Cerebrum
matter)
: basal ganglia
(gray matter)
Diencephalon : thalamus hypothalamus
2. Midbrain
: Brainstem : Midbrain (Mesencephalon)
Pons (Meten)
MO(Myelen)
3. Hindbrain
: Cerebellum
Spinal Cord
1.
2.
3.
4.
5.
Cervical segments
Thoracic segments
Lumbar segments
Sacral segments
Coccygeal segments
Spinal Segment
Cervical vertebrae
Add 1
Add 2
Add 3
L1-L2 cord segments
L5 cord segment
Ventricular system
Lateral Ventricle
3rd ventricles
Cerebral aqueduct
4th ventricles
Central canal
CSF absorption
The main site of CSF absorption into the venous system is through the arachnoid
granulations especially those that protrude into the superior sagittal sinus.
Hydrocephalus
1. Obstructive Hydrocephalus : Overproduction of CSF, obstruction of CSF flow, or
interference with CSF absorption results in excess fluid in the cerebral ventricles
and enlargement of head. The excess CSF dilates the ventricles, thin the cerebral
cortex, and separates the bones of calvaria in infants. Although an obstruction
can occur any place, the blockage usually occurs in the cebral aqueduct or an
interventricular foramen. Aqueduct stenosis may be cause by a nearby tumors in
the midbrain or by cellular debris following intraventricular hemorrhage or
bacterial and fungal infections of CNS. In infants, the internal pressure results in
expansion of the brain and calvaria because the sutures and fontanella are still
open.
2. Communicating hydrocephalus : the flow of CSF through the ventricles and
into subarachnoid space is not impaired, however, movement of CSF from this
space into venous system is partly or
NEUROANATOMY
Broadman area :
1.
2.
3.
4.
5.
Area
Area
Area
Area
Area
2. C5-T1 : Tetraparesis
UMN
3. T2-L1 : Paraparesis
UMN
4. L2- S2 : Paraparese
LMN
Inferior Extremities :
Limb weakness : Limb weakness results from damage to the motor system at
any level from the motor cortex to muscle
Tone
Fasciculation
Atrophy /
wasting
Reflexes
UMN
Hypertonicity
(after a few
days to weeks
of spinal
shock)
Passive
movements
produce a
clasp knife
CLONUS +
Absent
Absent
LMN
Hypotonicity
Present
Present (within 2-3 weeks)
1.Tendon : exaggerated
Depressed / absent
2.Superficial : depressed / absent(abdominal, rarely
affected cresmateric)
3.Plantar response : Extensor
Flexor
Pathophysiology of atherosclerosis
Platelets circulating in blood containing thromboxane A2, a substance that
promotes their aggregation, while vascular endothelium secrets prostacyclin,an
aggregation inhibitor that balance this effect. These products are synthesized
after conversion of arachidonic acid into intermediate endoperoxides by
cyclooygenase enzymes.
If endothelial continuity is interrupted by trauma, atherosclerosis, etc, subsurface
collagen is exposed to blood and stimulates adhesion of platelets to vessels wall.
Platelet then discharge thromboxane A2, causing aggregation of adjacent
platelets.
As more platelets aggregate, fibrin network develops and stabilizes mass into
white thrombus, which then retracts into vascular wall. In some cases,
endothelium may later heal over without narrowing of lumen.
If thrombus develops later, red blood cells become enmeshed in platelet-fibrin
aggregate to form red thrombus, which may grow and block vessel lumen.
Either platelet-fibrin aggregates or more fully formed clots break off, with
embolization into distal arterial branches
STROKE
1. Gejala dan tanda klinis yang berlansung Selma 24jam atau lebih akibat
gangguan fungsi otak fokal (atau global) yang terjadi tiba-tiba dan
berlangsung progressif atau menetap atau berakhir dengan kematian
tanpa penyebab yang lain selain gagguan cerebrovascular.
2. Stadium :
i.
Transient Ischemic Attack (TIA) : Serangan neurologic deficit yang
bersifat temporary akibat ggn peredaran darah otak secara
mendadak, menghilang engan cepat (<24 jam) tanpa gejala sisa.
ii.
Reversible Ischemic Neurologic deficit (RIND) : TIA, >24jam
iii.
Stroke in evolution : Stroke yang sedang berlangsung dan bersifat
proggresif dan dapat berakhir dengan completed stroke
iv.
Completed stroke : Stroke Hemorrhagic atau stroke non
hemorrhagic
3. Stroke Ischemic : kurangnya aliran darah ke otak sehingga mengganggu
kebutuhan darah dan O2 di jaringan otak, dengan tanda neurologic deficit
4. Klasifikasi of stroke ischemic berdasarkan Tria of Org 10172 in Acute
Stroke Treatment (TOAST) :
I.
Large-artery atherosclerosis (thrombus / emboli)
II.
Cardioembolism
III.
Small vessel occlusion (lacunar)
IV.
Stroke of other determined etiology
V.
Stroke of undetermined etiology
5. SI : thrombosis, emboli, pengurangan perfusi sistemik umum
6. Thrombosis : obstruksi aliran darah yg terjadi pada proses oklusi pada satu
pem darah atau lebih
7. Emboli: pembentukan material dari tempat lain dlm sistem vascular dan
tersangkut dlm pem darah tertentu sehingga memblokade aliran darah
8. Pengurangan perfusi : kegagalan pompa jantung atau proses perdarahan
atau hipovolemik
9. Anterior cerebral arteries, middle cerebral arteries, and posterior cerebral
arteries.
10.The anterior and middle cerebral arteries carry the anterior circulation and
arise from supraclinoid internal carotid arteries.
11.Anterior cerebral arteries (ACA): Medial portion of frontal and parietal
lobes and Anterior portion of basal ganglia and anterior internal
capsule.
12.Middle cerebral arteries (MCA) : Lateral portion of frontal and parietal,
Anterior and Lateral portions of temporal lobes, and gives rise to
perforating branches to the globus pallidus, putamen, and internal
capsule. MCA is the dominant vascular supply to the hemisphere.
13.Posterior cerebral arteries (PCA) : arise from basilar artery and carry the
posterior circulation. PCA give rise to perforating branches that supply