A.

Anatomi vaskularisasi otak (Stroke)

1. Circle of Willis: Anterior communicating, anterior cerebral, internal carotid, posterior communicating,
posterior cerebral
2. Anterior (Carotid Circulation): Sign and symptoms: hemispheric dysfunction aphaxia, apraxia,
agnosia, hemiparsesis, hemisensoric disturbance, visual field defects.
Anterior choroid: hippocampus, globus pallidus, lower internal capsule
Anterior cerebral: medial frontal, parietal cortex, subjacent white matters, anterior corpus callosum
Middle cerebral: lateral frontal, parietal, occipital, temporal cortex, subjacent white matters
Lenticulostriate branches: caudate nucleus, putamen, upper internal capsule
3. Posterior (Vertebrobasilar Circulation): Signs and symptoms: brainstem/ cerebellar problems, coma,
drop attack (jatuh tapi masih sadar), cranial nerve palsy, athaxia, crossed sensory motor deficit.
Hemiparsesis, hemisensory deficit, visual field defects.
Vertebral artery branches: posterior inferior cerebellar, medulla, lower cerebellum
Basilar artery branches:
Anterior inferior cerebellar: lower and middle pons, anterior cerebellum
Superior cerebellar: upper pons, lower midbrain, upper cerebellum
Posterior cerebral: medial occipital, temporal cortex, subjacent white matter, posterior corpus callosum,
upper midbrain
Thalamoperforate branches and thalamogeniculate branches: Thalamus (dari posterior cerebral artery)
 B. Stroke dan TIA (signs and symptoms)
Cerebral ischemia reduction in blood flow that lasts longer than several seconds, neurologic
symptoms + within seconds because neurons lack of glycogen rapid energy failure.
Cessation of flow lasts for more than a few
minutes infarction / brain tissue death, if
it is quickly restored can recover fully
and the patients symptoms are only
transient (TIA Transient Ischemic
Attack)
Transient Ischemic Attack all neurologic
signs and symptoms resolve within 24h
without brain infarct on brain imaging.
Stroke signs and symptoms last for >24h
or brain infarction is demonstrated
Syncope occurs when generalized
reduction in cerebral blood flow due to
systemic hypotension (cardiac
arrhythmia, myocardial infarction,
hemorrhagic shock)
Longer duration of low cerebral blood
flow infarction in the border zones
between the major cerebral arteries.
More severe instances, global hypoxia-
ischemia causes widespread brain injury,
sequel is called hypoxic-ischemic
encephalopathy.
Focal ischemia/infarction caused by
thrombosis of the cerebral vessels themselves or by emboli from a proximal arterial source or the
heart.
Intracranial hemorrhage bleeding directly into or around the brain, by a mass effect on neural
structures, form the toxic effects of blood itself, or increasing ICP.

Pathophysiology of Ischemic Stroke

1. Acute occlusion of intracranial vessels
2. reduction in blood flow to the brain region it supplies (depends on vascular anatomy,
occlusion site, systemic blood pressure
(Decrease in cerebral blood flow to 0 - brain tissue death within 4-10 mins; values <16-
18ml/100g tissue per minute infarction within an hour) (<20ml/100g tissue per minute
only ischemia without infarct, unless for hours/days) (Ischemic before infarcts: only transient
symptoms)
Ischemic penumbra: ischemic but reversibly dysfunctional tissue surrounding a core area of
infarction seen by MRI/CT. Can progress to infarction if no resolve, this is the goal of
revascularization therapy.
 Focal cerebral infarction: Necrotic pathway in which cellular cytoskeletal breakdown is rapid,
due principally to energy failure of the cell, or apoptotic pathway in which cells become
programmed to die.
Ischemia: Starving neurons of
glucose and oxygen
mitochondrial failure to
produce ATP membrane ion
pumps stop functioning and
neurons depolarizing
intracellular Calcium rises
Cellular depolarization causes
glutamate releases from
synaptic terminals these
extracellular glutamate make
neurotoxicity by activating
postsynaptic glutamate
receptors that increases
neuronal calcium influx
Degradation of membrane
lipids and mitochondrial dysfunction produces free radicals Free radicals causes
catalytic destruction of membranes and likely damage other vital function of cells.
Fever / Hyperglycemia worsens brain injury.

C. Transient Ischemic Attack

Stroke symptoms lasts only <24hrs, TIAs attack <1hours bawa ke rumah sakit!
Brain infarct on imaging stroke, no need to care about the symptom duration
TIA may arise from emboli to brain or from in situ thrombosis of an intracranial vessel, with TIA
occluded blood vessel reopens, neurologic function is restored
Risk of stroke after TIA 10-15% in the first 3 months, most events occurring in the first 2 days,
estimate risk with ABCD score. The risk of subsequent stroke in the first few days after TIA is high
give rtPA rapidly
Combine aspirin and clopidogrel can prevent stroke following TIA than aspirin alone.

D. Dysathria, Aphasia, Dyslexia

 E. 12 Cranial nerves

I. Olfactory - Smell - Sensory

II. Optic Vision - Sensory
III. Occulomotor Eyelid and Eyeball movement Motoric
IV. Trochlear superior oblique innervation, lateral and downward eye movement - Motoric
V. Trigeminal chewing, face and mouth, touch and pain - Mixed
VI. Abducens Lateral movement of eye Motoric
VII. Facial facial expressions, tears and saliva, taste - Mixed
VIII. Vestibulocochlear hearing, equilibrium, sensation - Sensory
IX. Glossopharyngeal taste, senses carotid BP - Mixed
X. Vagus senses aortic BP, slows HR, digestive organs, taste -Mixed
XI. Accesory trapezius and sternocleidomastoid, swallowing - Motoric
XII. Hypoglossal tongue movements - Motoric

F. Golden period of stroke and why?

G. Arrythmia dan stroke, why? in red
H. Babinski +, why? Upper motor lesion, lesion in CNS (Brain or Spinal Cord)

The neurophysiology of this reflex has not been completely elucidated. The account
given here follows the suggestions made by Kugelberg, Eklund, and Grimby (1960) and
is the result of their electromyographic studies. Each area of the skin of the body appears
to have a specific reflex response to noxious stimuli. The purpose of the reflex is to cause
the withdrawal of the area of the skin from the stimulus. This reflex is mediated by the
spinal cord, but influenced by higher centers. The area of skin from which the reflex can
be obtained is known as the receptive field of the reflex. To be more specific, a noxious
 stimulus to the sole of the foot, which is the receptive field, causes immediate flexion of
the toes, ankle, knee, and hip joints with attendant withdrawal of the foot from the
stimulus. Remember your own experiences with this reflex, an example being stepping
on a sharp object while barefoot. There is an instant involuntary flexion of all joints with
withdrawal. Another reflex in the normal individual is the great toe reflex: Stimulation of
the ball of the toe, which is the receptive field, causes extension (dorsiflexion) of the toe
with flexion at ankle, knee, and hip joints. The differences between these two reflexes are
in the receptive fields and the fact that the great toe is flexed in one and extended in the
other. The reason for the extension in the toe reflex is to remove the toe from the
stimulus.

The abnormal plantar reflex, or Babinski reflex, is the elicitation of toe extension from
the "wrong" receptive field, that is, the sole of the foot. Thus a noxious stimulus to the
sole of the foot produces extension of the great toe instead of the normal flexion
response. The essential phenomenon appears to be recruitment of the extensor hallucus
longus, with consequent overpowering of the toe flexors (Landau, 1971). The movements
of the other joints remain the same.

The corticospinal tract influences the segmental reflex in the spinal cord. When the
corticospinal tract is not functioning properly, the result is that the receptive field of the
normal toe extensor reflex enlarges at the expense of the receptive field for toe flexion.
Toe extension is consequently elicited from what is normally the receptive field for toe
flexion. The maintenance of territorial integrity of the receptive fields is apparently one
way in which the cortex exerts its influence under normal conditions.

I. Hipertrofi ventrikel di EKG, gambarannya seperti apa?

Atrium - P Wave pada AVR tinggi 2.5mm, lebar 2.5mm
Right Atrial Hypertrophy : >3 mm berarti P Pulmonal
Left Atrial Hypertrophy : lebar > 2.5mm P Mitral / P Wave berdefleksi di V1 > 1mm
Ventricle - R wave makin bertambah dari V1-V6
Right Ventricle Hypertrophy : Lebih tinggi dari S di Lead V1
Left Ventricle Hypertrophy : R di lead I dan AVL > 15mm (1.5cm) / R di V5 V6 >25mm

J. Lesi dimana? Stroke dimana? Which vascular