Cerebrovascular disease Flashcards
Definition of Stroke
Is a rapidly developing clinical symptoms and or signs of focal or global loss of cerebral function, lasting more than 24 hours or leading to death, with no apparent cause other than that of vascular origin.
Definition of Transient ischemic attacks
Transient focal neurological deficits lasting for less than 24 hours, usually minutes of vascular ischemic origin with complete recovery.
Causes of hemiplegia
1- Vascular (STROKE): either ischemic or hemorrhage.
2- CNS infections: brain abscess, encephalitis.
3- Brain tumors: meningioma, glioma, etc..
4- Demyelinating: DS, DEM.
5- Trauma: cerebral laceration, subdural hematoma.
6- Congenital cerebral palsy.
7- Hysterical: the patient suffers from paralysis although there is no organic
pyramidal tract lesion.
General clinical features of hemiplegia
1) Onset: is usually acute in hemorrhage, may be subacute in thrombosis, sudden in embolic, gradual in neoplasm, intermittent in D.S.
2) Cause: may be regressive in inflammatory causes, vascular, traumatic causes, Progressive in neoplasm.
3) Weakness: is usually affecting one half of the body UL, LL in equal degree or one may be affected than the other, weakness affects group of muscles, affecting fine movements more, distal muscles are more affected, progravity muscles are more affected than antigravity
- i.e. In UL→ Extensors are weaker
- In LL→ Flexors are weaker
4) Muscles tone:
- In acute lesions there is a shock stage lasting for 2-6 weeks, during which there is a complete loss of tone of the paralyzed side, after this stage tone gradually returns and spasticity appears
- In gradual lesions: spasticity develops from the start and affects thenantigravity muscles more than progravity muscles i.e., UL – flexors are more spastic LL – extensors are more spastic & adductors are more affected than abductors
5) Reflexes:
❖ Deep tendon reflexes in the affected limbs are exaggerated, pathological reflexes and clonus may be elicited.
❖ N.B: in the shock stage deep reflexes are lost or diminished)
❖ Superficial reflexes:
- +ve babinski sign.
- lost abdominal and cremasteric on the affected side.
6) Gait: is usually circumduction.
7) Other features: of sensory impairment, cranial nerves affection dependant on site of the lesions as shown later in discussion of localization
Localization of site of lesion in hemiplegia
1)Cortical lesion:
- Hemiplegia is incomplete, usually its monoplegia.
- Cloudiness of consciousness is common.
- Contra lateral cortical sensory loss in involvement of the parietal lobe.
- Convulsions, which may be focal or secondary generalized, in cases of irritative or extensive lesions.
- Higher mental functions disorders
2)Subcortical lesion: Same as cortical with more weakness
3) Capsular (Most common)
- Hemiplegia is complete
- Hemi hypothesia on paralyzed side (common)
- UMN facial and hypoglossal on the same side of paralysis (common).
- No convulsions, aphasia, or coma.
4) Brainstem (All have Crossed hemiplegia; contralateral hemiplegia, ipsilateral cranial nerve affection)
Mid brain: a) Webers syndrome: 3rd cranial nerve lesion
b) Benedicts syndrome: same as above + hemiataxia on contralateral (Red nucleus)
Pons: a)Millard gublers syndrome: 6th,7th lesion
b) Fovilles syndrome: ipsi loss of conjugate eye movement
Medullary a) Wallenberg: 9th 10th 11th affection, Horners syndrome, contra hemianasthesia
b) Avillis: 9th, 10th cranial nerve paralysis
c)Jacksons: ipsiliateral 11th and 12th CR N
5) Spinal cord lesion (Brown sequards syndrome)
In hemi lesion of the spinal cord in upper cervical segments, → hemiplegia may occur with the following features:
1- At the level of the lesions:
- Ipsilateral LMN weakness of muscles supplied by the affected segments.
- Loss of reflexes mediated by the interrupted segments.
- Loss of sensation (radicular) in the area supplied by the diseased segments.
2- Below the level of the lesion:
- Ipsilateral hemiplegia
- Ipsilateral deep sensory loss
- Contralateral superficial sensory loss.
Definition of ischemic stroke
Rapidly developing focal disturbance of cerebral function due to insufficient cerebral blood flow (hypoperfusion), which results in ischemia and neuronal injury, lasting for more than 2 hours or leading to death.
Causes of ischemic stroke
1) Embolic strokes (20%)
It’s due to embolism in the cerebral arteries coming from other parts of the arterial system.
Most commonly affect the middle cerebral artery (MCA).
a) Cardiac emboli (75% of cardiac emboli go to the brain).
▪ AF in MS, Atrial or ventricular thrombi, Rheumatic heart disease and Ventricular aneurysms.
b) Atherosclerotic emboli: Internal carotid artery and Aortic arch (less common).
c) Infectious emboli: bacterial endocarditis.
d) Paradoxical embolism: in patients with right-to-left cardiac shunt (e.g. persistent foramen oval or atrial septal defect).
2) Thrombotic strokes ( 40%):
- Caused by atherosclerotic obstruction of large cervical and cerebral arteries, with ischemia in all or part of the territory of the occluded artery.
a) Large vessel atherosclerosis ( 20%)
▪ Thrombus formation most commonly occurs at branch points in arteries (e.g., internal carotid artery bifurcation or where the MCA branches from the circle of Willis).
b) Small vessel occlusion (lacunar infarct) ( 20%).
3) Global cerebral ischemia:
a) Systemic hypoperfusion: shock or bilateral large artery atherosclerosis (e.g., of carotid arteries) → decreased effective oxygen delivery to the whole brain.
b) Hypoglycemia: repeated episodes of hypoglycemia (e.g., due to insulinoma) increase the risk of cerebral ischemia.
c) Severe and/or chronic hypoxia: hypoxemia (e.g., due to respiratory arrest) → global tissue hypoxia in the brain.
4) Other causes
a) Hypercoagulable states: e.g. Inherited thrombophilia (e.g., factor V Leiden mutation, protein C deficiency), Polycythemia, Hormonal contraceptive use, Hormone replacement therapy, Sickle cell disease.
b) Vasculitis (e.g., giant cell arteritis).
c) Arterial dissection (e.g., due to trauma or fibromuscular dysplasia).
risk factors of ischemic stroke
- Old Age (>65 y) [75% of all strokes].
- Race (African>Hispanics >Caucasians.
- Sex (Male more).
- Family history of ischemic stroke.
- Previous stroke, Transient ischemic attacks, or myocardial infarction.
- AF, Hypertension, Diabetes mellitus, Dyslipidemia, Smoking, Obesity, and physical inactivity.
- Cardiovascular disease and coronary artery disease.
Pathophysiology of Ischemic stoke
▪ Ischemic stroke is caused by focal cerebral ischemia: a localized reduction in blood flow sufficient to disrupt neuronal metabolism and function.
▪ If ischemia is not reversed within a critical period, irreversible cellular injury ensues, resulting in cerebral infarction.
▪An area called a PENUMBRA may result, denotes the part of an acute ischemic stroke that is at risk of progressing to infarction but is still salvageable if reperfused. It is usually located around an infarct core (which represents the tissue which has already infarcted or is going to infarct regardless of reperfusion).
▪ The primary aim of current acute stroke intervention is to prevent the penumbra from proceeding to established infarct.
Clinical picture of ischemic stroke
A. General:
- Symptoms develop in secs-mins
- Nausea and vomiting
- Hypertension is present acutely
- Neurologic deficit is variable
B. Specific picture:
1)Thrombotic strokes (Large artery stroke 40%)
- Usually during sleep
- May have “stuttering,” intermittent progression of neurologic deficits, or be slowly progressive (over 24-48 h.).
- Rarely loss of consciousness
- Emboli from incompletely thrombosed artery may precipitate an abrupt deficit. May have embolism from extracranial arteries affected by stenosis or ulcer.
2) Embolic strokes (20%)
▪ Immediate onset of neurologic deficits.
▪ Usually occurs during waking hours.
▪ Seizures may occur at onset of stroke.
Investigations in ischemic stroke
A. Imaging
1) Non-contrast CT brain (most used)
- Exclude mimics
- Infarction is hypodense
2) MRI
- Infarction seen immediately
-DWI-MR most sensitive
3) Carotid ultrasound (Carotid stenosis)
4) ECG (cardiac causes)
5) Laboratory markers in thrombophilia
B. Laboratory studies:
- CBC
- Basic laboratory evaluation of electrolytes, glucose, liver, and kidney function tests may reveal a stroke mimic or provide evidence of concurrent illness
- Cardiac biomarkers, Fasting lipid profile, Uric acid serum level.
- Coagulation parameters
- Thrombophilia workup: In unexplained stroke in young patient.
General principles in ttt of ischemic stroke
1) Stabilize the patient’s general condition.
2) Give therapy directed at specific aspects of stroke pathogenesis
3) Treat complications
4) Initiate early 2ry prevention measures to reduce incidence of stroke recurrence.
5) Begin rehabilitation measures.
Ttt of Acute ischemic stroke (CI and C)
1) Thrombolysis with recombinant tissue plasminogen activator (rt-PA): alteplase is the only FDA-approved medication for acute ischemic stroke. It must be given within 3-4.5 h. (golden time window) from the onset of symptoms.
Contraindications:
1. Intracranial hemorrhage (e.g., ICH or SAH) history or presence on imaging.
2. Brain CT demonstrates large infarction.
3. Elevated Blood pressure greater than 185/110 mm Hg.
4. Recent (within 3 months) severe head trauma or neurosurgical operation.
5. INR >1.7, thrombocytopenia, recent use of heparin or direct oral anticoagulants).
6. Intracranial neoplasm, or aneurysm.
7. Active internal bleeding.
Complications:
1) Bleeding.
2) Intracranial and extracranial hemorrhage.
3) Angioedema.
2)Intra-Arterial Mechanical Thrombectomy in : large artery occlusion in anterior cerebral circulation
Secondary Prevention of Ischemic Stroke (prevent recurrence)
1) Antiplatelet agents : (for thrombotic stroke)
- If there is no active bleeding or other contraindication.
- Aspirin: 75-325 mg/day. Significant reduction of recurrent stroke. or
- Clopidogrel (Plavix®): 300 mg load, then 75 mg/day.
2) Anticoagulants: (only with cardioembolic stroke) e.g., AF.
- Warfarin (Marevan): Indicated in hypercoagulable states; cardiac sources like AF or intracardiac thrombi.
- Dabigatran (Pradaxa®): Indicated in persistent or paroxysmal nonvalvular AF. Better than warfarin.
- Rivaroxaban (Xarelto®): factor Xa inhibitor. Reduce the risk of stroke and systemic embolism in nonvalvular AF. Better than warfarin.
- Apixaban (Eliquis®): Same as Rivaroxaban.
3) Risk Factors treatment:
a) Care of Blood Pressure (BP):
✔ Anti-Hypertensive drugs if the BP is above 200/120 mm Hg.
✔ Avoid sudden marked reduction of BP which decreases cerebral blood flow and worsens brain ischemia.
b) Statins and cholesterol-lowering agents:
✔ Shown to lower the risk of atherosclerotic mortality & vascular events, including stroke.
c) Smoking cessation, DM control, a low-fat low-salt diet, weight loss and regular exercise.
4) Other drugs may be used:
a)Piracetam (Nootropil®): It improves brain metabolism by increasing O2 consumption. It also decreases blood viscosity by reducing platelet aggregation.
b) Pentoxifylline (Trental®): It improves the microcirculation of the brain by increasing RBCs deformability and reducing platelet aggregation.
Definition of Transient ischemic attacks
A transient episode of neurological dysfunction caused by focal transient brain or retinal ischemia, with clinical symptoms typically lasting minutes up to ONE hour (maximum 24h) without evidence of acute infarction on brain imaging.
Same causes as Ischemic stoke
