Vascularssuppluvascularsupply

Front 1

What 2 arteries wrap around CN3

Back 1

Posterior cerebral and superior cerebellar

Front 2

What is the most common artery for berry aneurysm

Back 2

PCOM

Front 3

What is dysartheria

Back 3

It is a common speech disorder, problems with speaking and it is due to loss of muscles that we use in speech, speech is often stammered and stuttered, however they have no problem understanding speech. CAUSE OF THIS IS DEGENERATIVE NEUROLOGICAL DISORDERS LIKE BULBAR PALSY OR AMYOTROPIC LATERAL SCLEROSIS (ALS)

Front 4

What does vertebrobasillar arterial system supply

Back 4

It supplies everything in the posterior brain like brain stem and cerebellum

Front 5

Vertebrobasillar system consists of what vessels

Back 5

Vertebral a, single basilar a. at the pontomedullary junction, and paired PCA (posterior cerebral aa. At pontomesencephalic junction, and PCOM to anterior circulation

Front 6

What are the 3 cerebellar arteries

Back 6

Superior cerebellar, AICA and PICA

Front 7

What is the vascular territory SCA

Back 7

Arises from the top of the basilar artery at the level of rostral pons and supplies the superior cerebellum and bit of rostral laterodorsal pons

Front 8

What is the vascular territory AICA

Back 8

Arises form basilar at level of caudal pons and supplies the lateral caudal pons and a small portion of the cerebellum

Front 9

What is the vascular territory PICA

Back 9

Arises from vertebral artery and it supplies the lateral medulla and inferior cerebellum

Front 10

What is the blood supply to the midbrain

Back 10

PCA and penetrating branches of the basilar

Front 11

What is the blood supply to the pons

Back 11

Basilar artery

Front 12

What is the blood supply to the medulla

Back 12

Medial basilar

Front 13

What is the blood supply to the lateral

Back 13

Vertebral and PICA

Front 14

What structures make up the brain stem

Back 14

Midbrain, pons, medulla

Front 15

What is an embolism

Back 15

Cardiac origin

Front 16

Thrombosis

Back 16

In situ occurs at the site of a preexisting atherosclerotic stenosis

Front 17

Lacunar disease

Back 17

Small vessel occlusion in the setting of hypertension

Front 18

If we say brain stem is going down

Back 18

It is usually a warning sign for the vertebrobasillar ischemia

Front 19

What are some of the common signs of vertebrobasillar ischemia

Back 19

Dizziness (vestibular),

Front 20

CN3 or 4 lesion

Back 20

Midbrain

Front 21

CN 5,6,7,8, lesion

Back 21

PONS

Front 22

CN 9,10,12 lesion `

Back 22

Medulla

Front 23

Where would all of these lesion be localized

Back 23

In the brain stem

Front 24

What else is lesioned in the brain stem

Back 24

CN and long tracts, and lesion in the brainstem to any of long tracts will have a contralateral body deficit i.e. corticospinal, spinothalamic, medial lemniscus

Front 25

What are the exceptions to the contralateral problems due to lesion in brainstem

Back 25

1)

Front 26

2)

Back 26

Cerebellar peduncles which cause ipsi motor ataxia (discoordinated movements)

Front 27

3)

Back 27

Damage to the cranial nerves will result in ipsi head sensory or motor defects

Front 28

So another name for lesions of the brainstem is

Back 28

Alternating because we see both contralateral and ipsilateral problems

Front 29

What If we have upper midbrain damage, esp. of the lesion is above the red nucleus

Back 29

Impaired consciousness, flexion +, so patient is going to have flexor (decorticate) posturing, also there is CN3 palsy, and unilateral and bilateral pupil dilation and ataxia. THE REASON WE DON’T WALK AROUNF FLEXED IS THAT THE RUBROSPINAL TRACT HAS A STRONG NEGATIVE INHIBITION FROM THE CORTEX, BUT WHEN THERE IS A LESION, THAT INHIBITION IS GONE AND THE PATIENT IS FLEXED. This has good prognosis

Front 30

What if we have upper pontine damage

Back 30

Impaired consciousness, patient shows decerebrate or extensor posturing since the lesion is below RED NUCLEUS, here we have abducens palsy or horizontal gaze palsy, (IF THE LESION IS ON THE RIGHT, CAN TURN THE EYES TO THE RIGHT AND HAVE A LEFT GAZE PREFERENCE), WE HAVE BILATERAL SMALL BUT REACTIVE PUPILS, prognosis here is bad

Front 31

WHAT NYSTAGMUS IS NOT SEEN IN AN UNCOSNCIOUS PATIENT

Back 31

CALORIC NYSTAGMUS, BECAUSE THERE IS NO SACCADE

Front 32

What if there is a lesion in the medulla

Back 32

Bad prognosis, respiratory arrest, vertigo, ataxia, nausea, vomiting, autonomic instability and hiccups

Front 33

What are some of the most common brainstem lesions

Back 33

Lateral medullary syndrome, medial pontine base, and midbrain

Front 34

What Is lateral medullary syndrome

Back 34

It is a lesion in the lateral medulla mainly due to vertebral artery, main structure that is involved is inferior cerebellar peduncle (ipsi ataxia), vestibular nuclei (vertigo, nausea, nystagmus), CN5 (ipsi facial loss of pain and temp), nucleus ambiguus (hoarseness, dysphagia), nucleus solitarius (ipsi ↓taste), descending sympathetic fibers (Horner’s syndrome), spinothalamic tract (contra body ↓ pain and temp). The disorder is also called Wallenberg syndrome, lateral tegmentum is involved, not too much motor involvement prognosis is good.

Front 35

What if there is a lesion in the middle pontine base

Back 35

Caused by lacunar disease, mainly due to ↑ chronic BP, also called Ataxic Hemiparesis and the ataxia is same side as the weakness. There is a ↑# of motor tracks that run through here. The lesion happens because there is circumferential brr. from the basilar artery is not lesioned.

Front 36

1-

Back 36

Corticospinal tracts – UMN, contralateral leg arm weakness

Front 37

2-

Back 37

Corticobulbar tracts- UMN, contralateral face weakness, these people have central 7, with dysartheria. Assuming that the lesion is on the right, these people have facial weakness on the left side since it is UMN it is going to be left lower ¼, and they will be able to close their eye on the left but not tight

Front 38

3-

Back 38

Abducens nerve- ipsi paralysis of lateral rectus, this happens because the cell bodies are in the tegmentum

Front 39

4-

Back 39

Pontine nuclei and pontocerebellar tracts- contralateral ataxia which is on the same side of the weakness. This happens because the pontine nuclei send their fibers (w/c cross the midline) to medial cerebellar peduncle and they MCP sends it to the cortex and at this point they are called MOSSY FIBERS

Front 40

What is the cause of midbrain lesions

Back 40

It could be due to infarcts in the PCA and vessels from the top of the basilar A, it is also called top of the Basilar syndrome, could be due to an embolus 1- if the lesion occurs in the Occulomotor nerve, it will → to Moritz Benedikt syndrome (which shares some of the characteristics with the Weber syndrome, like eye down and out, drooping eye lid, dilated, non-responsive pupil, and contralateral tremor.

Front 42

What are some of the common signs of vertebrobasillar ischemia

Back 42

Dizziness (vestibular),
Diplopia and dyscongugate (supra on infra nuclear eye pathway)
Blurred vision or other eye (eye movement pathway)
Incoordination/ataxia (cerebellum)
Dysartheria or dysphagia (corticobulbar)
Numbness (somtaosensory)
Hemi or quadra paresis (corticospinal)
SOMNOLENCE (PONTOMESENCEPHALIC RETICULAR FORMATION OF BILATERAL THALAMI), these patients are in a coma and they cant keep the patient awake

Front 43

What are the exceptions to the contralateral problems due to lesion in brainstem

Back 43

1) Descending sympathetic hypothalamic fibers, lesions always result in Horner’s which is ipsi to the side of the lesion in the brain stem (Ptosis, Anhidrosis, miosis)
2) Cerebellar peduncles which cause ipsi motor ataxia (discoordinated movements)
3) Damage to the cranial nerves will result in ipsi head sensory or motor defects

Front 44

What Is lateral medullary syndrome

Back 44

It is a lesion in the lateral medulla mainly due to vertebral artery, main structure that is involved is inferior cerebellar peduncle (ipsi ataxia), vestibular nuclei (vertigo, nausea, nystagmus), CN5 (ipsi facial loss of pain and temp), nucleus ambiguus (hoarseness, dysphagia), nucleus solitarius (ipsi ↓taste), descending sympathetic fibers (Horner’s syndrome), spinothalamic tract (contra body ↓ pain and temp). The disorder is also called Wallenberg syndrome, lateral tegmentum is involved, not too much motor involvement prognosis is good

Front 45

What if there is a lesion in the middle pontine base

Back 45

Caused by lacunar disease, mainly due to ↑ chronic BP, also called Ataxic Hemiparesis and the ataxia is same side as the weakness. There is a ↑# of motor tracks that run through here. The lesion happens because there is circumferential brr. from the basilar artery is not lesioned.
Deficits:
1- Corticospinal tracts – UMN, contralateral leg arm weakness
2- Corticobulbar tracts- UMN, contralateral face weakness, these people have central 7, with dysartheria. Assuming that the lesion is on the right, these people have facial weakness on the left side since it is UMN it is going to be left lower ¼, and they will be able to close their eye on the left but not tight
3- Abducens nerve- ipsi paralysis of lateral rectus, this happens because the cell bodies are in the tegmentum
4- Pontine nuclei and pontocerebellar tracts- contralateral ataxia which is on the same side of the weakness. This happens because the pontine nuclei send their fibers (w/c cross the midline) to medial cerebellar peduncle and they MCP sends it to the cortex and at this point they are called MOSSY FIBERS

Front 46

What is the cause of midbrain lesions

Back 46

It could be due to infarcts in the PCA and vessels from the top of the basilar A, it is also called top of the Basilar syndrome, could be due to an embolus 1- if the lesion occurs in the Occulomotor nerve, it will → to Moritz Benedikt syndrome (which shares some of the characteristics with the Weber syndrome, like eye down and out, drooping eye lid, dilated, non-responsive pupil, and contralateral tremor.
2- Weber’s syndrome- this is caused by a lesion in the mid brain and basically we take out of the cerebral peduncle (PTO) we have eyeball down and out, drooping of eye lid, dilated non-responsive pupil, and contralateral UMN paralysis (because PTO is knocked out)
3- occulomotor palsy- this lesion is infranuclear, and we get the same symptoms as before, eye lid down and out, drooping of the eyelid, dilated non responsive pupil