The following slideshow contains the overview of blood supply of the brain viz. arterial and venous; Blood brain Barrier, Cavernous Sinus. It also has the various Neuropsychiatric manifestations related to alteration in the blood supply of brain.
1. Presented by : Dr. Aditya
Kashyap
Moderator : Dr. Sireesha S.
2. • INTRODUCTION
• BLOOD SUPPLY OF
BRAIN
• ANTERIOR CIRCULATION
• POSTERIOR CIRCULATION
• CIRCLE OF WILLIS
• VENOUS DRAINAGE
• BLOOD BRAIN BARRIER
• APPLIED ANATOMY
• CEREBRAL BLOOD FLOW IN
VARIOUS CONDITIONS
• ANEURYSM
• AV MALFORMATIONS
• CORTICAL VENOUS
THROMBOSIS
• STROKE
RELEVANCE
• POST STROKE
PSYCHIATRIC
MANIFESTATIONS
• Post Stroke Depression
• Pathological crying
• Post Stroke Catastrophic
Reaction
• Post Stroke Apathy &
Aggressiveness
• Post Stroke Mania &
Anxiety
• Post Stroke Psychosis
• Post Stroke Dementia
• FINAL NOTE
• REFERENCES
3. • The brain receives
about 15% of the
resting cardiac output
and accounts for 25%
of the body’s O2
consumption.
• The entire blood
supply of brain
depends on 2 sets of
branches from the
dorsal aorta.
• The vertebral arteries
from the subclavian
arteries.
• The internal carotid
arteries are the
branches of common
carotid artery.
5. 1. Vertebral Artery
Origin
Course
Branches
i. Post. Inf. Cerebellar A.
ii. Meningeal A.
iii. Posterior Spinal A.
iv. Small branches to
Medulla
v. Spinal branches
vi. Muscular branches to
deep muscles of neck
INSKULLINNECK
6. 2. Basilar Artery
Origin
Course
Branches
i. R & L Post. Cerebral A. – receive the Posterior Comm. A. of ICA to complete Circle of
Willis.
ii. Pontine A.
iii. Labyrinthine/Internal Auditory A.
iv. Ant. Inf. Cerebellar A.
v. Superior Cerebellar A.
7.
8. • The Circle of Willis is
formed by:
• Right & Left
Vertebrobasilar terminal
branch – Posterior
Cerebral Artery
• Right & Left ICA and its
branches –
• Middle Cerebral Artery
• Anterior Cerebral Artery
• Anterior Communicating
Artery (single)
• Posterior Communicating
Artery
10. Common Carotid Artery
Internal
Carotid A.
External
Carotid A.
1. Corticotympanic
A.
2. Pterygoid A.
3. Meningo-
hypophyseal
trunk
4. Inf. Cavernous A.
5. Capsular A.
6. Sup.
Hypophyseal
Artery
7. Ophthalmic A.
8. Post. Comm. A.
9. Ant. Choroidal A.
10.MCA
11.ACA
1. Sup.
Thyroid
Artery
2. Ascending
Pharyngea
l Artery
3. Lingual A.
4. Facial A.
5. Occipital A.
6. Posterior
Auricular
A.
7. Superficial
temporal
A.
8. Maxillary
11. • Origin
• Course
• Branches
i. Recurrent Artery of
Heubner/ Medial
Striate branch
ii. Ant. Communicating
A.
iii. Orbitofrontal A.
iv. Frontopolar A.
v. Callosomarginal A.
vi. Pericallosal A.
vii. Central branches
12.
13. • ACA supplies 2 main
functional lobes of
brain
Frontal Lobe
Parietal Lobe
15. • Origin
• Course
• Branches
A. Cortical Branches:
i. Lateral branch PCA
ii. Medial branch PCA
iii. Ant. Temporal Artery
iv. Post. Temporal Artery
v. Occipitotemporal
Artery
vi. Callosal Artery
vii. Calcarine Artery
16. B. Central Branches:
Posteromedial group
• Thalamoperforating
artery – to anterior 1/3
of thalamus,
hypothalamus, Globus
pallidus
Posterolateral group
• Thalamogeniculate
artery - geniculate
bodies and posterior
2/3 of thalamus.
• Branches to cerebral
peduncles and tectum
C. Choroidal Branches:
Posterior choroidal
artery – from PCA to
supply choroidal plexus
of lateral ventricle.
24. • Lateral to body of
sphenoid bone.
• Connected to opposite
sinus via intercavernous
sinus
• Receives blood from
Middle Cerebral Vein
• Drains into:
• Internal Jugular Vein via
Inferior Petrosal Sinus
• Transverse Sinus via
Superior Petrosal Sinus
• Dural Venous Sinuses
receive via Emissary
Veins from Extracranial
Veins.
26. • The cerebral endothelial cells
form tight junctions at their
margins.
• Foot processes from
astrocytes form a complex
network surrounding the
capillaries and this close cell
association is important in
induction and maintenance of
the barrier properties.
• In summary the BBB along
with other CNS barriers
together provide the stable
fluid microenvironment
that is critical for complex
neural function, and
protect the CNS from
chemical insult and
damage.
27. • Conditions which
cause dysfunction of
BBB
1. Stroke
2. Trauma
3. Infectious/Inflammator
y process
4. Multiple Sclerosis
5. Alzheimer’s Disease
6. Parkinson’s Disease
7. Epilepsy
8. Amyotrophic Lateral
Sclerosis
9. Systemic Lupus
NOVEL DRUG DELIVERY
SYSTEMS THROUGH BBB
Areas devoid of BBB
• Area Postrema
• Posterior Pituitary Gland
• Pineal Gland
• Median eminence of Hypothalamus
28. 1. Schizophrenia
• A review of regional cerebral blood flow (rCBF) studies in
schizophrenia shows the microvascular regulatory system may
be deficient, failing to selectively raise rCBF in areas of the
frontal and temporal lobes to respond to the physiological load
placed on brain.
2. Depression
• Studies suggest reduced rCBF in MDD, illustrated by
hypoperfusion in the frontal lobe, temporal lobe and limbic
system.
3. ECT
• Most of the above evidences are suggestive of definite changes in
rCBF following ECT in patients suffering from major psychiatric
disorders.
• During the ictal phase of ECT induced seizure, there occurs an up-
surge in blood pressure, consequently, there may occur gaps in
the continuity of BBB transiently, during which certain neuro-
chemicals may get released from circulation to brain parenchyma
29. • The word aneurysm comes from the Latin word
aneurysma, which means dilatation
Fusiform
Saccular
Dissecting
Ruptured
30. • Most Common Sites
1. Anterior
Communicating Artery
(30-35%)
2. Bifurcation of ICA and
Posterior
Communicating Artery
(30-35%)
3. Bifurcation of Middle
Cerebral Artery (20%)
4. Basilar Artery
Bifurcation (5%)
5. Remaining Posterior
Circulation Arteries
(5%)
• Risk Factors
a) Smoking
b) Hypertension
c) PCKD – 15%
prevalence
d) Coarctation of Aorta
e) Anomalous Vessels
f) Connective Tissue
Disorders
g) Vascular
malformations,
fistulae
h) Trauma
31. • Presents later in
childhood, more
frequently in adults in
2nd & 3rd decade
• C/F – Seizures,
Hemorrhage,
Progressive
Neurological
dysfunction or
Headache
• Complications
1. Hemorrhage into
surrounding tissue
2. Ischemia
3. Seizures
4. Brain cell death
• Diagnosis by MRI &
CT Cerebral
Angiography
32. • Cerebral venous sinus
thrombosis (CVT) is
clinically challenging and
mimics many neurological
conditions.
• Headache is the most
frequent symptom in
patients with CVT (80%).
• Recurrent Seizures and
Cranial nerve dysfunction is
seen with venous sinus
thrombosis.
• Psychiatric disturbances are
sometimes the presenting
symptoms
• The most common
neuroimaging finding was
hemorrhagic infraction
(84.3%), followed by non-
hemorrhagic infarction
(15.7%).
33. • Defined as a neurological impairment caused by
disruption in blood supply to a region of brain. It i
mainly of 2 types:
1. Ischemic Stroke
a) Athero-thrombotic infarction
b) Embolism
2. Hemorrhagic Stroke
34. • Identify 4 P’s
1. Parenchyma
2. Pipes
3. Perfusion
4. Penumbra
• CT Early Sign
1. Hypo attenuation of brain
tissue
2. Obscuration of Lentiform
nucleus
3. Dense MCA sign
4. Insular Ribbon sign
A core of irreversibly
infarcted tissue
surrounded by a
peripheral region of
ischemic but salvageable
tissue, without early
recanalization
36. • 15% of strokes are due to hemorrhagic infarcts
37. • Etiology:
i. Cardiac disease
ii. Large vessel disease
• Atherosclerosis
• Inherited metabolic
diseases
(Homocystinuria,
MELAS syndrome)
• Fibromuscular
dysplasia
• Infection
• Vasculitis (SLE, RA,
Sjogren syndrome,
PAN, Wegener’s
syndrome, IBD)
iii. Haematologic disease
iv. Migraine
v. Haemorrhagic – SAH,
Intraparenchymal
• Risk Factors and their
prevalence in Stroke in
Young
a) HTN, dyslipidemia,
diabetes : 45-60%
b) Smoking : 40-60%
c) Migraine: 10-35%
d) Pregnancy and
Puerperium: 5-10%
e) OCP: 10-22%
f) Illicit drug use: 3-12%
Important for PG viva exam
38. • Prevalence
Depression – 35%
Mania – Rare
Bipolar Disorder – Rare
Anxiety Disorder – 25%
Apathy – 20%
Psychosis – Rare
Pathologic affect – 20%
Catastrophic Reaction –
20%
• Neuropsychiatric
consequences of
stroke depend on
• Location & Size of
stroke
• Pre existing brain
pathology
• Baseline intellectual
capacity and functioning
• Age
• Premorbid Psychiatric
History
• Period of high risk for psychiatric
complications is 6 months following stroke
episode.
39. SYMPTOM NEUROANATOMICAL REGION
Depression Frontal Lobes, Left Anterior Frontal cortex, Anterior
Cingulate Gyrus, Sub genu of Corpus callosum, Basal
Ganglia, Left Caudate nucleus
Mania Inferomedial and Ventromedial Frontal cortex, Right
inferomedial Frontal cortex, Anterior Cingulate, Caudate
Nucleus, Thalamus & Temporo-thalamic projections
Apathy Anterior Cingulate Gyrus, Nucleus accumbens, Globus
pallidus, Thalamus
OCD Orbital or Medial Frontal cortex, Caudate nucleus, Globus
pallidus
Disinhibition Orbitofrontal cortex, Hypothalamus
Psychosis Frontal Lobes, Left Temporal cortex
40. • Prevalence varies overtime
with peak at 3-6 months
after stroke.
• Duration of major PSD – 9
months
• Spontaneous remission
can occur in 1-2 years post
stroke (Robinson et al)
• Causes of PSD –
Biopsychosocial factors
Biological – disruption of neural
circuits & neurochemicals,
Genetic cause
Psychological – presence of
poor coping skills
Social – disability, limited social
support, loss of independence
may overwhelm coping skills
• Diagnosis of PSD is difficult
due to
Language Disorders
Cognitive impairment-
anosognosia or lack of insight
Overlap between symptoms of
depression and medical
condition
• Left Prefrontal lesions are
more apt to be associated
with acute depression and
may be complicated by
aphasia, resulting in
inability to express
symptoms
41. • Also known as
emotional incontinence/
post stroke
emotionalism.
• Between 11-35% after
stroke (Parvizi et al.)
• Associated with
brainstem and
cerebellar lesions.
• Sudden paroxysms of
either laughter or crying
irrespective of ambient
mood state.
• Can be triggered by non
specific stimuli or low
Pseudobulbar Affect
• Defined as an emotional
disturbance that causes
uncontrollable crying or
laughing secondary to
stroke or any other
neurological condition
42. Post Stroke Mania
• Associated with right
sided lesions.
• Expansive or irritable
mood, decreased need for
sleep, increased goal
directed activity,
recklessness, disregard
for social constraints,
talkativeness, racing
thoughts, excessive
laughter or giggling, and
poor judgement.
Post Stroke Anxiety
• Majority also have PSD
• Associated with Right
sided lesions.
• Risk of Anxiety
Depression is 26% and
39% in men and women
respectively.
• More common in Cortical
than Subcortical stroke.
• Discrete episodes of
panic, tonic levels of
increased anxiety,
increased sweating,
worrying and decreased
sleep
43. Post Stroke
Catastrophic
Reaction
Outbursts of emotion,
that occurs when unable
to perform simple tasks.
Associated with PSD
and Basal Ganglia
lesions.
Maybe due to release
phenomenon due to
subcortical damage
Associated with
expressive aphasia
Post Stroke
Apathy
Presents with profound
lack of initiative without
tearfulness,
sleep/appetite
disturbances,
hopelessness, or
suicidality
Difficult to appreciate in
the absence of
depression
Post Stroke
Aggression
Associated with
increased motor
dysfunction and
dysarthria
Lesions in the area
supplied by the
subcortical MCA –
inability to control anger
or aggression.
Lesions nearer to the
frontal pole – irritability
and aggression.
44. • Rare complication.
• Include paranoia,
delusions,
hallucinations (visual
more common),
reference ideas,
disorganized thoughts
and regressed motor
behaviour.
• More prone to have
comorbid epilepsy.
• Psychotic episodes
can be a
manifestation of
complex partial
seizures secondary to
stroke.
• Correlate with right
sided lesions and
cortical/subcortical
atrophy
45. • Temporal relationship
between stroke and onset
of dementia.
• Stepwise progression of
cognitive decline.
• Evidence of
cerebrovascular disease
on examination.
• Small vessel disease is
most frequently observed
vascular pathology.
• Series of deep white
matter infarcts.
46. Unilateral
Sensorimotor
dysfunction.
Abrupt onset of
cognitive
dysfunction and
aphasia.
Difficulty with
planning, goal
formation,
organization and
abstraction
Cortical
Vascular
Dementia Affects
Fronto-subcortical
circuitry.
Results in
executive
dysfunction,
cognitive slowing,
difficulties with
abstraction,
apathy, memory
problems and
decreased ability
to perform ADL.
Subcortical
Vascular
Dementia
Changes in instrumental activities of daily living that require complex
organizational and problem-solving skills are more likely more prominent in a
patient with Vascular Dementia compared to Alzheimer's Disease
47. • Despite abundant literature available, unfortunately the psychiatric disorders
after CVA are often undiscovered clinically.
• It is therefore imperative for a clinician to screen, recognize and to monitor these
psychiatric symptoms for any progression on every follow up visit.
• Neurology and psychiatry should work in collaboration to address these
neuropsychiatric phenomena.
• There is also a need of extensive physical therapy and occupational therapy to
improve clinical outcome.
1. Kaplan & Saddock Comprehensive
textbook of Psychiatry 10th Edition
2. Adam & Victor Principles of Neurology
10th Edition
3. Clinical Neuroanatomy by Vishram
Singh
4. S Rizvi, Danish et al. Post Stroke
Psychiatric Syndromes. Psychol
Behav Sci Int J. 2018; 9(5): 555771
5. Martinelli I, Sacchi E, Landi G, Taioli
E, Duca F, Mannucci PM. High risk of
cerebal-vein thrombosis in carriers of
a prothrombin-gene mutation and in
users of oral contraceptives.N Engl J
Med 1998;338:1793-97.
6. Amit Singh et al. How Electroconvulsive
Therapy Works?: Understanding the
Neurobiological Mechanisms; Clinical
Psychopharmacology and
Neuroscience 2017;15(3):210-221
7. José M. Ferro, Lara Caeiro and Maria
Luísa Figueira ; Neuropsychiatric
sequelae of stroke ; Published online 11
Apr 2016 in Nature Reviews -Advance
Online Publication
8. Marta Tajes et al. The blood-brain
barrier: Structure, function and
therapeutic approaches to cross it; Mol
Membr Biol, 2014; 31(5): 152–167
9. Dorothy Sit et al. A Review of
Postpartum Psychosis; Womens
