TREATMENT:

A. Athero trombotic infarct and TIA

1. Patient should remain horizontal position on the first day unless edema is
prominent.
2. Reactive hypertension after ischemic stroke is prevalent and has tendency
to decline without medications during the first few hospital days;
therefore, treatment of previously unappreciated hypertension is deffered
until later when neurologic deficit is stabilized; avoid antihypertensive
drugs in the first few days unless there is active MI or if BP is high enough
to pose a risk to other organs.
3. Thrombotic agents: rTPA
4. Acute surgical revascularization: if the ICA has just become thrombosed,
immediate removal of clot or the performance of a bypass procedure may
restore function; if interval is longer than 12 hours, little value cerebral
edema and increased ICP.
5. Anticoagulant Drugs:
a. Low-molecular weight heparin : Nadoheparin at 4000 U subcutaneously
given within first 24 hours.
6. Anti-platelet drugs:
a. ASA- acetyl moiety combines with platelet membrane and inhibits
platelet cyclooxygenase, preventing thromboxane A2 and
prostacyclin
b. Ticlopidine- 250 mg bid, inhibits platelet aggregation induced by
adenosine PO4; does not inhibit cyclo-oxygenase
c. Clopidogril- an ADP receptor antagonist that competitively inhibits
ADP from binding to platelet receptors, blocking amplification of
platelet aggregation.

d. Dipyridamole- 23% relative risk reduction in stroke compared to

50mg ASA
7. Surgery:
8. Physical therapy should be started early to prevent contracture and
periarthritis.

Ischemic Penumbra:
- Tissue surrounding the core region of infarction which is ischemic but
reversibly dysfunctional
- Maintained by collaterals
- Can be salvaged if reperfused in time
- Primary goal of revascularization therapies
- Damaged by:
-hypoperfusion
-hyperglycemia
-Fever
-Seizure

Treatment to avoid Ischemic Penumbra 5Hs:

Hypotension
Hypeglycemia
Hyperpyrexia
Hypoxemia
Hyponatremia to salvage ischemic neuron

ISCHEMIC PENUMBRA: PATHOPHYSIOLOGY OF THERAPEUTIC WINDOW

TIME-BASED PLOT OF CEREBRAL BLOOD FLOW (mL per 100mg tissue per min),
which demonstrate the concept of increasing infarct volume growth that can be
attenuated by freezing the penumbra with neuroprotection. The untreated infarct
core is light plus darker blue. With neuroprotection, the infarct core volume (b1-a1)
will be attenuated to b2-a2 betwwen t1 and t2. However by t3, infarct volume will
have gradually increased in volume to value at C.
Note:
Cerebral Blood Flow:
20mL/100g/min (Normal function)
8-18 mL/ 100g/min (Neuronal dysfunction)

min
(N3uronal death)

Approach to Diagnosis:

Objectives:
-

To confirm the vascular nature of the lesion

The pathological type of the vascular lesion
The underlying vascular disease
Risk Factors present

Diagnostic Modalities:
Non-Invasive:
-

CT Scan
MRI Scan
MR Angiography
EEG

CT Scan:
-Mandatory initial investigation
- Infarct appears as hypodense area
IMAGE
MRI
DWI Hyperacute Infarction Stage
Angiography
CT Findings
MR Finding in Cerebral
CBC
ECG

Acute Ischemic Stroke:

-

Result from thrombo-embolic occlusion of intracranial arteries

Various patterns can be seen on CT scan in early & late stages

Middle Cerebral Artery

-

75% of all ischemic events

Sxs vary between minor sensory or motor deficits
More patients are scanned earlier to rule out hemlorrhage and large
infarcts due to thrombolytic therapy

Hyperdense MCA sign

-

Clot is visible as hyperdense in MCA

Most evident along the horizontal part
Appears as vessel segment of higher density than other parts of same
vessel, contralateral MCA and BA
Not an unequivocal sign of occlusion
Does not represent ischemic change in parenchyma