2. HAEMORRHAGIC STROKE.

ETIOLOGY, CLINICAL FEATURES, DIAGNOSTIC, EMERGENCY TREATMENT

Occurs within the brain substances, but rupture through to the cortical surface may produce associated subarachnoid
bleeding.
It results from a weakened vessel that ruptures and bleeds into the surrounding brain. The blood accumulates and
compresses the surrounding brain tissue.

Etiology:

Hypertension
Aneurysm
Malformation of blood vessels (basis of all hemorrhage, the thinned vessel wall ruptured)
Amyloid vasculopathy
Neoplasm
anticoagulants
Coagulation d/o (haemophilia)
Drug abuse, vasculitis, trauma
Idiopathic

Clinical pictures:
Supratentorial hematoma

Cerebellar hematoma

Pontine hematoma

Mass effects:
Sudden onset headache followed by rapid of loss cons or
gradual deterioration in cons level over 24-48 hrs
Focal signs:
Hemiparesis, hemisensory loss and hormonymous,
hemianopia. Third nerve palsy indicates transtentorial
herniation
Sudden onset of headache with subsequent effects developing
either acutely or subacutely
Cerebellar and brainstem symptoms and signs (severe ataxia,
dysarthria,nystagmus,vertigo, vomiting)
Sudden loss of cons, quadriplegia, resp irregularities, pinpoint
pupils, pyrexia, dysconjugate eye movement,death.

Diagnostics:

CT Scan determines the exact site and size of the haematoma and excludes other pathologies
Angiography performed immediately if clinical state requires urgent operation, to identify a possible arteriovenous
malformation or aneurysm.
If negative angiography, a late MRI may demonstrate a cavernous angioma

Treatment:
Surgical clipping of aneurysm
- decompression, trepanation
Without surgery if the hemorrhage complication does not decrease blood below 30mm 3
- give anti hypertensive drugs

3. Ischemic stroke. Etiology, pathogenesis, clinical features of diseases, emergency treatment.

In an ischemic stroke, blood supply to part of the brain is decreased, leading to dysfunction of the brain tissue in that area.
Etiology and pathogenesis
there are several factors that can lead to the ischemic stroke of the brain. As we know, the general complication is that the
ischemic happens due to insufficiency of blood supply to the brain, which is caused by:

Atherosclerosis
Cardiac emboli
Cryptogenic factor

Atherosclerosis

Tissue damage or intima of external carotid artery leads to plague formation

What is the need of atherosclerosis anyway? Actually, it is for the normalization of blood flow and condition. Normally, if
the tissue damage occurs, lipid band form is form to repair the blood vessels. However if the disorder of lipid
metabolism happens, the multiple band form occur and cause the obstruction to the blood flow.
Reposition of thrombosis happened when the surface of the plague formed, consequently decreases the area of lumen
of the vessel.
After the plague mass ruptured, it will form emboli.

Cardiac emboli

Any pathological reaction that can cause blood disturbance, and leads to formation of emboli
For example: a) valve diseases
b) Inflammation of the heart endocarditis
c) Arrhythmia
Internal carotid artery is first affected, because the lumen is bigger and emboli tend to go there.

Cryptogenic
Also known as unknown or unspecific etiology. It may consist:

Vasospasm
Rheological properties of blood.
Properties of the vessel vasculitis (in case of dzs of vessels)

Clinical features and manifestations:

Sudden paralysis of a leg, arm or one side of the face

Sudden trouble speaking or understanding speech
Sudden vision problems, such as blurred or double vision
Sudden loss of coordination or problems with balance
A severe, sudden headache without apparent cause
Sudden numbness, weakness or dizziness

weakness or paralysis, usually on one side of your body

lack of awareness of one side of your body (usually the left side)
loss of sensation on one side of your body
difficulty swallowing
extreme tiredness and sleep problems
problems with speech, reading and writing
problems with vision - such as double vision, or partial blindness
memory and concentration difficulties
difficulty controlling your bladder and bowel movements (incontinence) or constipation
behavioural changes

Treatment
Etiological treatment
Pathological treatment:

antiplatelet
aspirin give during the first attack of stroke, and throughout the whole life
- to prevent recurrent stroke
- 3.75 mg/1st day, 75mg on the next day
antihypertensive drug
to control the blood pressure and vital function of blood
increase metabolism and increase collateral circulation
Pyracetam (dose dependant drug)
Aktovegin
Cerebrolysin
Mexidol (antioxidant)
vasodilators
kaventon
euphylline

Symptomatical treatment:

depends on the symptoms of diseases that appeared.

4.Subarachnoid Hemorrhage. Etiology. Clinical pictures. Diagnosis. Treatment.

Intracranial vessels lie in the subarachnoid space and give off small perforating branches to brain tissue. Bleeding from these
vessels or from an associated aneurysm occurs primarily into this space.
Some intracranial aneurysms are imbedded to the brain tissue, and their rupture causes intracerebral bleeding with or without
subarachnoid hemorrhage.
Etiology.

Head trauma
Ruptured aneurysm
Age range 40-60 years old

Clinical pictures:

Severe headache
Loss of consciousness from minutes to hours
Seizures
Meningeal signs
Secondary hydrocephalus (headache, motor function deficiency)

Diagnosis:

CT
Lumbar puncture
Focal meningeal signs
Investigation of CSF
- increase RBC
- Xanthochromia
- increase pressure

Treatment:

Control the rheologic props of blood [HPT] clopedagril, dipyridamole

Diet statin [atherosclerosis]
Control the DM, obesity control level of glucose
Smoking, alcohol, hypodynamic control

How teenage (girls) get stroke?

- through oral contraceptive and smoking plus with liver diseases
How teenage (boys) get stroke?
- drugs abuse (cocaine)
How normal people get stroke?
- by drinking excessive energetic drink, esp with alcohol because have sibutramine which predispose to stroke.
5.Transient Ischemic Attack (TIA). Etiology, Pathogenesis, clinical features, and treatments.
TIA are attacks are episodes of focal neurological symptoms due to inadequate blood supply to the brain.
Attacks are sudden in onset, resolve within 24 hrs o less and leave no residual deficit.
These attacks are important as warning episodes or precursors of cerebral infarction
Pathogenesis:

A reduction of cerebral blood flow below 20-30ml 100g/min produces neurological symptoms. The development of infarction is a
consequences of the degree of reduced flow and duration of such a reduction. If flow is restored to an area of brain within the
critical period, ischemic symptoms will reverse themselves.
TIAs maybe due to:
1. Reduced flow through a vessel (haemodynamic explanation):
A fall in perfusion pressure, e.g. cardiac dysarthria associated with localized stenotic cerebrovascular dzs.
2. Blockage of the passage of flow by embolism (embolic explanation):
Arising from plaques in aortic arch/extracranial vessels of from the heart
Symptomatology of TIA
Anterior part of brain (90%)
-carotid territory hemiparesis, hemisensory disturbances, dysphasia, monocular blindness
Vertebrobasilar territory of brain (7%)
- loss of consciousness, bilateral limb motor/sensory dysfunction, binocular blindness, vertigo, tinnitus, diplopia,dysarthria
In many cases, it may cause:

Deterioration of cons level

Homonymous hemianopia of the contralateral side
Contralateral hemiplegia
Contralateral hemosensory disturbance
Gaze palsy to the opposite side eyes deviated to the side of lesion.
Examination of neck reveals: absent carotid pulsation at the angle of the jaw with poorly conducted heart sounds along
the internal carotid artery.

Treatment:

Anticoagulant therapy Heparin

Thrombolytics agent associated with rapid recanalisation of occluded vessels. Streptokinase is not used nowadays
because of the risk of intracranial hemorrhage.

Specific measures:

Decreasing blood viscosity

Neuronal rescue
Treatment of edema mannitol

Prevention of further stroke attack

The recognition of risk factors and their correction to minimize the risk of further events forms a necessary and important step in
long-term treatment.

Control hypertension
Emphasize the need to stop cigarette smoking
Correct lipid abnormality
Give platelet antiaggregation drugs (aspirin or in selected cases ticlopidine) to reduce the rate of reinfarction
Remove or treat emboli source (long term anticoagulation in arterial fibrillation)

Treat inflammatory or vascular inflammatory dzs

Stop thrombogenic drugs, esp oral contraceptives.