my summary for blood supply of brain

2. ARTERIES OF THE BRAIN
The brain is supplied by two major
important arteries:
• INTERNAL CAROTID ARTERY
• VERTEBRAL ARTERY

3. ANATOMY OF INTERNAL CAROTID ARTERY
The internal carotid artery arises as one of the two terminal branches of the
common carotid artery. It proceeds superiorly to the base of the skull where it
enters the carotid canal. As it enters the cranial cavity, the internal carotid
arteries pair giving off the following branches to form the anterior circulation:
1. OPTHALMIC ARTERY
2. POSTERIOR COMMUNICATING ARTERY
3. MIDDLE CEREBRAL ARTERY
4. ANTERIOR CEREBRAL ARTERY

4. ANATOMY OF INTERNAL CAROTID ARTERY

5. ANATOMY OF VERTERAL ARTERY
Each vertebral artery from the first part each subclavian artery in lower part of the
neck and passes superiorly through the foramen transversum of 6th cervical
vertebra. On entering the cranial cavity through the foramen magnum each
vertebral artery gives off a small meningeal branch. Continuing forward, the
vertebral artery gives off three additional branches before joining the basilar
artery:
1. POSTERIOR INFERIOR CEREBELLAR ARTERY
2. POSTERIOR SPINAL ARTERY
3. ANTERIOR SPINAL ARTERY
The vertebral arteries forms the posterior circulation.

6. ANATOMY OF VERTERAL ARTERY

7. THE BASILAR ARTERY
The basilar artery travels in a rostral direction along the anterior aspect of the
pons. Its branches in a caudal to rostral direction includes:
1. ANTERIOR INFERIOR CEREBELLAR ARTERY
2. SEVERAL SMALL PONTINE ARTERIES
3. SUPERIOR CEREBELLAR ARTERY
The basilar artery ends as a bifurcation, giving rise to two posterior cerebral
artery.

8. CEREBRAL ARTERIAL CIRCLE
“CIRCLE OF WILLIS”
The Circle of Willis is an anastomotic system of arteries that encircles the
stalk of the pituitary gland and provides important communications
between blood supply of forebrain and hindbrain.
The circle is formed when the ICA enters the cranial cavity bilaterally and
divides into ACA and MCA. The anterior cerebral arteries are united by
ACoM artery . These connections form the anterior half of the Circle of
Willis (anterior circulation). Posteriorly, the basilar artery formed by left
and right vertebral arteries branch into a left and right PCA, forming the
posterior ciculation. The PCAs complete the Circle of Willis by joining
the ICA system anteriorly via PCoM arteries .

9. CIRCLE OF WILLIS

10. CIRCLE OF WILLIS

11. CIRCLE OF WILLIS

12. ANTERIOR AND POSTERIOR CIRCULATIONS

13. VASCULAR TERRITORIES OF THE SUPERFICIAL
CEREBRAL STRUCTURES

14. VASCULAR TERRITORIES OF THE SUPERFICIAL
CEREBRAL STRUCTURES

15. VASCULAR TERRITORIES OF THE DEEP
CEREBRAL STRUCTURES

16. BLOOD VESSELS SUPPLYING THE BASAL
GANGLIA AND THALAMUS

17. BLOOD SUPPLY TO THE INTERNAL CAPSULE
AND GLOBUS PALLIDUS

18. SUMMARY OF SUPERFICIAL AND DEEP
BLOOD SUPPLY TO THE CEREBRAL
HEMISPHERES

19. BLOOD SUPPLY OF BRAINSTEM

20. CEREBRAL ANGIOGRAM

21. CEREBRAL ANGIOGRAM

23. MEDIAL MEDULLARY SYNDROME (A)
• Medial medullary syndrome is most frequently the result of occlusion of the
vertebral artery or the anterior spinal artery.
• Medial medullarysyndrome presents with a lesion of the hypoglossal nerve as the
cranial nerve sign and lesions to both the medial lemniscus and the corticospinal
tract.
• Corticospinal tract lesions produce contralateral spastic hemiparesis of both
limbs.
• Medial lemniscus lesions produce a contralateral deficit of proprioception and
touch, pressure, and vibratory sensations in the limbs and body.
• Lesions of the hypoglossal nerve in the medulla produce an ipsilateral paralysis
of half the tongue with atrophy. Upon protrusion, the tongue deviates toward
the side of the lesion.

24. LATERAL MEDULLARY (WALLENBERG)
SYNDROME (B)
• Lateral medullary syndrome results from occlusion of the PICA. The cranial
nerves or nuclei involved in the lesion are the vestibular or the cochlear parts of
CN VIII, the glossopharyngeal and the vagus nerves, and the spinal nucleus or
tract of V. The long tracts involved are the spinothalamic tract and the descending
hypothalamic fibers.
• Spinothalamic tract lesions produce a pain and temperature sensation deficit
in
the contralateral limbs and body.
• Lesions of descending hypothalamic fibers produce an ipsilateral Horner
syndrome (i.e., miosis, ptosis, and anhidrosis).

25. • Lesions of the vestibular nuclei and pathways may produce nystagmus, vertigo,
nausea, and vomiting. If there is a vestibular nystagmus, the fast component will
be away from the side of the lesion.
• Lesions of the vagus nerves exiting the medulla may produce dysphagia
(difficulty in swallowing) or hoarseness. The palate will droop on the affected
side, and the uvula will deviate away from the side of the lesion.
• Lesions of the glossopharyngeal nerve result in a diminished or absent gag reflex.
• Lesions of the spinal tract and nucleus of the trigeminal nerve produce a loss
of just pain and temperature sensations on the ipsilateral side of half the face.
Touch sensations from the face and the corneal blink reflex will be intact. In
lateral medullary syndrome, the pain and temperature losses are alternating;
these sensations are lost from the face and scalp ipsilateral to the lesion but are
lost from the contralateral limbs and trunk.
• Taste sensations may be altered if the solitary nucleus is involved.

26. MEDULLA LESIONS

27. MEDIAL PONTINE SYNDROME (A)
• Medial pontine syndrome results from occlusion of paramedian branches of the
basilar artery. At a minimum, this lesion affects the exiting fibers of the abducens
nerve and the corticospinal tract. The medial lemniscus may be affected if the
lesion is deeper into the pons, and the facial nerve may be affected if the lesion
extends laterally.
• The long tract signs will be the same as in medial medullary syndrome, involving
the corticospinal and medial lemniscus, but the abducens nerve and the
facial nerve lesions localize the lesion to the caudal pons.
• Corticospinal tract lesions produce contralateral spastic hemiparesis of both
limbs.
• Medial lemniscus lesions produce a contralateral deficit of proprioception and
touch, pressure, and vibratory sensations in the limbs and body.

28. • Lesions of the abducens nerve exiting the caudal pons produce an internal
strabismus of the ipsilateral eye (from paralysis of the lateral rectus). This
results in diplopia on attempted lateral gaze to the affected side.
• Lesions of the facial nerve exiting the caudal pons produce complete
weakness
of the muscles of facial expression on the side of the lesion.
• Lesions of the facial nerve may also include an alteration of taste from the
anterior two-thirds of the tongue, loss of lacrimation (eye dry and red), and loss
of the motor limb of the corneal blink reflex.
 If a lesion extends dorsally to include the abducens nucleus (which includes
the horizontal gaze center in the PPRF), there may be a lateral gaze paralysis
in which both eyes are forcefully directed to the side contralateral to the lesion.

29. LATERAL PONTINE SYNDROME (B)
• Lesions of the dorsolateral pons usually result from occlusion of the anterior
inferior cerebellar artery (caudal pons) or superior cerebellar artery (rostral
pons). The long tracts involved will be the same as in lateral medullary syndrome,
the spinothalamic tract and the descending hypothalamic fibers. The cranial
nerves involved will be the facial and vestibulocochlear in the caudal pons, the
trigeminal nerve in the rostral pons, and the spinal nucleus and tract of V in
both lesions.
• Spinothalamic tract lesions produce a pain and temperature sensation deficit
in
the contralateral limbs and body.

30. • Lesions of descending hypothalamic fibers produce an ipsilateral Horner
syndrome (i.e., miosis, ptosis, and anhidrosis).
• Lesions of the vestibular nuclei and pathways (caudal pons) produce nystagmus,
vertigo, nausea, and vomiting. Again, the fast phase of the nystagmus will be
away from the side of the lesion. Lesions of the cochlear nucleus or auditory
nerve produce an ipsilateral sensorineural hearing loss.
• Lesions of the spinal tract and nucleus of the trigeminal nerve result only in a
loss of pain and temperature sensations on the ipsilateral side of half the face.
• Lesions of the facial nerve and associated structures produce ipsilateral facial
paralysis, loss of taste from the anterior two-thirds of the tongue, loss of lacrimation
and salivation, and loss of the corneal reflex.
• Lesions of the trigeminal nerve (rostral pons) result in complete anesthesia of
the face on the side of the lesion, weakness of muscles of mastication, and deviation
of the jaw toward the lesioned side.

31. PONS LESIONS

32. MEDIAL MIDBRAIN (WEBER) SYNDROME
Medial midbrain (Weber) syndrome results from occlusion of branches of the
posterior cerebral artery. Exiting fibers of CN III are affected, along with
corticobulbar
and corticospinal fibers in the medial aspect of the cerebral peduncle.
Third-nerve lesions result in a ptosis, mydriasis (dilated pupil), and an external
strabismus. As with any brain-stem lesion affecting CN III, accommodation and
convergence will also be affected. Corticospinal tract lesions produce
contralateral
spastic hemiparesis of both limbs. The involvement of the cortico-bulbar
fibers results in a contralateral lower face weakness seen as a drooping of the
corner of the mouth. The patient will be able to shut the eye (blink reflex is intact)
and wrinkle the forehead.

33. MEDIAL MIDBRAIN (WEBER) SYNDROME (B)

34. BASILAR ARTERY STROKE
• Locked-in Syndrome
• Ventral pontine syndrome
• Loss of corticospinal and corticobulbar tracts
• Bilateral paralysis (quadrapalegia)
• Patient can blink (upper brainstem intact)
• Contrast with vegetative state
• Motor function intact
• Cortical dysfunction

35. TOP OF THE BASILAR SYNDROME
• Very rare
• Occlusion of upper basilar artery (usually embolic)
• Changes in the level of consciousness (coma)
• Visual symptoms: hallucinations, blindness
• Eye problems:
• 3rd nerve palsy
• Loss of vertical gaze
• Problems with convergence
• Usually no significant motor loss

37. MAJOR CLINICAL SYNDROMES OF THE MCA,
ACA, AND PCA TERRITORIES

38. MAJOR CLINICAL SYNDROMES OF THE MCA,
ACA, AND PCA TERRITORIES

39. MAJOR CLINICAL SYNDROMES OF THE MCA,
ACA, AND PCA TERRITORIES

40. WATERSHED INFARCTS
When a cerebral artery is occluded, ischemia or infarction occurs in the territory
supplied by that vessel, with regions near other vessels relatively spared. In
contrast, when the blood supply to two adjacent cerebral arteries is
compromised, the regions between the two vessels are most susceptible to
ischemia and infarction. These regions between cerebral arteries are called
watershed zones.
• Watershed infarcts can produce proximal arm and leg weakness (“man in
the barrel” syndrome) because the regions of homunculus involved often include
the trunk and proximal limbs.
• In the dominant hemisphere, watershed infarcts can cause transcortical
aphasia syndromes.

41. WATERSHED INFARCTS

42. WATERSHED INFARCTS MRI

43. LATERAL MEDULLARY SYNDROME MRI

44. ACUTE BILATERAL MEDIAL MEDULLARY
INFARCTION MRI