteries , middle and anterior cerebral
artery branches should be the focus
- Duplex US of neck & transcranial Doppler of
intracranial arteries
2) Posterior circulation – vertebrobasilar system –
extracranial & intracranial vertebral arteries, basilar
arteries & posterior cerebral arteries should be the
focus

23. Confirm the diagnosis
3) CT angiography or MR angiography of neck
and head arteries – done when the screening
test do not fully define the lesion and more
characterization is warranted and when surgery
or interventional treatment by an arterial
catheter may be indicated

24. Confirm the diagnosis
• Cardiac Evaluation:
1) ECG & 24 Holter - ? AF as source of emboli
2) Echocardiography- for all patient suspected for
embolic stroke
a) TEE- examines the atria, atrial region and the
aorta
- to exclude ascending aortic atheromatous
disease, look for patent foramen ovale or atrial
septal aneurysm
b) TTE-

25. • Blood tests:
1) FBC
2) PT, INR, APTT
3) Thrombin Time
4) LIPIDS

26. Blood tests:
Hypercoagulable Studies:
1) Protein C, Protein S, antithrombin III
2) Lupus Anticoagulant
3) Anticardiolipin antibodies
4) Activated protein C resistance/ factor Leiden
mutation
5) Prothrombin Mutation

27. Antiphospholipid antibody testing is
recommended in:
1. Hx of Lupus or sx compatible with Lupus
2. Fx suggestive of Antiphopholipid Syndrome:
a) Miscarriages
b) Venous thrombosis
c) Migraine headaches
3. Cryptogenic stroke / TIA at young age

28. http://crisbertcualteros.page.tl