Applied Vascular Anatomy of CNS 2 5 2020

SAVE OFFLINE

Applied CNS Vascular Anatomy By Khaled Osama Aboshaera Assistant Professor of Neurology Assiut University

ACA origin and Segments • ACA arises as the medial branch of the bifurcation of ICA at the level of anterior clinoid process. • The ACA divided into five segments (A1–A5).

MCA ICA

A1 Perforators

Distal A1 Perforators from its inferior surface

Optic nerve, Optic chiasm, Optic tracts

Heubner’s Artery (ies)

Lat. part of ventral surface of ant. limb of internal capsule, Lower 1/3 of head Caudate, Medial 1/2 of Glopus Pallidus, Septal nuclei, Anterior perforated substance

Proximal A1 Perforators from its superior surface Pcom The left-hemisphere distribution represents maximal perfusion volume, and the right represents minimal perfusion volume.

Genu & Posterior limb of IC, Rostral Thalamus, Pallidum, Putamen Suprachiasmatic anterior Hypothalamus,

Proximal A1 Perforators • Infarction of the hypothalamus may cause transient memory disorders or more protean psychological manifestations of anxiety, agitation or a feeling of weakness

Heubner artery ( red )

Proximal A1 perforators ( blue )

Thalamoperforate (PCA) Anterior choroidal (ICA) ( pink ) ( mauve )

Lateral lenticulostriatal arteries (MCA) ( yellow )

Recurrent artery of Heubner (H) • It commonly takes its origin from distal A1 or proximal A2 segments, rarely from the AcomA. In a few cases, it can have a common origin with frontopolar artery. • Occlusion: • Facio-Brachial monoplegia: Face & UL weakness (prox. ˃ distal) (2-3 + 3-4 NIHSS) • Dysarthria ± Soft whispering voice (1-2 NIHSS) • ± Dystonia • No Sensory (Total NIHSS 6-9)

H H

MCA

ICA

Subcallosal branch of ACOM

•

Supply: Anterior commissure, Lamina terminalis, septum pellucidum, Preoptic hypothalamic region, anterior pillars of fornix, columns, midline & paramedial basal forebrain, cingulum, rostrum & genu of corpus callosum

•

Sometimes, it can be well developed. It can extend between both pericallosal arteries along the corpus callosum supplying it and also the adjacent parts of the cerebral hemispheres. It also called (median artery of the corpus callosum, median callosal artery, arteria pericallosa triplex).

•

Occlusion: – Anterograde amnesia: if infarction confined to midline & paramedial basal forebrain. – Persistent & spontaneous confabulation: In cases of additional mesial frontal lobe damage

M1 ICA

Cortical Branches of ACA • Branches:

– Medial Orbito Frontal (orbfa) – Fronto Polar (fpa) – Calloso-marginal (callo)

• Anterior Internal Frontal (aif) • Mid Internal Frontal (mif) • Posterior Internal Frontal (pif)

• Paracentral (pcla) – Peri-callosal (peric) • Superior Internal Parietal (sipa)

• Inferior Internal Parietal (iipa)

Frontal Pole (Medial & lateral surface)

Fronto Polar Medial Orbito Frontal Olfactory bulb, Olfactory tract, Gyrus rectus , Medial orbital gyrus Transient memory impair. Anxiety Agitation Disinhibition

Contralateral Primitive reflexes (grasp, sucking) Paratonia (Gegenhalten) If dominant Trans-cortical motor aphasia (1 NIHSS) Impaired detection tasks Impaired go/no go tasks If non-dominant Perseveration Impersistance

If Bilateral Executive dysfunction Lack of initiatives (Abilia)

Trans-cortical motor aphasia •

Reduced spontaneous speech and preserved repetition

A3 (Precallosal Segment) • It gives off the callosomarginal artery (callo) Posterior Paracental Lobule Internal Frontal Mid Internal Frontal

Anterior Internal Frontal

Medial part of Supplementary motor (SMA) & Premotor

Paracentral lobule LL monoparesis (Distal > Prox.) (2-3 NIHSS) Cortical sensory loss in the LL (1 NIHSS) Homolateral ataxia, Crural paresis (2 NIHSS) If Bilateral Disinhibited bladder Total 5-6 NIHSS

Hemiparesis: LL > UL (2-3 + 1-2 NIHSS, total 3-5); Prox. > Distal Gait Apraxia Mirror writing (SMA) If dominant Alien limb Impaired bimanual coordination Inter-manual conflict Transcortical motor aphasia (SMA) If non dominant Motor neglect (SMA) Pusher syndrome

(A4 )

(A2)

Alien-hand signs • Motor perseveration: spontaneously occurring simple, repetitive, stereotyped movements of the hand. Patients are unable to stop them voluntarily or restrain them with the other hand. • Compulsive manipulation of tools: patient could not help grasping a familiar object placed before him and using it appropriately with her right hand against her will. These movements could not be inhibited by an examiner’s verbal command or the patient’s left hand. • Utilization behavior: a phenomenon similar to the compulsive manipulation of tools, in that objects in front of the patient are used, but this syndrome is distinctively different because of its lack of compulsiveness, its bilateral hand involvement. • Diagonistic dyspraxia: peculiar dissociative movement in which one of the patient’s hands (usually the left) acts at cross-purposes to the other (e.g., putting on one’s clothes with the right hand, immediately followed by pulling them off with the left hand). It is due to damage to the body of corpus callosum. • Unclassified alien-hand signs: simple or purposeless movements of either the right or left hand. Due to damage to contralateral medial frontal lobe and the genu and body of the corpus callosum.

A4 Superior Superior precuneus Internal Parietal Inferior Internal Parietal

Inferior precuneus, adjacent cuneus

Peri-callosal

• Meningeal branch can arise from the precallosal segment supplying inferior part of the falx. It anastomoses with branches of middle meningeal artery descending along the falx. It can also be connected with meningeal branch of PCA

Body of Corpus Callosum Limb-shaking TIA: LL Callosal Disconnection Syndromes Lt Ideomotor Apraxia Lt Dysgraphia Lt Tactile Anomia Lt hemispatial neglect Rt constructional disturbance Bilateral crossed pseudoneglect Crossed visuomotor ataxia (ataxie optique) Crossed avoiding reaction of the left hand (A4 )

(A2)

Callosal disconnection syndrome 1. Lt ideomotor apraxia: inability to execute learned skilled movements with the Lt hand according to verbal commands, in contrast with correct and flawless performance with the Rt hand. 2. Lt agraphia: linguistic errors in spontaneous writing by the Lt hand. whereas when using the right hand, the patient will make no linguistic errors even when he has paresis or grasp reflex. 3. Lt tactile anomia: inability to name subjects placed in the left hand. 4. Lt hemispatial neglect: 5. Rt constructional disturbance: may occur. 6. Bilateral crossed pseudoneglect: both visual and tactile line-bisection tasks showed that the Rt hand made errors to the Rt when the task was performed in the Lt hemispace, and the Lt hand made errors to the Lt when the task was performed in the Rt hemispace, despite no clinical signs of hemispatial neglect or extinction. 7. Crossed visuomotor ataxia (ataxie optique): The patient’s hand will fail to reach & grasp an object placed in the peripheral visual field of the opposite side. 8. Crossed avoiding reaction of the Lt hand: The patient is unable to mobilize the Lt hand with any effort, when he intended to reach and grasp the stimulus placed in the Rt hemispace.

ACA Occlusion (Total NIHSS 12-17) 1- Contralateral Heubner (6-9 NIHSS) a. Faciabrachial weakness b. LL weakness Paracentral (5-6 NIHSS) c. Cortical sensory loss over leg and foot d. Primitive reflexes e.g. grasp, sucking reflex Frontopolar e. Gegenhalten Callosomarginal 2- Gait apraxia Precallosal 3- Ideomotor Apraxia, Dysgraphia, Tactile Anomia of the lt hand 4- If Dominant – Trans-cortical motor aphasia Frontopolar (1 NIHSS) – Impaired detection tasks – Impaired go/no go tasks – Alien limb – Impaired bimanual coordination Callosomarginal – Inter-manual conflict 5- if non dominant – Perseveration Frontopolar – Impersistance Precuneal (1-2 NIHSS) – Lt Spatial neglect

Heubner

Callosomarginal

Paracentral

Bilateral ACA infarction • Causes: bilateral ACA vasospasm following rupture of an ACA/ACoA aneurysm, or occlusion of an ACA in the presence of a hypoplastic A1 segment or an azygous distal ACA. – Cortical Paraplegia, (6-8 NIHSS) – Cortical sensory loss of both LL (1 NIHSS) Paracentral – Disinhibited bladder Orbitofrontal – Disinhibited behaviour – Impaired executive function, – Mental confusion. (1 NIHSS) Frontopolar – Lack of initiatives (Abilia) – Transcortical motor Aphasia (1 NIHSS)

MRI Patterns Extensive Unilateral

Ant to central sulcus

Deep Territory

Extensive Bilateral

Post to central sulcus

Intermediate Territory

MCA • It rises from terminal ICA (its largest branch,75% of its caliber) lateral to optic chiasma. • •

• •

M1- Horizontal / Sphenoidal Segment: passes horizontal in lateral direction & slightly anteriorly to enter in sylvian fissure, then turns 90 at the genu of the MCA. M2- Insular Segment: running vertically on the surface of the insula, terminates at the circular sulcus of the insula. M3- Opercular Segment: running laterally and exiting the insular cistern, following the curvature of operculum, ends at the surface of the Sylvian fissure after two 180 turns. M4- Cortical Branches: emerge from the Sylvian fissure, follow along the sulci and gyri, and extend over the cortical surface of the cerebral hemisphere.

M1 (Horizontal / Sphenoidal) • M1 gives off two types of branches: – Perforators: Lenticulostriate arteries – Cortical branches: • Tempro-polar & anterior temporal arteries (AT) • Sometimes also orbitofrontal branch (O)

Lenticulostriate arteries (lena) • They arise along the length of the M1 commonly from its superior surface. • When M1 is short, dividing early in its distal branches, the perforators arise from superior branch or from a branch of M2. • The branches can be subdivided into medial, intermediate, and lateral groups. • The medial branches have a straight course, the intermediate a slightly tortuous course, and the lateral display the typical S-shaped aspect.

ACA MCA

ICA

M1 • Medial LS: the least constant & can be replaced by perforators of ICA-T or A1. • Lateral LS: the largest one called Charcot‘s artery of cerebral haemorrhage.

Lenticular striate artery infarction Three hemi syndrome: • Cont. hemi-paresis • Cont. hemi-hypoesthesia • Cont. homonymous hemi-anopia • If Dominant: Transcortical motor / sensory aphasia Proximal single lenticulostriate artery territory infarction lesion (extending to the basal surface of MCA)

Distal single lenticulostriate artery territory infarction lesion (not extending to the basal surface of the MCA)

Lenticular striate artery infarction Lacunar Syndromes

Ant. Limp

Pure Dysarthria Dysarthria

Capsular genu $ Mastication, palatal, pharyngeal, ipsilat. vocal cord weakness

Dysarthria clumsy hand $

7th,

12th,

Dysphagia, x hand fine mov. ± micrographia

G

Pure motor Hemiparesis UL ˃ LL

Ataxic hemiparesis LL Weakness, UL Ataxia Cheiro-oral $ Perioral & distal UL sens dysfun.

Post. Limp

Bi/tri-furcation of MCA • The M1 divides distally into 2 or 3 branches (bi-trifurcation). Its length varies, being on average of 16 mm in length. It can be very short, and so the bitrifurcation may be located near the bifurcation of the ICA. (a) In the bifurcation pattern, (64–90%) (3+3) • Anterosuperior trunk: orbitofrontal (O), operculofrontal (OF), central (C). • Posteroinferior trunk: ant.&post. parietal (P), gyrus angularis (G), temporal (T). (b) In the trifurcation pattern, (12–29%) (2+3+1) • Anterosuperior trunk: O, OF • Middle trunk: C, P, G • Posteroinferior trunk: T

Premotor • • • •

Faciobrachial monoplegia (Distal ˃ Proximal) Brachial syndrome: weakness of hand & arm Limb kinetic apraxia If Dominant: ✓ Frontal opercular syndrome: Brocas aphasia + facial weakness ± arm weakness. ✓ Agraphia ± acalculia. ✓ Pure anarthria; ✓ Aphemia or pure apraxia of speech • If Non-dominant: ✓ Cortical dysarthria ✓ Motor impersistence ✓ Hemineglect • If bilateral: Facio-lingo-pharyngo-musticatory diplegia

OF

Prefrontal • • • •

Transient tonic deviation of eyes & head toward the lesion Apraxia of conjugate gaze to the opposite side If dominant: Trans-cortical motor aphasia If non-dominant: Lt motor neglect

• • • •

C P G

O

Orbitofrontal Contralateral forced grasping Social disinhibition; Senseless, Inappropriate playfulness, Compulsive joking & laughing

T

Precentral

Postcentral

• Focal weakness in the arm, wrist, hand, or fingers • Writing tremor (infrequent) • UL ataxia with asterixis (rare) • Segmental action myoclonus (rare) • If bilateral: (Foix–Chavany–Marie syndrome): ✓ Loss of voluntary control of facial, pharyngeal, lingual, and masticatory muscles ✓ Preserved reflexive and automatic functions ✓ Anarthria or severe dysarthria

• Posterior operculum syndrome ✓ Isolated cheiro-oral sensory loss

Anterior Parietal

OF

C P G

O T

• Spectrum of acute hemisensory dysfunction (rare): from hemisensory neglect to “pseudothalamic $” • Posterior operculum syndrome (rare) • Parietal ataxia • If dominant ✓ Conductive aphasia ✓ Ideomotor apraxia, ✓ Alexia, Phonogic agraphia • If non-dominant: ✓ Hemisensory neglect, Acute hemiconcern ✓ Postrolandic motor hemineglict ✓ Visuo-spatial & visuo-constructive impairment

OF

Posterior parietal

C P G

O T

• Contralateral homonymous lower quadrantanopia • Hemisensory cortical impairment • Mild transient motor weakness, rarely ± ataxia or dystonia of UL • Parietal kinetic ataxia without proprioceptive deficit • If dominant: ✓ Transcortical sensory aphasia / sensory aphasia, ✓ Anomic aphasia, ✓ Phonological agraphia and alexia, ✓ Ideomotor apraxia, ✓ Left word eye tracking impairment (x pursuit) ✓ Asymbolia of pain • If non-dominant: ✓ Spatial Left hemi-neglect without weakness , ✓ Asomatognosia, Ansognosia ✓ Visuo-spatial memory impairment ✓ Optic Ataxia: ✓ Dressing & constructional apraxia. ✓ Acute confusional state (Spatial delirium) • If bilateral: ✓ Balint’s $ ✓ Altitdinal neglict

OF

O

• -

C

Angular

• In distal occlusion: P ✓ Contralateral hemianopia or lower quadrantanopia ✓ Optic ataxia • In proximal occlusion: G ✓ Transient motor weakness ✓ Contralateral hemianopia or lower quadrantanopia T ✓ Prevalent neuropsychological impairments. ▪ In the dominant side: - Angular lexical Alexia with agraphia (angular) - Transcortical sensory aphasia In bilateral - Ideomotor Apraxia Bálint’s syndrome, - Grestman $: (Angular & Supramarginal): Psychic gaze paralysis, Acalculia, Agraphia, Finger agnosia, Rt-Lt Visual inattention, Disorientation. ± Optic ataxia - Anomic aphasia ± anterograde & partially retrograde amnesia - Wernicke’s aphasia ▪ In the non dominant side: - Hemispatial neglect with sensory predominance, - Asomatognosia, - Visuo-constructive & visuo-spatial disturbances, constructional apraxia

Temporal • Contralateral homonymous upper quadrantanopia • Visual hemineglect • If Dominant: ― Global aphasia → Sensory aphasia → Pure word deafness OF ― Isolated pure alexia with agraphia, ― Conduction aphasia (Less often ), ― Anomia (ant. temporal), ― Impaired verbal memory O • If non-dominant: ― Sensory aprosidia, Expressive instrumental amusia, ― Impaired nonverbal memory ― Hemineglect (auditory, somatosensory, visual). ― Constructional apraxia ― Asymmetrical catalepsy with perseveration of posture, more in the Lt limbs (rare) ― Behavioral changes: • Acute confusional state (most often) • Acute agitated delirium (less often ). • Delayed poststroke depression • If bilateral: ― Cortical deafness, Pure word deafness ― Rejection behavior

C P G T

Superior Division • • • • • •

Cont. Hemiparesis/plegia: UL >LL Cont. Hemihypoethesis. No homonymous hemianopia. Conjugate gaze to the hemiplegic side. If dominant: • Broca’s dysphasia • Post-stroke depression If Non-dominant: • Acute confusional state • Visual perceptual disorders • Hemi-inattention or hemispatial neglect, • Dysarthria or dysprosodia • Denial of hemiplegia (and denial of eye closure with confabulations about what they claim they see through their closed eyes

Inferior division • • •

•

Cont. homonymous hemianopia Cont. cortical sens. loss (graphaesthesia & stereognosis) If dominant: – Temporal: Wernicke’s dysphasia (post. temporal), Anomia (ant. temporal), Impaired verbal memory – Parietal: Asymbolia of pain, Left word eye tracking impairment (x pursuit) – Angular & Parietal: Ideomotor Apraxia – Angular: Anomia , Angular lexical Alexia with agraphia , – Angular & Supramarginal: Grestman $: Acalculia, Agraphia, Finger agnosia, Rt-Lt Disorientation If Non-dominant: – Parietal: • Left hemi-neglect, Agnosia for the left half of external space • Ansognosia & Asomatognosia • Visuo-spatial memory impairment • Optic Ataxia: • Dressing & constructional apraxia. • Acute confusional state – Temporal: • Amusia, Sensory aprosidia, • Impaired nonverbal memory

MCA Total Occlusion It is mainly attributable to cardiac or artery-to-artery embolism • • • • • • •

Cont. hemiplegia: UL (cortical & capsular) ˃ LL (only capsular) Cont. hemianesthesia including the face (spino-thalamic tract) Cont. homonymous hemianopia (Optic radiation) Conjugate gaze to I/L side (destructive), to c/l side (irrelative) (Frontal eye field) Altered sensorium (due to edema) If Dominant: Global aphasia (motor aphasia, word deafness, anomia, jargon speech), Agraphia, Gerstmann $ (acalculia, alexia, finger agnosia, Rt-Lt confusion), Ideomotor apraxia If non-dominant: — Parietal: • Left hemi-neglect, Agnosia for the left half of external space • Ansognosia & Asomatognosia • Visuo-spatial memory impairment • Optic Ataxia: • Dressing & constructional apraxia. • Acute confusional state — Temporal: • Amusia, Sensory aprosidia, • Impaired nonverbal memory

Centrum ovale infarcts •

•

•

The centrum ovale (or centrum semiovale) is the central white matter of the cerebral hemispheres, including the most superficial part of the corona radiata and the long association bundles. It is supplied by long perforating medullary arteries (2–5 cm) originating from the superficial (pial) MCA (usually as single territories without interdigitation with adjacent branches) and the anterior choroidal artery. Centrum ovale infarcts in isolation account for only 1.2% - 2% of all strokes.

Centrum ovale infarcts Small ˂1.5 cm

More frequent

Large >1.5 cm

Less frequent, less than ¼

Often silent, In symptomatic patients, the Stroke onset is usually acute & stabilizes within neurological deficit develops over several hours few minutes. in at least half of the patients. lacunar syndrome (mainly in UL): Pure motor stroke is the most frequent pattern, but pure sensory and sensorimotor stroke and ataxic hemiparesis can be observed. Choreoathetosis or dysphasiaare also uncommon.

Similar to large superficial or extended MCA territory infarcts, including neuropsychological impairment (dysphasia, visuospatial dysfunction, and hemineglect) and motor, sensory, or visual field dysfunction.

Small infarcts are frequently round or ovoid.

Large infarcts with irregular geographic margins following the inner border of cortex.

Small vessel disease is the most common. May be artery-to-artery or cardiac embolism

Hemodynamic failure associated with severe ICA disease in up to ¾ of the patients. Artery-to-artery or cardiac embolisms can be found in some cases.

MRI Patterns Occlusion of Deep branches (33%) Lat. Lenticulo-striate arteries

Occlusion of Main stem (M1) (10%)

Occlusion of one trunk (M2) (57%) Antero-superior trunk (18%)

Postero-inferior trunk (14%)

PCA Origin •

• •

Parent artery: – In 75% of cases: both PCAs arise from bifurcation of basilar artery – in 20%, 1 PCA has its origin from ipsilateral ICA – in 5%, both originate from respective ipsilateral ICA (as direct continuation of pCom) Site of origin: – within interpeduncular cistern Relation to surroundings: – lies above 3rd nerve – circles midbrain above tentorium.

PCA Segments • P1 / Peduncular segment: from basilar tip to PComA, runs in the interpeduncular fossa,. – Mesencephalic / interpeduncular – Posterior thalamo-perforators (P)

•

P1

Mesencephalic / interpeduncular br: – Supply: • Cr. Nv. Nuclei 3 – 4 • Red nucleus (Sup. Med. part) • Medial leminiscus • Decussation of Sup. Cerebllar Peduncle – Occlusion: • Benedict's $: Ipsi. 3rd & cont. hemiplegia + Ataxia (rednucleus / Medial mid brain) • Claude's $: Ipsi. 3rd & contr. cerebellar ataxia (rednucleus / cerebral peduncle) • Hemiataxia, Intention tremor: Red nucleus or Dentato-rubro-thalamic tract • Contralat. Delayed action tremors (my be myoclonus or athetosis) • Vertical gaze (4th nerve palsy) & conversion disorder

P1 •

Posterior thalamo-perforators: – Supply: • Ant 1/3 of thalamus: midline, centro-median, medial, ventro-lateral, reticular • Hypo-thalamus, Sub-thalamus – Occlusion: • Transient loss of consciousness or somnolence • Behavioural changes: confusion, agitation, apathy • Recent memory loss • Contr. hemiballismus: subthalamic nucleus

• Bilateral occlusion of proximal PCA or top of basilar artery: Extensive infarction in the midbrain and subthalamus →Coma, unreactive pupils, bilateral ∆ signs, decerebrate rigidity.

P2

• P2 / Ambient segment: in ambient cistern from PComA, runs around the midbrain – Peduncular or basal br. of midbrain – Dorsolateral br. of midbrain – Thalamogeniculate (G) – Med. post. choroidal (M) – Lat. post. choroidal (L) – Ant temporal (AT)

P2 •

Peduncular or basal br. of midbrain: – Supply: 3rd root, med. 1/5 of CP – Weber's $: Ipsi. 3rd & contr. Hemiplegia (medial mid brain / cerebral peduncle) • Dorsolateral br. of midbrain or collicular artery: – Sup. Cerebellar P., Lat. 1/5 of CP, – Med. & Spinal leminiscus • Ant temporal: – Uncus

•

P2

Thalamogeniculate br.: – Supply: • Post 2/3 of thalamus: part of VL, VPL • Superior & inferior colliculi, pineal gland – Occlusion: Contralateral • Sensory: Transient hypoesthesia followed by an agonizing, searing or burning pain (Thalamic Déjérine-Roussy $) • Ataxia: Dysequliprium (thalamic astasia) / Hemiataxia / Hemiataxia-hypoesthesia syndrome / Ataxic tremor • Involuntary movement: Athetoid posture (thalamic hand) mild choreo athetoid mov • Motor: transient mild hemiparesis

Small Lesion affecting the lateral thalamus 4 patients had mainly sensory deficits with paraesthesias in the distal UL. Discrete motor weakness was observed in 1 patient.

P2 •

Infarction in the lateral thalamus in the territory of thalamogeniculate artery branches also cause motor abnormalities. – Due to: • Interruption of extrapyramidal fibers from basal ganglia, via ansa lenticularis • Interruption of cerebellofugal fibers from superior cerebellar peduncle & red nucleus that synapse in ventrolateral nucleus of the thalamus, • Infarction of posterior limb of internal capsule adjacent to ventrolateral thalamus – Result in contralateral: • Abnormal movements: chorea or athetosis, • Abnormal posture: flexion & entrapment of the thumb in the fist. • Ataxia • Slight hemiparesis: usually not severe, and improve rapidly

• •

P2

Med. post. choroidal arteries: – 3rd & 4th ventricle, MGB, Tectum of midbrain, Fornix – Part of thalamus: VPM, Post. Part of medial, Sup. Med. Pulvinar Lat. post. choroidal arteries: – Supply • Lateral ventricle, Med. ½ of LGB, Hippocumbus • Part of thalamus: Inf. Lat. Pulvinar, LD – Occlusion: Isolated infarct is rare • Partial hemianopia: contralat. homo. quadrantanopia or horizontal secoronopia • Asymmetric optokietic response • ± hemisensory loss, transcortical aphasia, memory disturbances.

P3 • P3 / Quadrigeminal segment: on the surface of the quadrigeminal plate to calcrine fissure – Hippocampal (H) – Middle & posterior temporal / occipito-temporal (PT) – Posterior pericallosal / medial central (S)

P3 •

Hippocampal artery: – Supply: Parahippocampal gyrus. – Occlusion: • In the dominant side: Persistent amnesia that can last at least 6 months • In the non dominant side: defective long-term, nonverbal memory. Para-hipocampus

P3 •

Middle, and posterior temporal / occipito-temporal arteries: – Supply: Lingual, medial and lateral occipitotemporal gyri. – Occlusion in the dominant side: • Verbal memory impairment (Med. temp. & hippocampal involvement) • Transcortical sensory aphasia (Fusiform) • Color agnosia (Fusiform & Lingual) • Visual agnosia (Fusiform) • Anomic aphasia (Post temporal) • Agitated delirium (postero-inferior temporal lobe) – Occlusion in the non-dominant side: • Achromatopsia: (Fusiform & Lingual) • Prosopagnosia: (x faces) (Fusiform) • Landmark agnosia (Lingual & Para-hipocampus) • Constructional apraxia • Visual inattention

Para-hipocampus

Lingual

Fusiform

P3 •

Posterior pericallosal / medial central artery: – Supply: • Spenium of CC – Occlusion if in dominant side: • Alexia without agraphia: patients write, speak, and spell normally, but fail to read words and sentences and cannot name colors

P4 • P4 / Distal segment – Parieto-occipital (PO): Inferior Parietal lope – Calcarine (CA): Occipital lope

AT

TO

Parieto-occipital (PO) • •

•

Supply: Cuneus & Precuneus Occlusion in the dominant side: – Alexia with agraphia (Lt angular gyrus, the anatomical residence of literacy) – Gerstmann’s syndrome (Angular & Supramarginal): acalculia, alexia, finger agnosia, Rt-Lt confusion – Conduction aphasia (inferior parietal lobe) Occlusion in the non-dominant side: – Neglect of the contralateral visual field – Constructional apraxia – ± disorientation to place

Angular gyrus

Supramarginal gyrus

Calcarine artery occlusion • •

•

• •

Contralateral homonymous hemianopia with macular sparing. Visual perseverations consist of: (i) Seeing an object within the field of vision repeated, sometimes multiple times, in the defective hemifield, despite continued gaze fixation (ii) After turning one’s gaze to the hemianopic field, seeing an object that was formerly in view (iii) continuing to see an object (palinopsia) as an afterimage, despite the fact that the object or the viewer has moved The field defect may be limited to a quadrantanopia. – Superior quadrantanopias are caused by infarction of the lower bank of the striate cortex or the inferior optic radiations in the temporal occipital lobes. – Inferior quadrantanopia is due to infarction of the upper calcarine bank or involvement of the upper optic radiations in the inferior parietal lobe or occipital lobe. At times, the visual defect is a homonymous scotoma involving the fixation macular region (occipital-pole infarcts). Unformed visual hallucinations of brightly colored scenes & objects (Release hallucination) (Peduncular hallucinosis)

PCA Stenosis •

• •

Visual symptoms: the most common, can be negative (hemianopia, homonymous hole or scotoma) or positive (photopsias and visual illusions). Photopsias described as flashes of light, striped vision, colored objects, or geometric objects in one visual field. These positive phenomena are identical with those described in classical migraine, except that in patients with PCA stenosis, the attacks are briefer and the visual phenomena do not develop or progress over minutes as do migraine auras. Sensory symptoms (Paresthesias): relatively common, most often involving face & hand. Occasional symptoms: limb clumsiness, dizzy feelings, brief periods of confusion.

PCA occlusion •

The clinical findings depend heavily on the portion of the PCA occluded, on the location and extent of infarction, and on the side of the occlusion. • The most common location for occlusions is in the ambient segment, affecting one or more of the hemispheric branches. • Unilateral PCA territory infarcts can conveniently be divided into four groups, each having characteristic findings: (i) Extreme proximal occlusion (P1): causing midbrain, thalamic, hemispheric infarctions (ii) Proximal ambient segment occlusion (P2), before the branching of the thalamogeniculate arteries: causing lateral thalamic & hemispheric infarctions (iii) Large hemispheric infarctions (P3): often involving calcarine, parietooccipital, and posterior temporal artery territories. (iv) Single PCA branch occlusion (P4): predominantly involving the calcarine artery

Artery of Percheron • Bilateral paramedian involvement of the brainstem & thalamus can also occur even with unilateral PCA occlusions, as penetrating arteries to the rostral brainstem can arise from a common trunk off one of the PCAs, called the artery of Percheron. • Patients with these bilateral infarcts often have prolonged stupor or coma, or later, hypersomnolence, amnestic deficits, and vertical-gaze palsies.

Total PCA occlusion • •

Right homonymous hemianopia. Hemiparesis or hemianesthesia (Infarcts extending to thalamus & internal capsule)

Bilateral P3 & P4 occlusion

– Bilateral Calcarine: • Striate cortex: Cortical blindness with preserved light reflex. • Visual association areas: the patient is unaware of the blindness or may even deny it (Anton's syndrome). • Patients who are cortically blind may be able to avoid bumping into objects and may blink to visual threat. The most frequently posited explanation for this “blindsight” is preservation of extra-geniculate optic pathway involving connections between superior colliculus & peristriate cortex. Some patients have bilateral hemianopias, with sparing of parts of the visual field, or bilateral scotomas. • Bilateral inferior-bank infarcts: (more common) (after rostral basilar artery occlusion): – Upper-quadrant attitudinal hemianopias, – Loss of the ability to revisualize the form of an object or people (occipitofugal system or what pathway), but they can revisualize and picture directions and place relationships (visuospatial system or where pathway in the superior bank).

Bilateral P3 & P4 occlusion

– Bilateral Calcarine:

• Bilateral superior-bank infarcts: (less common) (after severe hypotension, with infarction in the posterior PCA–MCA border-zone regions): x visual association areas – Bélint’s $: • Simultanognosia: x appreciate the meaning of the whole of an image • Palinopsia: abnormal recurring visual imagery; persistence of a visual image for several minutes despite gazing at another scene • Optic ataxia: failure to grasp an object under visual guidance • Occulomotor apraxia: inability shift gaze voluntary & on command at a position or object • Decreased visual attention: affect mainly peripheral field – tunnel vision • Spatial disorientation: loss of spatial reference and memory – lost in space – Difficulty in revisualizing directions, locations and relationships – Disorientation to place

Bilateral P3 & P4 occlusion – Bilateral Posterior Temporal: • Prosopagnosia: (x faces) (Rt Fusiform) • Color agnosia: (Lt Fusiform & Lingual) • Restless, hyperactive state: (Lingual & Fusiform gyri) • Agitated delirium: (limbic cortex) – Bilateral Hippocampal: • Acute Amnestic Syndrome – Malignant PCA infarction: • On rare occasions, large bilateral PCA strokes can be associated with severe edema → increase ICT with irreversible 2ndry brain injury → death – DD: Acute metabolic edematous posterior leukoencephalopathy or a capillary-leak syndrome following acute elevation of BP, seen in hypertensive encephalopathy, eclampsia, and administration of antineoplastic drugs such as cyclosporine. Infarcts tend to be mostly cortical or corticosubcortical, whereas acute edema predominantly or exclusively involves white matter

Thank You