Comprehensive Guide to Stroke: Definition, Types, Clinical Evaluation, and Localization

Name: STROKE LOCALIZATION | Dr. Archith Boloor
Uploaded: 2026-01-12T12:46:39.861108+00:00
Channel: THE WHITE ARMY
Description: Summary and key takeaways on Comprehensive Guide to Stroke: Definition, Types, Clinical Evaluation, and Localization, covering Introduction Stroke is an acute
THE WHITE ARMY
Jan 12, 2026
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5 min read
YouTube video ID: Y6nUTCjPUyw
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Introduction

Stroke is an acute or rapidly progressing focal neurological deficit of vascular origin. The WHO defines it as a neurological deficit that cannot be explained by any non‑vascular cause.
It can involve the cortex, subcortical regions, brainstem, cerebellum, or spinal cord, but the classic exam scenario focuses on hemiplegia.
Two Core Questions in Every Neurological Case

Nature of the illness – Is the stroke ischemic (thrombotic or embolic) or hemorrhagic?
Site of the lesion – Where in the nervous system is the damage located?
A thorough history can provide up to 90 % of the diagnosis; examination confirms it.
Types of Stroke

Category	Sub‑types	Typical Frequency (overall)
Ischemic	• Thrombotic (≈80 %) • Embolic (≈15 %)	8 : 1 : 1 ratio (thrombotic : embolic : hemorrhagic)
Hemorrhagic	• Intracerebral hemorrhage (ICH)	1 : 1 with embolic
Age‑related patterns - Elderly (>45 y) – Thrombotic strokes dominate. - Young (<45 y) – Embolic strokes become most common (≈4 × thrombotic), followed by thrombotic and then hemorrhagic.
History Elements that Point to the Stroke Type

Timing of onset
Thrombotic: Often wakes the patient up with symptoms (≈4 a.m.) due to a hyper‑coagulable morning surge (high plasminogen‑activator inhibitor).
Embolic / Hemorrhagic: Occur during activity; patient is awake when deficit appears.
Deficit at onset
Embolic: Maximal deficit immediately; no progression.
Thrombotic: Deficit evolves step‑wise (core + penumbra).
Hemorrhagic: Progression due to edema; may be accompanied by headache, vomiting, or signs of raised intracranial pressure.
Progression – See above.
Key Risk Factors

Non‑modifiable: Age, male sex.
Modifiable: Hypertension (95 % of hypertensive strokes are thrombotic), diabetes, dyslipidaemia, smoking, alcohol, post‑menopausal status.
Pro‑thrombotic states (young patients): Pregnancy, antiphospholipid syndrome, protein C/S deficiency, factor V Leiden, oral contraceptives, polycythaemia, leukocytosis, hyper‑homocysteinaemia (often B12 deficiency), malignancy, HIV, TB.
Embolic sources: Cardio‑embolism (atrial fibrillation, rheumatic heart disease) – most common in <45 y; Athero‑embolism from carotid plaques – more common in older adults.
Hemorrhagic triggers: Uncontrolled hypertension, amyloid angiopathy (lobar bleeds in the elderly), intracranial aneurysms (sub‑arachnoid), AV malformations (young), anticoagulant/antiplatelet therapy.
Localization of Hemiplegia

Site	Typical Features	Vascular Territory
Internal capsule	Contralateral dense hemiplegia (equal arm & leg weakness), contralateral UMN facial palsy, contralateral hemisensory loss, homonymous hemianopia (if optic radiations involved)	Lenticulostriate branches of MCA, anterior choroidal, posterior communicating arteries (all end‑arteries)
Cortex	Non‑dense hemiplegia (upper‑limb‑dominant brachial or lower‑limb‑dominant crural), aphasia (dominant left cortex), apraxia (non‑dominant), seizures, possible facial palsy (UMN type)	ACA supplies medial leg area; MCA supplies lateral face/arm area
Subcortex (watershed)	Variable motor deficit, often without cortical signs; may present with pure motor or pure sensory lacunar syndromes	Border zones between ACA/MCA or MCA/PCA
Midbrain	Contralateral hemiplegia + ipsilateral third‑nerve palsy (Weber syndrome); possible red‑nucleus tremor, ataxia	Posterior cerebral artery (PCA) branches
Pons	Contralateral hemiplegia + ipsilateral facial (LMN) palsy ± abducens palsy (Millard‑Gubler syndrome)	Basilar artery perforators
Medulla	Medial medullary syndrome: contralateral hemiplegia, ipsilateral tongue weakness (CN XII), internuclear ophthalmoplegia, contralateral loss of proprioception. Lateral medullary (Wallenberg) syndrome: ipsilateral facial pain/temp loss, contralateral body pain/temp loss, Horner’s syndrome, dysphagia, hoarseness, ataxia, hiccups.	Vertebral artery (lateral) or PICA (medial)
Cervical spinal cord (≥C4)	Ipsilateral hemiplegia (same side as lesion) affecting both arm and leg; often due to trauma or rare vascular occlusion.	Anterior spinal artery
Special Terminology

Dense hemiplegia – Equal arm and leg weakness; points to internal capsule involvement.
Brachial hemiplegia – Upper‑limb predominance.
Crural hemiplegia – Lower‑limb predominance.
Crossed vs. uncrossed hemiplegia – Determined by lesion relative to the pyramidal decussation (above = crossed, below = uncrossed).
Cruciate hemiplegia – Rare lesion at the decussation producing opposite‑side arm/leg weakness.
Brain‑Stem Syndromes at a Glance

Weber (midbrain): Contralateral hemiplegia + ipsilateral oculomotor palsy.
Millard‑Gubler (pons): Contralateral hemiplegia + ipsilateral facial (LMN) and abducens palsy.
Medial medullary: Hemiplegia, tongue deviation, internuclear ophthalmoplegia, loss of proprioception.
Lateral medullary (Wallenberg): Ipsilateral facial pain/temp loss, contralateral body pain/temp loss, Horner’s, dysphagia, ataxia, hiccups.
Imaging and Management Pearls

CT scan – First‑line, rapid (≈5 min) to rule out hemorrhage; may miss early ischemic changes.
Diffusion‑weighted MRI – Gold standard for detecting acute infarct within minutes; guides thrombolysis.
Blood pressure – In acute ischemic stroke, avoid aggressive lowering (maintain MAP to perfuse penumbra) unless BP > 220/120 mmHg or thrombolysis is planned (target <185/110 mmHg).
Thrombolysis – Recombinant tissue plasminogen activator (rt‑PA) given within 3 h (up to 4.5 h in selected patients) after ruling out bleed.
Hemorrhagic stroke – Manage intracranial pressure, reverse anticoagulation, control BP aggressively.
Stroke Mimics

Migraine with aura, hypoglycaemia/hyperglycaemia, electrolyte disturbances, seizures with post‑ictal paresis (Todd’s paralysis), brain tumours, cerebral venous thrombosis, functional (psychogenic) hemiplegia.
Key Take‑aways for Clinical Practice

A focused history (time, activity, deficit pattern) narrows the stroke type.
Recognize the pattern of motor and sensory loss to localize the lesion (internal capsule → dense hemiplegia; cortex → non‑dense, aphasia/apraxia; brain‑stem → crossed signs).
Know the vascular territories (anterior circulation = ACA/MCA/Kerotid; posterior = vertebro‑basilar) to anticipate imaging findings.
Early imaging (CT → MRI) determines eligibility for reperfusion therapy.
Manage blood pressure judiciously and be aware of contraindications to thrombolysis.
Always consider stroke mimics; a normal MRI/CT with transient symptoms may represent a TIA (symptoms <1 h, no infarct).
Accurate history, recognition of characteristic motor‑sensory patterns, and knowledge of vascular anatomy allow clinicians to pinpoint the stroke type and lesion site without needing to view the original video, guiding timely imaging and appropriate acute management.
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Full Transcript YouTube

So this is the common neurological
disease that you encounter and you do
get this in your exams. So by definition
the definition of
stroke stroke is an acute onset or a
rapidly progressing. So it's an acute
onset of disease. So it's an acute
disease and it could be a focal
neurological deficit. Very rarely stroke
can produce a global deficit and the
ethiology for stroke is vascular.
So when we talk about the ethiology of
stroke it is vascular. So when we mean
stroke it's a acute onset of a focal
neurological deficit that can be due to
a vascular ethiology. So when you see
the WH definition the WHO when it
defines stroke it says that it is a
focal neurological deficit that cannot
be attributed to anything other than
vascular. So they do not use it as
vascular. they say it cannot be anything
other than vascular that is called as
stroke. So by meaning when we have a
stroke we are dealing with a basic
problem in the vascular problems in the
uh central nervous system that we're
talking. So it's a um disease we are
talking it can affect various parts of
the brain. It can affect the cortex. It
can affect the subcortical regions. It
can affect the brain stem and also the
spinal cord also can get involved in
stroke. But the classical uh discussion
when we go on to uh a stroke when we are
discussing we are basically discussing
about
hemiplegia. So this is the case that is
usually kept for you in the exam
hemoplegia. So they keep a case with
hemoplegia and you are expected to do
the evaluation take a good history and
do examination and come about to what is
the cause for hemiplegia and why this
structural abnormality has occurred in
this patient. So whenever we give a
neurological case the two questions that
are always to be answered is one is the
nature of
illness what is the nature of the
disease and second is the site of
illness or the site of lesion. So these
are the two things that we have to uh
arrive when we take a history and
examine and please remember in nervous
system examination or nervous system
history uh good history can give you a
90% diagnosis. you have to just do a
examination to confirm your diagnosis.
So a good history would give you the
diagnosis uh in almost complete
diagnosis can be given. So when we mean
by the nature of the illness as we said
the cerebrovascular accident is always
going to be a vascular ethiology. So the
problem is in the vessel. So the two
types of problems can happen. So it
could be either due to
eskeeia or it could be due to a
hemorrhage. So it could be due to an
eskeemic stroke or a hemorrhagic stroke.
By far the large amount of strokes that
we have are eskeemic strokes only. So if
you go on to the ethiology of eskeeia
the basic two categories that could come
under eskeemic stroke either you have a
thrombotic
stroke or you have an emolic stroke. So
these are the two ethiologies that come
under the eskeemic stroke. The
hemorrhagic strokes basically are the
intra cerebral
hemorrhages. So these are the three
varieties of stroke. If you say a
natural uh stroke which we are seeing in
elderly if you see the ratios of these
two disease these three diseases the
thrombotic strokes is eight times more
common emolic and uh the hemorrhage is
one time that common. So if you take 10
strokes if you see the ratio is 8 is to
1 is to1. So thrombotic strokes by far
is the commonest stroke that you would
get as you go in the elderly. But if you
see a younger patient, we call it a
stroke in young. Stroke in young is
whenever the stroke is less than 45
years of age. If you see the ratio in
such observations, the most common
stroke that you get in young strokes is
emolic strokes. That's almost four times
there. Thrombotic strokes would be
second followed by hemorrhagic strokes.
So the ratio changes there. So it's not
only important for us to just know about
the thrombotic strokes with the advent
of lot of diseases metabolic diseases
that have come your young strokes are
becoming more and more common. So we
have to also consider these two other
ethologies of stroke. So to know the
ethology of stroke or the nature of
illness the most important thing that
would come into is the history itself.
So you should have a good enough history
and based on that history you'll be able
to get a reasonable diagnosis about what
is the nature of illness. So when we say
the nature of illness it's a whole class
on itself when we take uh the nature of
illness. But I think in today's session
since we are discussing localization I
will briefly touch about uh how do you
assess the nature. So the first question
that you're going to ask is timing of
the stroke. So what time did the stroke
happen? That's the first question. The
second question is deficit at
onset. Deficit at onset. And the third
important question is progression of
deficit. So these are the three
questions that you have to very very
carefully concentrate on in your history
which will help you to localize the type
of stroke that you have. So if you take
the thrombotic strokes, if you see the
thrombotic strokes, the thrombotic
strokes occur early morning. So 4:00
a.m. is the time when thrombotic strokes
happen. Now why does this happen? Why
the blood is more prothrombotic at 4:00
a.m. in the morning? Remember
hypercogability is what makes it and we
have various factors. The main factor
that you have is something called as a
plasmogen activator inhibitor. The
levels of which govern the stroke
happening. So that is the reason why all
thrombotic event be it uh thrombotic
stroke be thrombotic MI or any other
thrombosis occurs at 4:00 in the
morning. So the thrombotic strokes the
patient will wake up with the stroke.
That's very important you have to
remember. Whereas the emolic stroke and
the hemorrhagic stroke both occur during
activity. So both uh emolic as well as
the hemorrhagic stroke there is activity
that is needed only with the activity it
will come. So they don't occur at sleep.
So that's the first question that you
have to ask when did the stroke occur?
What was the patient doing? So if he was
doing something and all of a sudden the
stroke has happened so it's more likely
to be an emolic or hemorrhagic stroke
but yes if the patient woke up with a
neurological weakness then it's more
likely to be a thrombotic stroke. You're
most often right based on the timing.
Second important part you have to ask in
history is
the deficit at onset. Now remember
emolic stroke the deficit is maximum at
onset. So the patient gets a deficit
that will be the maximum at onset. So
the deficit will be maximum. If they
have a hemiparasis or a hemiplegia they
have it they have it maximum at onset.
There is no progression of deficit.
Whereas in contrast in thrombotic
strokes there is a nice stepwise
progression of stroke what we call it as
a stroke in progression. I think the
ethophysiology would have known there is
an eskeemic core surrounding which we
have a eskeemic penumbra and that gets
affected that's why the deficit
progresses. So there is a progression of
deficit which is very characteristically
seen in case of thrombotic stroke
because the region that is the pis
eskeemic penumbra which is surrounding
that also gets involved. What happens in
hemorrhagic? Remember when blood comes
out of the vessel it produces a lot of
edema. So whenever there is so much of
edema that's happening again the deficit
will progress. Okay. So remember the
deficit is maximum at onset in emolic
stroke. So based on these two questions
you can make out what type of stroke it
is. Supposedly a patient has woken up in
the morning and he says he went to the
washroom he was having slight weakness
there. Then he came back and slept. By
the time he woke up again he had more
weakness. By another one hour he had
facial weakness there. And by another
two hours the patient had complete
hemoplegia and he was not able to walk.
So that is the classical thrombotic
stroke. Whereas if a patient was doing a
work and all of a sudden he falls and
then he has complete weakness on one
side complete loss of weakness that is
emolic stroke. So that occurs during
activity. Hemorrhagic stroke. The other
important feature which almost always is
there there are signs of raised
intraranial tension. Patient can have
headache. Patient can have projectile
vomiting that could be there. So that if
it is there would suggest more of a
hemorrhagic stroke but please remember
the raised intraranial tension can also
occur when you have a large eskeemic
region. So it's not uh specific for
hemorrhagic stroke but yes if it is
there in a patient then it's more likely
to be a hemorrhagic stroke. The other
important factor that you have to always
remember when you tell the type of
stroke is the risk
factors. So based on the risk factors
you can localize what type of stroke or
what type of stroke that we are having.
Now supposedly we are talking about the
commonest stroke that's a thrombotic
stroke. So most important non-modifiable
risk factor
age and male gender. So these are two
important non-modifiable risk factors
that you have for thrombotic stroke. So
thrombotic strokes this is the important
thing. The other important risk factor
for thrombosis please remember
hypertension. Again a very common
question they ask you is hypertension.
What type of strokes do you get?
Remember the most common type of stroke
in hypertensives is thrombotics. 95% of
the strokes in hypertensive is
thrombotics. But yes please remember
hemorrhagic strokes are almost always
seen in hypertensives. But the most
common type of stroke that you get in
hypertensives is thrombotic. The other
important risk factors for thrombosis
diabetes. If the patient has
disipidmia, if the patient has
uh
smoking,
alcohol, post-menopausal females are the
risk factors for that. If a young
patient is getting thrombosis,
supposedly he's less than 45 years and
he's developing thrombosis, that's when
you have to consider a pro-thrombotic
state. Anybody in the chat can answer
what are the common proth thrombotic
states that we
have? People can unmute and answer. Is
it possible?
Yes sir, it's possible sir. Yeah.
Anybody? One of you can unmute and
answer because sir pregnancy. Okay.
Pregnancy. Yes. Okay. Pregnancy is a
prothrombotic state. But more important
when we talk about prothrombotic we
don't say nothing physiological.
Pregnancy is
physiological. Any other
protid antibodies thrombophilia. Okay.
So antifhospholipid antibbody syndrome.
Thrombophilas as you said there are
thrombophilas where you have
deficiencies of certain factors. OCP
pills. Yes. OCP pills is correct.
Remember the polyythemeia polyythemia is
an important risk factor. Leukemas are
important risk factors and again
remember there are uh inflames of
inflammation of the vessel can happen as
the yeah vasculitis. Okay. Vasculitis
could occur either primarily due to a
vascular disorder or more importantly we
have two infections that are common in
our part which produce vasculitis.
Anybody? What are those two infections
where you have vasculitis? Syphilis.
Syphilis is the disease of the past. We
don't see it now that often. Hepatitis B
and C. No, that is common. I do agree.
Two important diseases which produce a
stroke
infections. I was talking about two
infections. Polyarteritis. No doer.
That's connective. That is a connective
tissue disorder. We're talking about
infections which produce vasculitis.
Okay. HIV. HIV. Please remember HIV and
tuberculosis. These are two common uh
infections. Again, we see it very often.
Both of these infections can produce.
Okay. Both of these infections produce
uh vasculitis and they produce strokes.
So when you see a thrombotic stroke in a
young patient, we have to think of
prothrombotic states. So get the blood
counts and then see if there is
polyythemia, thrombocytosis etc. And a
very common disorder especially in India
what you get is related to an amino
acid. Anybody can tell
me hyper homocyine. Yes very important
hyper homocyinemmia and also remember
it's common in pure vegetarians because
vitamin B12 deficiency produces hyper
homocyinemmia. So these are the causes
of thrombosis. So these are the risk
factors that you'll assess for whenever
there is thrombosis. Now if you come to
the second ethiology which we discussed
is
emolism. So emolism the clot has to
arise from somewhere and go. So the two
important sites it can arise from one is
the heart called as the cardio
emolism and the second more often is
from the vessels itself called as
etherolism. So from a large vessel
kerotid or the iotites arising the clot
or the plaque which can dislodge and it
can go and cause emolic strokes. So
again remember in young patients it is
more often cardioism that we're looking
for whereas in uh patients who are older
part of it you can see it is more of
aolism. So older patients get
atheromolism whereas younger patients do
get cardioism. So younger patients you
would most importantly ask for history
of rheumatic heart disease or you can
ask for histories of uh uh atrial
fibrillation. And please remember the
most important cause of cardiamolism is
atrial fibrillation. So you will have to
take history of that in the patient. So
young patient amolic stroke cardiamolism
elder patient emolic stroke is
atheromolism. The third type of stroke
is hemorrhagic strokes.
Again remember hemorrhage can occur in
younger patients can occur in older
patients. Older patients the most
important ideology is
hypertension. Uncontrolled hypertension.
Please remember not any hypertension.
Remember hypertension I told you is the
most important risk factor for
thrombosis. But when you have an
uncontrolled hypertension that's where
you can get hemorrhage. Also you have uh
elderly patients can have one more
common disease in elderly which can
produce hemorrhage. Anyone can tell me
which is the other disease we get if a
85 year old person comes with
hemorrhage. Aneurysms are common in
young patients not subdural hematoma.
Subdural hematoma is not a it produces
symptoms like stroke but that doesn't
classify as stroke. You don't call it a
stroke which is the other disease which
happens as you age which is the other
degeneration that happens in the vessels
which can make them bleed. Uh highin
degeneration of the highin degeneration.
Okay. Okay. It's something like highin
degeneration what we call it as an
amiioid angopathy. So remember
hypertension and amioid andopathy are
the two important diseases which occur
in elderly which produces hemorrhage. So
one yeah one thing that you to always
remember is hypertension never produces
hemorrhages into the loes. Please
remember hypertension produces
hemorrhages at various sites but it does
not produce hemorrhages in the various
loes. The most common site of
hypertensive bleed is the basil ganglia.
So it goes to the basil ganglia. It can
go to the putamin as the commonest site
there. It can go to the pawns. it goes
to the
thealamus and
cerebellum. So 90% of hypertensive
bleeds occur at this site. It never
comes to the lobe. Okay? Very very
rarely you can get lowar hemorrhages.
But in contrast amoid causes lowbar
hemorrhage. Lowbar hemorrhage. So uh
this is what you have to remember for
hemorrhage in elderly persons. You can
get aneurysms. Okay. But again remember
the aneurysms. Where are the aneurysms
located? Where are the aneurysms
located? Circle of vis. Circle of phis.
So where is the circle of vis located?
Inside the brain or outside? Inside.
Outside.
It's in the base. Now it is not inside
the substance of the brain. So if there
is aneurysmal bleed, what type of
hemorrhage do you produce?
What type of hemorrhage? It produces
subaractid hemorrhage. Okay. It doesn't
produce intraerable hemorrhage. produces
subarnite hemorrhage. If you see younger
patients coming with hemorrhage, the
most important ethiology in young
patients which produce hemorrhage are AV
malf formations. Okay, AV malfformations
are the most common ethiology of
hemorrhage in young patients. Also
remember patients who are on
antiplatelets,
anti-coagulants and certain other drugs
can produce hemorrhage. So these are the
risk factors that we have to understand.
So what we discussed so far is to get to
the nature of the illness. So to see
what is the disease that we are talking
about the nature of the illness is
governed by a good history and the risk
factor analysis. Hope I'm clear so far.
So take a good history. The two
important questions which I told you is
the timing of the onset of the
neurological weakness the patient is
having. Second is what is the
progression? Whether there is maximum at
onset or it does progress. Next is the
risk factor analysis. So based on these
two things you can make out whether we
are dealing with thrombosis, we're
dealing with emolism or we are dealing
with a hemorrhage.
Next the most important part and the
point of today's discussion that we
are discussing that is
the localization or where is the disease
we are talking about. So localization of
stroke or what we call it as the site of
lesion. So as we discussed hemiplegia,
we're talking about hemiplegia only in
today's discussion. I'm not going to
describe the other neurological
problems. I'm going to discuss only
about hemiplegia. By meaning uh the word
hemiplegia means there is involvement of
the upper limb and lower limb on one
side of the body on one side of the body
that is hemoplegia. What do you mean by
hemiparasis? And what do you mean by
hemiplegia? Hemoplegia means the power
is 0 by five. Whereas hemip parasis
means it is not 5 by five. So it is
lesser than it might be four, it can be
three, it can be two but it is not zero.
So when you say hemiplegia it is
complete paralysis and when we say
hemiparasis it means a partial weakness
partial weakness but it is one side of
the body. That is what you have to
remember. The next term that you have to
remember whenever we discuss hemiplegia
is the term what we call as dense
hemiplegia. Now this is a very important
term that you have to understand what do
you mean by dense hemoplegia? Anybody
can tell
me what is dense hemoplegia? Both upper
limb and lower limb weakness that is
there in any hemoplegia. Same grade of
weakness in both upper limb and lower
limb weakness in upper limb and lower
equal weakness very important. So dense
hemiplegia means upper limb is equalent
to lower limb. So the power of upper
limb and the lower limb is equally
involvement that's when we call it as
dense hemiplegia means zero. So both are
zero by five part that when we say dense
hemiplia we can say dense hemiparasis if
it is 3x 5 or in both upper limb and
lower limb. If supposedly the upper limb
is 3x5 but the lower limb is 0x 5. This
is not dense where the upper limb is uh
less involved and the lower limb is more
involved. That does not become dense. So
when we say dense it means upper limb
and lower limb are equally involved. Now
what's the importance for us to
understand whether it is dense he
semipllegia or not? Please remember
dense he semiplegia always means
internal capsule involvement.
Now why does internal capsule
involvement produce dense hemiplesia?
Please remember internal capsule is a
very small area that's there and the
entire corticpinal tract which supplies
the entire one half of the body is
located in that very very very small
area. So it's a very small area and at
the genu and the posterior limb of the
internal capsule the pyramidal tract is
one which is going to go down and that
small area all the fibers are there. So
that is if that part is involved both
the upper limb and lower limb will get
involved equally and that is what we
call it as dense hemiplegia. So dense
hemiplegia is pathogammonic of internal
capsule leion. Okay, internal capsule
leion is the one which produce dense
hemipleia. All other types types of
lesions do not produce dense hemiplasia.
Sometimes you could have upper limb
which is more involved. Sometimes you
can have lower limb that is more
involved. If upper limb is more
involved, we call it as brachial
hemiplegia. So brachial hemiplegia means
we have a hemoplegia but the upper limb
is more involved than the lower limb.
Whereas if the lower limb is more
involved than the upper limb, we call it
as crural
hemoplegia. Okay. So if the upper limb
is more involved, we call it as brachial
and if the lower limb is more involved,
we call it as crual hemiplia. So that's
the first term that we have to
understand that is what is dense
hemiplegia and what is not dense
hemiplegia. The next point that you have
to understand is what is crossed
hemoplegia.
Sorry. What is crossed
hemiplegia and what is uncrossed
hemiplasia? Yes. Anybody can tell me
when lower level of pawns is involved
then it is a cross hemiplasia. If it is
above that then it is. Now what do you
mean by crossed? The cytoion I agree
it's in the not in the pawns it's below
the medula. Ipsilateral ipsilateral
facial and qualateral. weakness of the
lower. It's not necessarily facial. It's
not necessarily facial.
So remember the pyramidal tract if you
see the pyramidal tract is arising from
the cortex and from there the pyramidal
tract comes down. It goes through the
internal capsule goes to the midbrain
pawns at the lower part of the medula
it's going to decate and go to the
opposite side. So supposedly you have a
lesion on this side on the right side.
I'm talking here the hemoplegia will
always be on the left side. So you have
one-sided involvement the lesion will be
the hemoplegia will be on the opposite
side but supposedly if you have a lesion
below the decarcation okay you have a
lesion below the decarcation you will
have hemiplegia on the same side so
leftsided leion leftsided hemoplegia now
you have the cranial nerves so you have
various cranial nerves that are there so
supposedly we can take an example of one
of the cranial nerves like third cranial
nerve so if I say third cranial nerve
It's located somewhere in the midbrain.
Here you have the 12th cranial nerve
that's located in the medula there. So
supposedly you have a lesion above the
decassation above the decassation. So
decisionation is here the cranial nerve
will be on one side the hemiplegia will
be on the opposite side. But if you have
a lesion below the decarcation that's
specifically for the 12th nerve the
cranial nerve and the hemoplegia will be
on the same side. So the word crossed
and uncrossed basically refers to the
decassation. So if you have a lesion
above the decision you do get crossed
hemiplegia. If you have a lesion below
the decassation you get uncrossed
hemiplesia. So these are some of words
that you have to remember. Supposedly
sometimes in the MCQs or sometimes if
you answer well they'll ask you if if
you have the lesion at the decision what
sort of hemoplegia do you get?
Please repeat. Okay. So, okay. You want
me to repeat what is crossed and
uncrossed? Okay.
So, okay. Let me draw the pyramidal
tract for you. So, here is the right
sided cortex. Here is the leftsided
cortex. And here the pyramidal tract is
arising from the cortex. Okay? And there
the pyramidal tract enters through the
internal capsule. And there it goes down
to the cortical spinal tract. It goes
through the midbrain. It goes to the
pawns and comes to the medula. At the
lower part of the medula, it is going to
decate and go to the opposite side. Is
that clear so
far? Okay. So if you have a lesion above
here, supposedly I have a leion here.
So if I have a lesion here on the right
side if I'm taking a lesion
there hemoplegia will be on the left
side because the decarcation is here but
supposedly I take a lesion here in the
lower part of the medula here after the
decarcation leftsided leion will produce
leftsided hemipleia whereas right sided
leion will produce rights sided
hemiplegia is that much clear so far
okay now coming on to the cranial nerves
that are there now supposedly you have
the various cranial nerves you know that
the third and fourth cranial nerves are
located in the midbrain. The 5 6 7 8 are
located in the
pawns. The 9 10 11 12 are located in the
medula. So this is the cranial nerves
that is arranged. So supposedly I take a
leion at the
midbrain. Okay, I'm taking a median in
the right sided midbrain. So what
happens? The right sided cranial nerve
getting involved. So the cranial nerve
is on the right side. Which side is the
hemoplegia? It's not yet crossed. So the
hemoplegia is on the left side. Is it
clear? So cranial nerve is on one side.
Hemiplegia is on the opposite side. Now
if I take a lower lower part of the
medula where the decursation has already
occurred. The most common cranial nerve
that's located is a 12th cranial nerve
there. Now if I take the lesion and this
side so I'm taking a right sided lesion
I'm taking here. So already decation has
happened there. So the hemoplegia will
be on the right side. The cranial nerve
also 12th cranial nerve is also on the
right side. So this is uncrossed
hemoplegia and this is crossed
hemiplegia. So above the decarcation you
have cranial nerve on one side and
hemoplegia on the opposite side. Whereas
below the decarcation if at all you'll
have the hemoplegia and the cranial
nerve on the same side. That's what we
call it as crossed and uncrossed. It's
basically for the brain stem only
because crossing we know occurs at the
brain stem. So all your internal capsule
uh cortical lesions all are uncrossed.
All are crossed hemoplegias only. Only
the brain stem lesions can be crossed or
uncrossed. If it is crossed that means
it's above the decarcation. If it is
uncrossed it becomes below the
decarcations. Hope I'm
clear. The question that I'd asked I
think somebody answered in the chat.
What do you get if you have a lesion at
the decarcation? So if you have a lesion
at the decarcation what you get is the
what you get is something called as a
cruciate
hemoplegia. So cruciate hemoplegia is
the one you get at the decation you get
one-sided upper limb the opposite side
lower limb. So if you have rights sided
upper limb the left lower limb will be
involved. So it's like a cross that's
because of the fiber arrangement. So
that's a question that's asked if
supposedly you answer all questions they
ask you what do you get that so you get
crucial hemiplegia at the sight of
decision it's rare to get that because
generally you get quadriplegia at that
site so the terms that we have described
so far we described what is hemoplegia
what is hemiparasis then we described
what is dense hemiplegia then we
described what is brachial hemiplegia
then we described what is coral
hemiplegia and then we described about
the term that is crossed or uncrossed
hemiplia. Hope I'm clear so
far. Okay, we'll proceed. Now coming on
to hemiplegia and its localization. So
when we say hemiplegia when a patient of
stroke is given to you, what are the
sites of hemoplegia that you could have?
So
hemiplegia can occur at various sites.
Okay. The first and the most common site
that we encounter hemiplegia is internal
capsule. So internal capsule is the
commonest site of hemiplegia that you
have. The second site is above the
internal capsule what we call it as the
cortex. The third site could be in
between the internal capsule and the
cortex what we call it as a subcortex.
The next site are the brain stem. So in
the brain stem you have three important
sites that is the
midbrain, the
pawns and the
medula. So the midbrain pawns and medula
and the last site is the spinal cord.
The cervical spinal
cord above C4.
Now let's understand this a little more.
Remember internal capsule is the most
common site followed by the cortex then
the subcortex midbrain pawns medula.
These together form the brain
stem brain stem. So these are the sides
of hemiplegia. Okay. If there is
hemoplegia it has to be one of these
sides. Okay. Why do I say cervical
spinal cord? Why can't a thoracic or
lumbar spinal cord cause it? Because
remember the upper limb fibers. The
upper limb fibers are given. What is the
upper limb topmost root value? Deltoid
is C5. So above that. So C4 is where the
upper limb fibers are given. So
supposedly the upper limb fibers are
given already. If the upper limb fibers
are given after that you can't get
hemoplegia. You can only get lower limb
weakness. So you can get hemiplegia in
the spinal cord disease if the level is
in the cervical cord above C4. So these
are the sites of hemiplegia.
that you can get in your exams. So what
we have to understand is how do we
localize each of these sides of
heiplesia.
Okay. So uh before we go on to that just
remember we could the internal
capsule the internal capsule the cortex
and subcatics belongs to something
called as an anterior
circulation. Anterior
circulation. What do you mean by
anterior circulation?
Anti-irculation stands
for what vessel anterior
circulation is the keroted and its
branches. So the internal capsule cortex
and subcortex belongs to anterior
circulation the keroted circulation.
Whereas the brain stem and the spinal
cord belong to your posterior
circulation which is nothing but
vertebra basilar. So vertebro basilar
this is what you have to understand.
Yes. So keroted circulation includes
both ACA and MCA whereas basilar
includes the vertebral the basil that's
coming and the branches of that. So
let's move further and we'll try to
localize and tell what are the features
of each of these strokes that we could
get. So before we go on to that we
should know the functional anatomy of
the nervous system or how the fibers are
arranged. So let's briefly discuss that
now. So as we discussed all your
pyramidal tract is going to start from
the cortex. So this is the cortex I'm
drawing here. So this is the
midline. So this is the cortex. So the
bed cells the post central gyus where is
there your motor homunculus there from
the bet cells the pyramidal tract is
going to originate. So the pyramidal
tract is going to originate from there
from all these tracks here coming down
as the corona radiator and it converges
onto the internal capsule. So that's
the most important site that we have. So
that's the internal capsule. So these
fibers are going to converge at the genu
and the posterior limb of the internal
capsule. From there it's going to form
the pyramidal tract and it's going to
come down medially. It comes down
through the
midbrain. Then it's going to come down
through the pawns and then it's going to
come down through the
medula. So it's going to come down
medially from the uh midbrain, the
pawns, the medula and the lower part of
the medula. That's where it's going to
cross over and go to the opposite side
spinal cord. It's going to form the
anter antrolateral corticospinal
tract. So this is how our pyramidal
tract is originating. So you have the
pyramidal tract on both sides. You have
it on the right as well as you're having
it on the left. So if I can draw the
leftsided pyramidal tract also would
come like that and go down decate here
and go to the spinal cord. So this is
how the pyramidal tract is getting
involved. So we can have a lesion
anywhere starting from the cortex.
Here the next important site we have
discussed is the internal capsule.
That's the second site that we have.
Between the internal capsule and the
cortex you have the subcortics as a
site. You can have a leion in the
midbrain, the pawns, the
medula and the cervical spinal cord
above C4. So these are the sites where
you can get hemiplia. So how do we
localize each of these sites? Because
hemoplegia is there in all the sites. So
how do you localize this each of these
sites? Basically it is by the company
the hemoplegia keeps. So what is there
along with the hemiplegia? So hemiplegia
plus what else is there that helps us to
decide where is the site of lesion.
Okay. So before we go on to actual
localization a little more brief on the
anatomical part of
it. You have the cranial nerves as uh I
think you would have learned in your
anatomy or in your neuroanatomy. There's
something called as a rule of fours.
Anybody can tell me what is the rule of
four? For cranial nerves you have
something called as a rule of
four.
So anybody
[Music]
orig from midbrain four 5 6 7 8 third
and fourth from midbrain uh 5 6 7 8 from
pawn and 8 and 10 12 from medula okay so
that's the uh one one of the rules so
there are four rules of gates described
four rules
Four rules here is described. So the one
is the cranial
nerves. Four originate from the
pawns. Four above and four below. So the
ones which are originating from the
pawns as you have described it five 6 7
and 8. The ones which is arising from
the medula is 9 10 11 and 12. And the
one which is arising from above that is
third and fourth will come from the
midbrain. However, you have your uh
uh one and two is direct communication.
So there is no nucleus that is there for
one and two. Three and four have their
nucleus in the midbrain. So that's the
first rule of uh gates. The second rule
of gates is very important for us for us
to localize the hemoplegia because uh
gates based on this rule only we can
make out where is the site of lesion of
this cranial nerves only four cranial
nerve located
medially. Remember in the diagram which
we drew here for
the
sorry for the uh pyramidal tract we have
drawn it here you can see that the
pyramidal tract is located medially in
the brain stem it's located medially so
only four cranial nerves are located
medially which are the four cranial
nerve nucleus which are located medially
3 6 12
okay one more and four and four and four
So 3 4 6 and 12.
Yeah. 3 4 6 and 12 are the four cranial
nerves which are located medially. Okay.
So what's the relevance of this? Anybody
can tell me what's the relevance of
knowing that these are located medially
motor nuclei. Yeah. This is the motor
nuclei. The other motor nuclear are
located laterally like you have
five sorry 5 6
7 8 9 10 11 no they are located
laterally six is not okay what's the
importance for us to know whether this
is medially located or laterally located
why do you have to be knowing
that how does it
help anyone why do you have to know this
Okay. Syndromes. Okay. Uh it's important
for us to know because we are talking
about stroke and stroke is a vascular
disease. So stroke is a vascular disease
we're talking about. So this medial
part, the medial part of the brain stem
is supplied by one blood vessel. The
lateral part is supplied by one more
vessel. So it's the different blood
vessels that are there for different. So
since the pyramidal tract is located in
the middle these cranial nerves are more
likely to get involved with pyramidal
tract. So supposedly I say a medial
medularary syndrome. So if I say medial
medularary syndrome, which cranial nerve
do you expect to get
involved? 12. Yes. If I say it's a
lateral pontine syndrome, which cranial
nerves do you expect to get
involved? Five and seven. in the lateral
part of the pontine syndrome. So that's
why we have to know. So that's the
second rule that we discussed is one is
the four cranial nerves are located
where they located. Second is only four
of the cranial nerves are located which
are located in the four cranial nerves
are located in the medial part. The rest
cranial nerves nucleus is located in
laterally. So these are the two
important force. The there are two more
rules of force. I'll come to that when
we are discussing the brain stem. Okay.
Now the next part before we go on to the
cranial nerves, why cranial nerves are
involved in stroke? So remember each of
these cranial nerves have the
nucleus just a minute. I think
I'm so each cranial nerve has a nucleus
there. So supposedly I'm talking about
the third cranial nerve. Where is the
third cranial nerve nucleus located?
Where's the third cranial nerve of
nucleus located? Superior chiculus area.
No, which which structure which we
discussed so far?
We're talking about the midbrain. So
third cranial nerve nucleus is located
in the midbrain. So when we take the
midbrain, third cranial nucleus will be
located. So you have the right side
third cranial nerve nucleus and the left
side third cranial nerve that is there.
Both these cranial nerves get corticle
fibers from both sides. You understand?
The
right-sided third nerve nucleus gets the
cortical nuclear fibers from both right
side and left side. So if you have a
lesion above the midbrain, okay, if
supposedly I have a leion in the
internal capsule, will this cranial now
get
involved? Will the cranial nerve get
involved? Will you get a manifestation
of the cranial nerve? No sir. No.
Because it has bilateral representation.
So the cranial nerves will get only
manifest only if okay cranial nerves
will get manifested only if you have
bilateral corticonuclear involvement if
the involvement is on both sides. Okay,
if the involvement is on both sides,
supposedly you get a lesion on the up
here as well as up here. What we call it
as a pseudo bulbar paly or else the
cranial nerve will only get involved if
the cranial nerve nucleus gets involved.
So supposedly we have a midbrain lesion.
You have a classical syndrome called as
Weber syndrome. We'll be discussing it
where the midbrain is involved. So there
you'll have a lesion which is there and
that can produce a lower motoring type
of cranial nerve involvement. So all
cranial nerves are not involved in
stroke basically because of this reason.
So cranial nerves are not involved
because these cranial nerves have
bilateral corticonuclear representation.
The only exception for
this the exception for
this yeah I'm trying to draw with the
thicker pen but I don't know for some
reason. Okay now let's see. No, it's
still becoming thin. Just give me a
moment. Highlighter could be better.
Okay, let's try the highlighter.
That highlighter is in which color?
Okay, it's black. So, the only exception
for this rule is the facial nerve. No,
it's not
coming. The facial nerve nucleus,
remember the facial nerve nucleus is
located in the
pawns. Pawns. The facial nerve nucleus
has two parts. You have an upper part
and you have a lower part.
So the upper part of the facial nerve
nucleus gets supply from both
sides. So the upper part of the facial
nerve nucleus gets supply from up by
right side as well as the left side.
Whereas the lower part of the facial
nerve nucleus which is there in the
pawns gets supply from contraateral
side. Please remember not ipsilateral
contraateral side. Now why do you have
to know this? We have to know this
because this upper part, if you see the
face
here, this is the representation of the
face. The upper part of the facial nerve
nucleus will supply the upper part of
the face. That's still the eye. Whereas
the lower part of the facial nerve
nucleus supplies the lower part of the
face. Now supposedly we said this this
lower part of the facial nerve nucleus
has only one-sided supply that is from
the opposite side. That is why in all
strokes we get facial nerve paly because
one part of the facial nerve nucleus
that's the lower part of the facial
nerve nucleus is getting only one-sided
supply. Okay. So you get involvement of
the lower part of the face. The upper
part of the space is spared. The upper
part of the face is spared. Now why the
upper part of the face is spared? Please
remember the nucleus which supplies the
upper part of the face gets supply from
both sides. That's why the upper part of
the face is spared. Now
this type of paralysis where only the
lower part of the face is involved is
called as the upper motor neuron type of
facial nerve paly. So upper motor neuron
type of facial nerve paly. By upper
motor neuron type of facial nerve paly
we mean it is a corticon nuclear paly
that's happening. that is it's not at
the nuclear level it is above the
nucleus. So how do you identify a um
facial paly versus element facial paly?
In um facial palsy the upper part of the
face is spared. Okay. So upper part of
the face is spared only the lower part
of the face gets involved. Only the
lower part of the face is getting
involved and that is basically because
of the upper part of the fish nucleus is
supplied by that. So this is the
exception. This is an exception. Similar
to that, please remember in the 12th
nerve you have goglosses. Okay, 12th
nerve nucleus 12th nerve supplies
various muscles of the tongue. There is
one which supplies the golosses. So that
also has similar pattern. Okay, that's
why in most of the stroke patients you
will find slight deviation of the tongue
because of that nucleus which is
supplying to the geneoglosses gets
involved. But that's not a very
important thing. Just remember about the
facial nerve nucleus that is the most
important thing that you have to
remember. So all cranial nerves get
involved in stroke but they do not
manifest because they have bilateral
corticonuclear representation. So that
is what you have to understand. Facial
nerve nucleus does not uh get that why
the facial nerve is involved because the
facial nerve nucleus the lower part has
only one-sided that is the contrateral
supply. Okay. So after knowing this
much, let's start with the localization
of the stroke. The most common site of
stroke that we
encounter, the most common sight of
stroke that we encounter is internal
capsule. Now the question often asked is
why is internal capsule the most common
sight of stroke? Why is internal capsule
the most common sight of stroke?
For some reason I am like yes anybody
can answer me in that why is internal
capsule the most common sight of
stroke. Okay some would say that is end
arteries. Correct. That's one reason end
arteries. That's one reason for why it
is internal capsule. Please remember
internal capsule has a very wide uh
blood supply. Okay, it's a very small
area. It has multiple blood supplies
that you have. So internal capsule is
supplied by the middle cereal artery. It
is supplied by the anterior coridal
artery. It is supplied by the poster
communicating artery. So multiple blood
supply is there but still all these
arteries are end arteries. So please
remember all of these arteries which
supply the internal capsule are end
arteries. So there is
no anastmosis that's happening. So if
any one of the arteries get involved,
you do get internal capsule stroke. So
internal capsule stroke is the commonest
because of that reason. Okay. So what
are the features that will be there in
internal capsule lesion. So we have
already discussed the diagram that time
where we discussed how the pyramidal
tract is
arranged. I think here. Okay. So you're
able to see that there. So you have the
pyramidal tract that starts from one
side and it's going here through the
genu and internal genuine
uh poster limb of the internal capsule.
This part where it is getting going
there. So here if it gets involved so
what is the most important feature
they'll have? So we have already
discussed the first and most important
feature they have is
hemiplegia. What sort of hemiplegia?
Internal capsule dense hemiples. What do
you mean by dense hemiplegia? Upper limb
and lower limb are equally involved.
Which side will be the
hemoplegia? Same side or opposite side?
Opposite side. Yeah. So contrateral
dense hemiplegia is the first and most
important feature of internal
capsule. Clear. The second feature as we
said the cranial nerve which is involved
in all types of stroke. What is that?
Seventh nerve. Seventh. So seventh nerve
paly will happen. What type of seventh
nerve paly? Upper motor neuron type.
What do you mean by upper motor neuron
type? Upper part of the face is paired.
Which side will be this paralysis?
Contraateral because the cranial nerve
nucleus of the seventh gets opposite
side supply. So contrateral seventh
nerve paly. That is the two important
features that are there and which you
will find in almost all stroke patients.
The other features remember the internal
capsule has various limbs isn't it? What
are the limbs of the internal capsule?
You have the anterior limb genu and
posterior limb that is there. So we said
the pyramidal tract is going somewhere
here. What is located in the anterior
limb and the poster limb? Rest of it.
What are the other structures that are
there? The anterior limb and poster
limb. Yes. What are the other
structures? What is there in the
anterior limb post capsule? You have
sensory fiber.
Cortical spinal is in the genuine and
postal limbo only you have sensory
tracks remember from the corticopontine
fibers corticopontine fibers are also in
the genuine okay there are sensory
tracks which go from the thealamus to
various parts of the cortex so you could
have a thealamo frontal you could have a
thealamo parietital so a lot of
radiations that are going there which
carry sensory problem so whenever the
sensory gets involved you get something
called as hemiensory
loss. Which side will be the hemisensory
loss? Contraateral. So this is a third
feature that you can get in internal
capsulation. Contrateral dense
hemipleia, contrlateral seventh cranial
nerve involvement, contrlateral
hemiensory loss. And sometimes when you
have a big lesion there, you have
certain fibers that are running on
either side of the internal capsule.
Okay? It's running from front to back.
What are those
fibers?
Any fibers which are running from the
front and going onto the
occiput anyone?
Association fibers. Okay. Somebody has
written in the chart it is the optic
radiations. Okay. Optic radiation. So
when the optic radiation gets involved
what is the deficit that is called as
homonymous hemianopia. Hommonous
hemianopia. So homonymous
hemianopia. So what do you mean by
homonymous hemiopia? What does the word
homonymous hemiopia mean?
Visual loss on the same uh side one
nasal one one side it's nasal nasal one
side it's nasal other side it is
temporal. So these are the four
characteristic features of an of a
internal capsule. So please remember if
you find these features in an uh patient
it is suggestive of an internal capsule
lesion. Now do you find it in all
patients with internal capsulation? Do
you find it this you would have seen a
lot of stroke patients in your walls but
do you find these uh findings in all
patients?
No, you generally do not find. Okay, you
generally find the dense hemoplegia and
maybe sometimes you find the sensory
problem because the fibers are at
different different parts of the
internal capsule, different parts of the
internal capsule and each part is
supplied by different blood vessel. Can
anyone of you tell me the blood supply
of the internal capsule in brief?
Anterior limb, posterior limb, genu.
Anterior is by recurrent artery of
ebena. Genu and which part? Which part
of anterior is supplied? Anterior and go
by recurrent artery
of and go the anterior limb the
posterior limb and genu is divided into
upper part and lower part. Okay, upper
part and lower part. You understand? So
if we say this is the internal capsule
I'll divide it
into anterior genu and poster the upper
part and the lower part. So upper part
is supplied
by
what the main blood
supply which is the main blood supply of
the internal capsule middle cerebral.
What is that? Which branch?
Charcoord artery
lenticloroid branch of the middle
cerebal artery supplies this part. Okay.
As you said the lower part of the
anterior limb is supplied by Yes. What
you said that time?
Cubinous artery. Hubin's artery that's
there. The genu, the lower part of the
genu is supplied by
char codes. Okay, charco artery or
direct branches of the ICA. Whereas the
posterior limb totally supplied by
either the PCOM or the direct branches
of ICA. So there are different blood
supply for different parts of the
internal capsule. So since the
fibers are located at different sides,
so you do not get all these features. So
supposedly I give you a patient of
internal capsule lesion and he has all
the features of internal capsule
leion. What is your inference? He has
all these four features are there. So
what does it mean to
you? It definitely means internal
capsule. But what else does it mean to
you? Block at koted level.
Internal caroted artery. Block at
caroted level. Agreed. Internal caroted
art. That will not only supply the
internal capsule. No, that will supply
the entire thing. You'll have entire
cortex going. I'm talking about internal
capsule
only. But all these features are there.
So what does it mean to
you? I've told you the fibers are at
different different part. Here there are
some fibers. Here there are here there
are. So what can involve all the fibers?
What type of lesion can involve all the
fibers? All the vessels cannot get
blocked. Huh? All these five vessels
which we told cannot get blocked all of
a sudden. No. So what sort of lesion can
cause tumor compressing the internal
tumor compressing? Okay. Tumor is right.
But we are talking about stroke. Tumor
is absolutely correct. Whoever said
hemorrhage hemorrhage hemorrhage. So
please remember hemorrhage. So
supposedly if one of the vessel bleeds
there what will happen? The blood will
come out and the blood coming out will
start compressing the entire internal
capsule. So please
remember whenever in an stroke patient
you find all these features of internal
capsule your diagnosis becomes
hemorrhagic stroke.
Okay did you get that point? Is that
clear? So internal capsule is the
commonest structure involved.
Internal capsule has multiple blood
vessels. All are end arteries and each
getting blocked can produce various
manifestations. But the characteristic
manifestations are these four.
Contrlateral dense hemiplegia,
contrlateral and seventh cranial opaly,
contrlateral hemisensic loss and
homonymous hemi anopia. But all of them
are not usually seen because different
structures are there. If you find it in
a patient then we are dealing either
with a space occupying leion or a
hemorrhagic stroke.
Okay, so that's about the internal
capsule. By far the most common sight of
stroke. The second important site of
stroke we're talking about is
cortex. Now cortex as a site of stroke.
So if you say this is the motor
homunulus I'm drawing here. Are you able
to see that? Okay. So you have the how
are the fibers arranged? How are the
which fibers are located medially? Which
are located laterally? Can anyone tell
you leg fibers medally and upper fibers
later? Correct? So leg is somewhere here
located the face the trunk and the hands
will be located laterally. Correct? So
that's the arrangement that is there in
the motor homunculus. Why do you have to
know is because the blood supply is also
something like that. So the blood supply
that we have if you see this as the
blood supply here the medial part is
supplied by which vessel?
Antior anterior cerebral artery. Whereas
the lateral part is supplied by the
middle cerebral artery. So you remember
this the medial part is supplied by
anterior cerebral whereas the lateral
part is supplied by middle cereal
artery. So supposedly I say anterior
cerebral artery gets thrombos or
blocked. So which part of the body gets
involved most? Leg leg is getting
involved. So which side leg? Opposite
side leg isn't it? So you get monoplegia
of the leg or sometimes you can get
hemiplegia but that hemiplegia will have
lower limb more than upper limb
involvement. What do you call this
hemiplegia as
differential hemiplesia?
I I told the name for this beginning
coral coral hemoplegia. So lower limb
getting involved more than the upper
limb. Supposedly the middle cerebral
artery gets involved. You get
involvement of the hands as well as the
face hands and the face together gets
involved. So you get upper impredominant
hemoplegia or the brachial hemoplegia.
So what is very important for us to know
is in the cortical leion the upper limb
sorry thing
happened where did it go. So in a
cortical leion you have to understand
that the upper limb and lower limb are
never equally involved. It's always
either cural dominant or it is a
brachial dominant that you get. So it is
never dense. That is what we have to
understand in case of a cortical
lesion. The next features of a cortical
lesion that you have to understand in a
cortex whenever the cortex gets
involved. What are the other features
which will tell us that this is a cortex
that is getting involved. What are the
other functions of the cortex that can
get affected?
Speech. Speech. Very important. So
speech can get affected if you have a
dominant cortical involvement. So as we
have discussed in the dominant cortex
which is the dominant cortex in almost
majority of the population the dominant
cortex is the left cortex isn't it? So
leftsided. So if you have a leftsided
cortical involvement you can get
aphasia. So that's the second feature
that you could have ephacia. Yes. What
else could be there in a cortical
involvement?
Apexia. Apraia. What do you mean by
apexia? Skilled movement. The person
cannot do the skilled movements. Okay.
Inability to perform the skilled motor
activity. Again remember this is a
function of the non-dominant cortex. So
ephacia is dominant cortex. Epraxia is
non-dominant cortex. Will the facial
nerve get involved? Will you have facial
nerve involvement?
Dominant involvement. Yes, facial nerve
can get involved. So you can get a um
seventh nerve paly on the opposite
side. Okay. And a very important thing
that you have to remember always on
history if a patient gets
[Music]
seizures. Okay, patient gets seizures.
So if there is a seizure on history it
always says the patient has a cortical
involvement because seizure is nothing
but irritation of the cortex. There is
an irritation of the cortex. So if there
is a seizure that means there is a
cortical involvement. So history-wise
and examination wise you say this lesion
is in the cortex. If you have a
non-dense hemiplegia, if you have an
aphasia in a patient who has right-sided
hemoplegia or else if there is a
left-sided hemoplegia, sometimes the
patient can have apraxas and the patient
has seizure on history. And again
remember when the non-dominant
parietital lobe gets involved sometimes
uh non-dominant loc is not a feature.
LOC uh it is not uh I think somebody in
the chat has asked about uh loss of
consciousness. Again loss of
consciousness is not specific for the
cortex. Loss of consciousness uh can
occur in brain stem lesions. Loss of
consciousness occurs in raised
intraranial tension also. Uh so it's not
specific for the cortical involvement.
Okay. The other important as uh uh
somebody has already answered it in the
chat. If the non-dominant parietal lobe
gets involved, you get a symptom called
as hemi neglect. Okay. Please remember
this. The patient refuses to see the
side. So non-dominant parietital I told
you. So the right sided is a lesion. So
the patient has a leftsided hemiplegia
and the patient refuses to see that left
side. So his head is always turned to
the right. So it's a very very specific
leion of a non-dominant parietal lobe
lesion. So these are the features that
you'll have in a cortical uh stroke. In
a cortical stroke there are other
functions can be abnormal but please
remember ephesacia
apraxia non dense hemiplegia and
seizures if you have in a patient you
have a cortical lesion. Now do we get
effacia in an internal capsulation? A
very important question they ask you.
Patient has all the features. You have a
patient who has dense semipllegia and
has uh fac also. So what do you think?
Patient has
ephesia and there is dense semiplletia.
So what do you pro what is the problem?
You think
the middle cerebral artery. Okay. The
entire middle cerebral artery. But then
the patient will have other features
also if the MCA gets involved. So please
remember internal capsule can also cause
something like a motor efficacia. Okay.
Though it's not common. If there is a
dense hemoplegia and the other cortical
functions are normal then per say if the
internal capsulation can produce
something like a motor ephesacia but for
all practical purposes please remember
ephacia means dominant cortex. So it
could be a brokia it could be a
vernicia. Please remember your middle
cerebal artery finally comes and gives
out two branches. You have a superior
division and inferior division. The
superior division goes and supplies the
brokas area. The inferior division goes
and supplies the vaniciz area. So if the
superior division of the middle cerebral
artery gets involved, you get brokia. If
you have the inferior division of the
middle cerebal artery gets involved, you
get vaniciz. Supposedly you have a stem
of the middle cerebral artery getting
involved, you get something called as a
global ephacia. So you have the various
other syndromes of middle cereal artery.
We call it as M1 syndrome, M2 syndrome.
I think we'll uh discuss that maybe in a
further class. It's not very important
for undergraduate level. Please remember
internal capsule cortex. What are the 1
2 3 4 5 features. Now the next fe next
site which I told you is subcortex.
Again it's a not a very common site you
get uh subcortical involvements
generally whenever there is a something
called as watershed region. The
subcortical region is something called
as a watershed where the blood supply is
not individual. It depends upon the
other sides for the blood supply. So
whenever we have a hypotension or you
have a multi-infact state such lesions
would occur. Why do you get seizure in
stroke? When there is an infact is a
dead area. It causes as an iritative
focus. So it produces seizure. That's
the cause of seizure. So cortex is the
site where uh if you have an infact
produces a seizure because it's a dead
area. That's how you get
seizures. I was speaking about something
else. I was speaking about subcortics.
So subcortics remember they will neither
have features of cortex they will
neither have features of internal
capsulation. So they may have some sort
of a monoples but then they may the
speech etc may be normal. So those are
the lesions where you get subcortical
lesions. So more of in the imaging you
do an MRI and you find subcortical
influx clinically it will not be
difficult to make out that. So these are
the anterior circulation strokes. So if
you get a question on anterior
circulation
strokes please remember we are talking
about the middle cerebal artery the
anterior cerebral artery and the
keroted. So the sides are internal
capsule cortex and
subcortex. Now one question they ask you
supposedly the internal keroted itself
gets involved what will be the features
if the internal kerotid gets blocked
what other features the patient will
have other than hemoplegia hemisensory
loss and global aphasia. What else
feature will a patient will have if the
internal keroted artery is directly
getting blocked? MRO is fugax. Yes, very
important. This is one sign before the
MCA etc is given. The last branch that
is gives is the ofthalmic artery. So if
the internal keroted artery gets
involved, you get monocular blindness.
Amorosis fugas is a transient one. It's
a transient one. It's a TIA. But if you
have blindness, monocular blindness,
then that would indicate an internal
keroted artery getting involved. So ICA
stroke will have along with the MCA and
ACA features, it will also have a
patient will have monocular blindness.
Okay. So that is the anterior
circulation strokes. We'll go on to the
poster circulation stroke. But before
going to that as we discussed in the
anterior cerebral artery. Now can you
get paraplegia in a patient with stroke?
We are talking about hemiplegias in
stroke. Can you get paraplegias? Both
lower limbs involved. Can you get that
in
stroke? Okay. So this anterior cerable
artery which we discussed this is the
anterior artery we were talking about it
supplies the leg area. So there is one
more anterior cerebral artery on this
side which supplies the leg area there.
Now in a good amount of population you
have an abnormality called as an
unpaired anterior cerebral artery. What
do you mean by unpaired anterior
cerebral artery? Unpaired anterior
cerebral artery means there is only one
anterior cerebral artery. The other side
area is going to be supplied by the
anterior communicating artery. So you
have an anterior cerebral artery here
and through the anterior communicating
the other side cortex is getting
supplied. So supposedly this unpaired
anterior cerebral will get thrombos.
What will happen? This will also get
infacted and the opposite side also gets
infacted. So the lower limb on this side
and the lower limb on this side also can
get involved. So you can get paraplegia
in case of unpaired ACA thrombosis.
Please remember this. It's a common
anatomical variant. It's not a rare
condition. Unpaired ACA causes
paraplegia. If you have a paired ACA,
one side getting involved produces
opposite side lower limb involvement. Am
I clear with that? Unpaired ACA can
produce paraplegia. We're talking about
stroke. Some other fellows have written
of the other causes like they have
written about uh CVT as well as
hydrophilis. They are not part of stroke
but they are part of other conditions
where it can compress on both of the
frontal loes there and it can produce a
a bilateral weakness sort of features.
They can have paraplegia can be produced
due to
that. Okay. So coming on to the
posterior circulation stroke. By poster
circulation stroke we are meaning the
vertebra basilar circulation that is
happening there. So we are talking about
the sides of poster circulation stroke
the first
stripe the first we are going to look
what is the
midbrain. So what happens in the
midbrain? So if I
take
okay you have the midbrain there. So the
cranial nerves that are located in the
midbrain the two important cranial
nerves that are located the third and
the fourth cranial nerves are located in
the midbrain. So third and fourth
cranial nerve nucleus is located there
on both sides. So the pyramidal tract
comes like this and goes down. And so
what are the features they'll have in a
midbrain stroke? That's what is
important for us to make out. So in a
midbrain stroke if there is a lesion on
the right side here patient will have
hemoplegia. Which side hemiplegia?
Opposite side hemiplegia. So
contraateral hemiplegia will be there.
So contrateral hemiplegia that's the
first feature they'll have. The second
is the third nerve nucleus is getting
involved there. So what will they have?
They will have ipsilateral
ofia. Ipsilateral ofthalmopoplegia.
Please remember third nerve is involved
on this side. Hemipleia is on the
opposite side there. But the of
theopoplegia is on the same side. So
ipssilateral of theopoplegia.
Contraateral hemiplegia. This is the
classical syndrome. Anybody can tell me
what's the name of this syndrome?
Webers. Webers. Yes. This is called as
the Weber syndrome. The most common
syndrome that you have in a midbrain
stroke.
Ipsilateralia. Contrateral hemoplegia.
That's a common syndrome that you have
also for uh your other there are many
other syndromes that are located.
Remember there are other structures that
are there in the uh midbrain. What are
the other important structures that are
located in the midbrain? Anybody can
tell me red nucleus is present. So you
can have a red nucleus that is present
there. So red nucleus can get involved.
So if the red nucleus gets involved what
is the symptom the patient can get?
Tremors. Tremors very important. And
it's a coarse tremors the patient can
develop. Correct? So the patient can
have coarse tremors due to red nucleus
involvement. Correct. Any other
structure? Any other structure?
Sexia will be there.
Correct. Why do they get taxia? Why do
they getia? Can somebody tell me what
old tax cerebral pontine rubal fibers
are there? Cerebro pontine rubil. That's
a big word. Okay. Remember the brain
stem, the three parts of the brain stem,
midbrain, pawns and medula. How are they
connected to the
cerebellum? How are they connected to
the cerebellum? Pedunals. Pedunals. How
many pedunkles are there? Three. Three,
isn't it? Superior, middle, and
inferior. Superior connects the midbrain
to the cerebellum. Middle connects the
pawns to the cerebilum. and the inferior
connects the medulla to the cerebellum.
So all the blood supply to this pedunks
are going through the cerebilum are
going through the pedunals. So the
pedunkles get involved and there are
tracks in the pedunkles so they can get
tremors. Correct. That's a very
important feature. So the patient can
have tremors. Any other important
structure something black that's located
black substantia. Substantia isn't
it? So substantia is located
there. So if that gets involved what
will the patient have?
Rigidity. What is the disease? What is
the disease? Parkinson. Parkinson's.
What sort of Parkinson's? Both sides or
one side only?
Unilateral. Unilateral Parkinson's or
what we call it as a
hemiarkin. So remember midbrain
involvement produces two important
features. One is if
epsilateralia, contrateral hemiplegia.
So that is the classical syndrome of
Webers. Then you have the other
syndromes. You have various named
syndromes are there. You have the claude
syndrome where you have opposite side
atexia third nerve involvement. You have
a north nagel syndrome and you have as
you said the red nucleus involvement
producing coarse tremors. Hemi
Parkinson's because the substantion is
getting involved. So you can all have
all these syndromes. Also if you
remember in your anatomy there are other
nucleus that are located related to the
ocul motor which are there in the
midbrain you have something called as a
tegmentum and the tectum you heard of
it. So in the tectum you have various
nucleus like the pre-tectal nucleus the
edging vespal nucleus these are involved
with the light reflex the accommodation
reflex is involved reflexes. Yes. So
these also can get involved. Okay. In
ofthalmology you would have learned a
syndrome called as parod syndrome isn't
it node syndrome is a very important
syndrome which is involved in the
midbrain. So they have predominantly
problems with
the eye especially the ocul the 3 46
nerves that is not 346 the three and
fourth nerve especially
the light reflex and accommodation
reflex. So they have upgy pupilary
dilotation and they get a very classical
nestagmas called as the convergence
retraction nestagmas or otherwise called
as the kolas sign. So I think in
opthalmology you would have learned
about the parinaut syndrome. So midbrain
lesions midbrain lesions just remember
for simple reasons remember if the third
nerve is involved on one side hemiplegia
is on the opposite side you're dealing
with midbrain. Okay coming on to the
next site. The next side that we have is
the
pawns. So
pawns. So what are the structures that
are located in the pawns? So you have
the pawns here, right and left pawns. So
pyramidal tract is going. So if you have
a lesion here, you get
contraateral hemoplegia, isn't it? So
contrateral hemoplegia will be
there. The cranial nerves that are
located in the pawns, what are the
cranial nerves that are located in the
pawns? Sixth cranial sixth sixth and
seventh cranial. So sixth sixth and
seventh cranial nerve predominantly that
are located there. So you get paralysis
of these two nerves. So you get facial
now paly now. So seventh nerve paly is
coming and seventh nerve paly is now
which side will be the seventh nerve
paly? Which side will be the seventh
nerve paly? Ipssilateral isn't it? It
will be ipsilateral seventh n paly that
you're going to get because the seventh
nerve nucleus is getting involved there.
So ipssilateral seventh n paly
ipssilateral abdosense nerve paly that
is the lateral rectus will be paralyzed
whereas the patient will have hemoplegia
on the opposite side. So whenever you
have a lesion in the pawns you have
contrateral hemoplegia ipspipssilateral
seventh nalcy what type of seventh nalcy
now it's a nucleus getting involved. So
what type of paly will it be? UN or
LM? Will it be upper motor or a lower
motor?
Elemen type of facial pulsey. So how do
you identify element facial palsy?
How do you identify? Same side lower
face upper and lower both are getting
involved. So you have contrlateral
hemoplegia ipsilateral element type of
seventh nerve paly that is there. So the
entire face is getting involved isn't
it? So this classical syndrome is called
as
Millard gobbler. Yeah it's called as a
Millard gubler
syndrome. So that's the commonest
syndrome that you get in case of a
pontine stroke. You get milard gubler
syndrome where you have hemoplegia on
the opposite side and seventh nerve
involved plus or minus abducence nerve
involved on the opposite side of that.
So this is the Millard Gibbler syndrome.
Again you can have only abducence
involvement because remember the sixth
nerve is located centrally medially
whereas seventh nerve nucleus is located
laterally there. So with the hemoplegia
usually sixth can get involved. Okay the
seventh may not get involved. So you
have other syndromes also of the pawns
but important for us to know is the
Millard Gubler syndrome. That's the
commonest syndrome that we have. Okay.
Coming on to the next location that's a
very important location for us is the
medula. Okay. So we are talking about
the medula
now. So when we discuss the medula what
is important for us to know about the
medula is there are we discussed about
the rule of five that time sorry rule of
four. There are two other rules of four
that are there in the medula. There are
two more rules of four. So we have four
structures in the medula which are
located in the center which are located
in the center. Four structures which are
located in the center and there are four
structures which are located in the
side. So that's the next rule that we
have in the medula that we have to
understand. Now in medula what are these
four structures which are located in the
center. So center we can call it as
midline. So all of them start with M.
The central midline structures are
starting with M. So what are these M
structures which are located in the
center of the medula. So the first one
we have is the motor pathway or the
corticospinal
tract. Motorar pathway or the
corticospinal tract which we are
discussing. So the motor pathway.
The second M is the motor cranial nerve
which is the cranial nerve that's
located in the medula and it's located
medially which cranial nerve 12th
cranial nerve. So 12th cranial 12. Okay.
The next cranial next medial path with m
midline structure which starts with the
uh midd is the medial longitudinal
vessicle and the fourth m is the medial
laminiscus. So I'm just repeating in the
medula in the center or the midline you
have four structures which start with m.
What are they? Motor pathway, motor
cranial nerve 12, medial longitudinal
faces and medial laminus. So you have a
syndrome in the medula which involves
the medial part of the medula. We call
it as the medial medularary syndrome.
Okay. Medial medularary syndrome is a
syndrome of the medula which involves
the medial part of the medula. That's so
in that medial medularary syndrome you
have ailment of these four structures.
So if the motor pathway gets involved
what is the feature they'll have? If the
motor pathway is getting involved what
feature they'll have? They will have
hemoplegia. So which side will the
hemoplegia be? Which side will the
hemoplegia be? Contrateral weakness.
Okay. Again remember medula is the site
where the decation is happening isn't
it? So this is the medula. If you say
the decarcation of fibers the fibers
start from this side come and decate
onto the opposite side. So if you have
lesion above the decision helesia will
be contraateral. If you have a dec below
the decursation you'll have ipsilateral.
So this is the site where your crossed
and uncrossed comes. Till now the all
the hemiplias were crossed in the
medula. Above the decision you have
contrateral hemoplegia. Below the
decision you have ipsilateral
hemoplegia. That is what you have to
understand. So hemiplegia can be
contrateral or ipsilateral based on the
sight of decision. The second feature
they'll have is because of the
involvement of the cranial nerve 12. So
cranial nerve to val paralysis will be
happening in the medial medularary
syndrome. So there'll be paralysis of
the tongue. The tongue will be wasted
and it'll be deviated. Okay. So tongue
wasting and deviation will occur towards
the side. So that is the second feature.
They'll have 12th nerve involvement.
Next is they'll have involvement of this
medial longitudinal fac. Now what is
medial longitudinal physical? Anyone can
tell me what is medial longitudinal
physical?
Physical is gracious and physicist
cunat. No that is not medial
longitudinal faces.
Medial longitudinal faces. Horizontal
gaze. Horizontal gaze. Conjugate gauge.
Correct. So you have the gaze. gaze the
horizontal gaze. Horizontal gaze means
when you're looking onto the right side,
one eye lateral rectus should act, other
side medial rectus should act. What is
the nerve supplying the medial
rectus? Which nerve supplies the medial
rectus?
Three. Third. Third nerve. Which nerve
supplies the lateral rectus? Sixth.
Sixth. Sixth nerve. Where is the sixth
nerve nucleus located?
Pawns. Pawns. Pawns. Where is the third
nerve nucleus located? Midbrain.
Midbrain. So these two cranial nerve
nucleuses are located at two different
sides and one side third nerve should
get stimulated. Opposite side six nerve
should get stimulated. So to facilitate
this there is a group of inter neurons.
There is a group of inter neurons which
connect these two cranial nerves. That
is the sixth cranial nerve on one side
is connected to the third cranial nerve
on the opposite side. And that group of
inter neurons is called as medial
longitudinal physical. Now when you have
a medial longitudinal physical
involvement the deficit that you get is
called as in O. Have you heard of this
in O? Interuclear of them. Yeah it is
called as interuclear of themalmopia.
Now how do you make out this interuclear
of themopleia? What features the patient
will have? Same side there is adduction
paly
and contrlaterally uh the gaze is
impaired. Gaze is impaired or what else
will happen in the other eye? Distramus
is seen sir. Okay. So there will be
problem with adduction on one side
opposite eye there will be nestagmas. So
that is what you have to understand. So
otherwise for all practical purposes
please remember MLF involvement produces
inter
nuclearia loss of adduction on the same
side.
nstagmus on the abducting eye. So that
is what you get. Very important. MLFl is
one group of inter neurons. It is
starting from the medula. It is there
right up to the midbrain. So it is
located in the center of the midbrain.
Whereas in the center of the midbrain,
it
is it is there right in the center of
the midbrain that is there. So uh
because of that you can get this
involvement of the interuclear of
thermalopia and one disease where this
MLF is classically involved. One disease
sclerosis multiple sclerosis very good.
So multiple sclerosis is a disease
where MLF classically gets involved and
though in India we do not have so many
cases of multiple sclerosis in the west
multiple sclerosis is a very common
disease and they get a lot of
interuclear of themia but please
remember where is the interuclear of
them site of lesion is in the medial
longitudinal faces. Where is the medial
longitudinal faces located? It is
located in the medial part of the brain
stem. Okay. Okay. The fourth feature
that they have is due to this medial
laminiscus. What is this medial
laminiscus? What is this medial
laminiscus?
And grailus for correct. Correct. So it
is the continuation of
the faciculus cuniatus and graasilus. So
what do they carry?
Dorsal column sensory fibers fine fine
touch and propriception. Okay. Okay. So
joint position propriception vibration
fine touch is carried through this
pathway and that is going to the the
phalamus from this. So what will happen
if the medial laminosis gets get
involved? What what will be the problem
that the patient will have? Contrateral
reduction in propriioception contrateral
loss of proprioception. Please remember
it is contrateral loss of propriception
because it is decassated in the lower
part of the brain stem and come up. What
will the patient will be able to
appreciate pain and
temperature? Will the patient be able to
appreciate pain and temperature? Yes.
Yes. Because that is going to go from
the separate, isn't it? Spinal lamic.
It's on the lateral side. Spinalic.
Yeah. It is in the spinalamic. It's on
the lateral side of the brain stem. So
whenever you have a medial medularary
syndrome, you will have these four M's
that is getting involved. So what are
the four M's? Motar pathway. So the
patient will have hemiplegia motor
cranial nerve true. So the patient will
have tongue weakness. MLF medial
longitudinal physical. So the deficit is
inter nuclear of fourth M is medial
leiniscus involvement produces loss of
posterior column sensation in this
patient. So medial medillary syndrome
the other name for the medial medularary
syndrome is called as a gerine syndrome.
Okay. Jireine is D J E R R I A D is
silent there. So that is the medial
medary syndrome. Now coming on to the
fourth uh rule of four that we had. The
fourth rule of four that we
had. What are the three rules of four we
have finished so
far? Anyone can tell me what are the
three rules of fours we have
finished.
Division of the division of the four
based on the four cranial nerves. Okay,
correct. That's the first one. Second
one was midline there will be of motor
cranial nucleus. Correct. The third one
was and lateral there will be a four
nucleus that is third one was just now
what we discussed motor path midline
structures which are starting with M.
Coming on to the fourth rule that is we
have the four structures which are
located in the side of the medula side
which start with S. So we are discussing
the most important posterior circulation
syndrome that you have is the lateral
medularary syndrome. Please remember
lateral medularary syndrome is the most
important syndrome in the posterior
circulation. That's the commonest
syndrome that you get in the posterior
circulation.
That's the commonest syndrome you get in
the posterior circulation. So there are
four structures that are located in the
side which start with S. Okay. I think
somebody in the chat has already
mentioned the first structure that we
have is what we call it as the
spinoalamic
tract. So spinoalamic
tract if I zoom will the handwriting be
better or will it be less?
Okay. Uh spinoalamic tract. That's the
first S. The second S is something
called as a spinal tract of trigeinal.
Now that's the second S. The fourth the
third S is something called as a
sympathetic
tract. And the fourth S is what we call
it as the spino cerebellar tract.
So please remember we are talking about
the side of the brain. Still we're
talking about the lateral medularary
syndrome the most important lateral
medularary syndrome. It has four S's
because they are in the side. One is the
spinoalamic tract. Spinal tract of
triminal nerve sympathetic tract and
spino cerebellar tract. Now what is
spinothealamic tract? What is
spinoalamic tract
from spinal cordalamus?
Correct. What what what does it carry?
Pain and temperature. Correct. Pain and
temperature. Pain and temperature from
the body. Which side of the
body? If I'm talking about the right
side of the medula, which side body
spinal spinothalamic tract is there?
Opposite side. It crosses at the spine.
It causes the pain and temperature very
importantly crosses in the spinal cord
itself, isn't it? It crosses in the
spinal cord and ascends up. So
spinothealamic tract is the tract which
is carrying pain and temperature from
the opposite side of the body. Correct.
The next tract we're talking about is
spinal tract of the trigeinal nerve. Now
triminal nerve where is it located?
Triminal nerve.
Pawns. It is located in the pawns there.
But then you have a spinal tract of the
triminal nerve which comes from the
spinal cord and goes up. Okay. Which
carries the pain and temperature
sensation of the face. So that is in the
lateral part of the medula. Next is the
sympathetic tract which is required for
your pupils and the pupilary dilotation
or pupilary constriction that is
required is sympathetic tract that is
there as well as it's required for the
sweating of the face and then you have
the spino cerebellar tract. So these are
the four S's that are there in the site.
Now if these get involved what will be
the features? Okay. So supposedly you
have the spinoalamic tract that is
getting involved. What will happen?
Contrateral loss of pain. Contrateral
loss of pain
and temperature where
body isn't it? So body contrateral loss
of pain and temperature. Okay. Spinal
tract of fifth nerve. What will be the
problem?
There will be loss of pain and
temperature. Correct? Ipsilateral loss
of pain and temperature in the
face. Ipsilateral face. So please
remember in when we discussed about
internal capsule what is the sensory
problem I told you? Internal capsule
will
have hemiensory loss. That means
opposite side face and body complete
sensation loss. Hemiensory loss meaning
opposite side face and body to the sight
of leion opposite side if supposedly
right sided internal capsule leftsided
body as well as the face that is called
as hemiensory loss but what do you get
in lateral medillary you get crossed
sensory loss please remember this word
crossed sensory loss crossed
sensory cross sensory meaning same side
face opposite side body so whichever
side the facial sensation is lost Lo
that is the side where is the sight of
leion for so right sided lateral
medularary right sided facial sensation
lost opposite side left sided body
sensation is lost so that is what we get
cross sensory okay and only pain and
temperature is lost the posterior column
sensation is preserved correct why is
the posterior column sensation preserved
dorsal column because that is going
through the medial part of
the medula so In temperature lost dorsal
column sensation is preserved. What do
you call this deficit deficit?
Dissociative sensory loss. Dissociative
sensory loss. Very good. So
cross dissociative sensory loss you get
in case of lateral metallary syndrome.
And when the sympathetic tract gets
involved what is the problem you get?
Her syndrome. Her syndrome. Very good.
Yes. So Herner syndrome what are the
features?
Can one of you tell Miotosis,
anhydrosis, anhydrosis,
mosiosis. Correct. Tossis, meiosis,
and loss of celopillary reflex. Correct.
Loss of celio reflex. Somebody wants me
to repeat
something. What is the thing you wanted
to repeat? I could not catch that. Okay.
Uh, so harness syndrome. So the patient
will have meiosis andhydrosis loss of
celio reflex mild inopthalmos will be
there and spinal cerebilar tract when
the spinal cerebellar tract gets
involved what will they have spinal
cerebellar tract getting involved
atexia atexia atexia correct so spinal
cerebellar tract getting involved they
have
atexia so a patient with lateral
medularary syndrome will have crossed
sensory loss same side face opposite
side body patient will have horner
syndrome on that side patient will have
it atexia on that sideaxia is because of
the spinal cerebellar tract getting
involved what is this dissociative I
think somebody wants me to explain what
is dissociative sensory dissociative
sensory means one sensation is lost the
other sensation is preserved so remember
you have two tracks you have the
spinoalamic and you have the posterior
column sensation so posterior column
sensation is joint position
propriception fine touched whereas the
spinoalamic is pain and temperature. So
in some conditions you have pain and
temperature is lost and the other
sensation is preserved like in lateral
medularary syndrome you have only pain
and temperature is lost because
spinalamic is gone whereas in medial
medularary syndrome you have the other
one which is lost. So this is what we
call it as dissociative sensory loss.
But please remember the word
dissociative sensory loss is classically
described for which
disease? Which
disease? Which disease produces
dissociative sensory loss? Seringia.
Please remember siringia. Have you heard
of singomalia? There is a cavity inside
the spinal cord which dilates. So right
in front of the cavity the pain and
temperature fibers are crossing. So in
serumia you get classical dissociative
sensory loss. But you can get
dissociative sensory loss even in case
of lateral medary syndrome or medial
medary syndrome also. Which side will be
the hornness? Same side honors. Okay.
Same side will be the
honor. What are the other features this
patient will have? Lateral part of the
medula. What else is
located? We discussed that
time. What else is located in the
lateral part of the medula? Cranial
nerves, isn't it? What are the cranial
nerves which are located in the lateral
part? Ninth, 10th, 11th cranial nerves
are located. Eth is little up there. So
9th, 10th, 11th cranial nerve is
located. So whenever we have 9th, 10th,
11th cranial nerve involvement, the
patient will have horarsseness of voice.
They'll have nasal regurgitation.
They'll have loss of gag reflex. When
you check the gag reflex that will be
lost. So 9th, 10th, 11th cranial nerve
also will be involved. And a very
important feature in history to remember
is a very important symptom. Whenever
this symptom is there, you should always
suspect lateral medary. Anybody can tell
me what is that symptom? Hiccups.
Persistent hiccups. Very important.
persistent hiccups. Remember in the
lateral part of the medula there is a
nucleus. Okay, you have a nucleus. One
is for the vagus and one is for the
facial nerve. One is the NTS and the
other one is nucleus ambiguous. So these
can get involved and because of that the
patient can have persistent hiccups. So
whenever a patient with stroke complains
of hiccups you should always check for
you can you should always check for a
lateral medary syndrome. Now very
important syndrome why this lateral
medularary syndrome is so important for
us because that's the most common site
of poster circulation stroke again like
internal capsule had five blood supplies
the lateral part of the medulla also has
five or four blood supplies most
important one is the vertebral artery
then you have something called as a pah
pah stands for poster inior cerebellar
artery then you have the superior middle
and inferior cerebellar artery so all
these supply the lateral medary
very common MCQ they ask you what is the
commonest artery that is blocked in
lateral medary syndrome vertebral. Okay.
Uh please remember this is a question
which is debatable because two three
years back the artery which was always
considered as getting blocked was the
pah. Maybe two or three editions prior
if you see the books always they used to
say pah is the cause for the uh lateral
medary syndrome. But presently if your
MCQ is asked answer is vertebral artery.
So vertebral artery blocking produces
lateral medary syndrome. Okay. So that
is what you have to remember. The other
name for lateral medary syndrome or more
often it is called as Wenber syndrome.
Wallenberg syndrome. So please remember
again you can get a short notes clinical
features of Wallenburg syndrome. You're
going to write this three S4S. Then
you're going to write that there is also
ninth 10th cranial nerve involvement.
Now what is so uh special about this
stroke compared to all other strokes?
What is so special about stroke due to
lateral medularary
syndrome? What is so
special or what is the difference from
the other strokes that we have in
contrast to your lateral med syndrome?
Horner syndrome. Yes, Horner syndrome.
Yes, Horner syndrome you can have other
cause also but yes Heros syndrome is
specific. Whenever we say stroke what is
the first and most important thing that
we always speak about when your patient
has stroke. So what are you going to go
and check in the patient?
Hemopleia. Hemiplegia. Correct. You're
going to check for motor weakness.
You're going to check for reflexes
exaggerated reflexes. You're going to
check for Babinsky sign. Correct. So
will this be there in a patient with
lateral medularary syndrome? No sir.
Yes. That's a very important thing that
you have to remember. In case of lateral
medularary syndrome, this is a stroke
where your corticospinal tract is not
getting involved. So corticospactal
tract will not be involved. Very common
in the exam they say this patient has
left lateral medularary syndrome. Which
plantar will be
extensor? Which plantar will be
extensor?
None.
Patient has left lateral medularary
syndrome. Which planter will be
extensor? Right or left?
So both will be flexor.
Neither. Okay. So there is no cortical
spinal tract involvement. So you do not
have a plantar extensor. So this is a
stroke where you do not have plantar
getting extensor. That is what you have
to understand. So lateral medularary
syndrome is a common syndrome in the
posterior circulation. That's the most
common stroke that you get. But you do
not have motor weakness in these
patients. So this will finish your brain
stem syndromes. We told about the
midbrain syndrome. We told about the uh
pontine syndromes. And then we discussed
about the lateral and the medial
medularary syndromes. The last location
of
stroke is the spinal cord, isn't it? So
spinal cord you can get stroke. So as we
discussed in spinal cord stroke, what
should be the site where the spinal cord
should get involved to produce stroke?
It should be above
the C4 level. It should be above the C4
level. You can get spinal cord
involvement. So to produce hemiplegia,
one side should be weak. What sort of
lesion should be there in the spinal
cord?
Hem should have a hemisction of the
cord. What do you call that syndrome as
brown sequad syndrome? Again, it's a
very very rare uh uh thing to happen
because uh what's a common cause for
brown
sequinal cord should get cut.
Any bullet or stab injury? Yeah, bullet
or stab injury. It can't happen with
stroke. Why is can't you can't get it in
stroke? Why can't you get a brown squad
sort of picture in stroke? How is the
blood supply of the spinal cord? So
anterior spinal artery. Ant spinal
artery is there. There is poster spinal
artery is there. How do they supply?
They supply half one half. No one third
and 2/3. Ah they supply from front and
back. Isn't it? So if one gets blocked,
you'll have anterior 23 getting going.
So the patient will have paraplegia or
quadriplegia. So to get stroke due to a
vessel getting blocked in the spinal
cord is rare. So usually if you get a
spinal hemoplegia it's because either
due to trauma or a gunshot injury. So
they will have classical features of
brown sequad syndrome. So what are the
features of brown squad syndrome?
Same side there will be hemipleia.
Correct. Same side hemip
contrateral loss of pain and
temperature. Contrateral loss of pain
and temperature and ipsilateral loss of
all the posterior column sensation. So
posterior column sensation will be lost
on the same side. Hemiplegia will be on
the same side but the
uh pain and temperature will be lost on
the opposite side. So these are the
localizations of hemiplegia that we we
discussed. So so this is how you
localize
hemiplia. So we discussed about the
various sides of hemiplegia. We
discussed that you have a anterior
circulation. We have a posterior
circulation that is there. So anterior
circulation the sides we discussed
was what are the sites in the anterior
circulation we discussed? Lower limb
lower limb no anterior circulation. What
are the three sides? Internal capsules.
Internal capsu subcortex. That is the
three anterior circulation. The
posterior circulation sites we discussed
was midbrain, pawns, medula and rarely
the spinal cord. And we discussed how do
we localize based on each most common
site internal capsule. What are the
features? Contrlateral denseia,
contrlateral um facial paly,
contrlateral hemisensory loss and
homonymous hemianopia. We say cortex if
the patient has aphasia, apraxas or
seizures. And cortex never has dense
hemiplegia. It is either upper limb
predominant or lower limb predominant
hemiplegia that could be there in a
cortical
lesion. Midbrain third nerve on one side
hemiplegia on opposite side. The
syndrome is named Weber
syndrome. Pawns you have ipsilateral
element facial palsy contraateral
hemoplegia plus or minus seventh sixth
nerve involvement on the side and that
syndrome is called as Millard Gubler
syndrome. When we came to the medula, we
discussed that could be a medial
medlerary syndrome. There could be a
lateral medary syndrome. If there is a
medial medary syndrome, the four M are
getting involved. Motar pathway produces
hemiplegia. Hemiplesia can be
ipsilateral or contrlateral because
decursation. Second M is motor cranial
nerve 12. So the 12th nerve weakness
will happen. Third M is MLF medial
longitudinal physical deficitus
interuclear of thermoplia and the fourth
M that we have is medial leminiscus. So
the patient will have loss of posterior
column sensations. Coming on to the most
important lateral medularary syndrome
four S's that we had spinoalamic spinal
tract of triminal nerve sympathetic and
spinal cerebellar. So the patient has
crossed sensory loss same side face
opposite side
body syndrome ipsilateral atexia
horarsseness of voice loss of gag reflex
and hiccups as a symptom that they could
have. So that is lateral medillary
syndrome and the rest of the strokes
that you could have is the spinal
heiplegia where you have the classical
brown sick quad same side motor and
posterior column opposite side sensory
of pain and temperature lost. Now it is
important for us to localize because
clinically we can order for a specific
investigation. Remember whenever we
require the brain stem to be evaluated
MRI is always better. CT scan will not
pick and brain stem stroke since the
cranial nerves get involved the patients
can have various complications since
they will not be able to swallow they
can
[Music]
have problems with the aspirations and
aspiration pneumonas etc can happen with
that and also atexia is important
feature of poster circulation that is
the brain stem getting involved uh
whether the patient recovers or or what
is the recovery chances with stroke
basically ally depends upon the amount
of infact that is there. It doesn't
depend upon the site alone. It's the how
big is the inact. The in fact a big
infact in a non-critical area may not
produce any
deficits. Small inact in a critical area
the patient can succumb. So uh the
recovery depends upon the sites that is
involved, the size of the infacts and
the coorbids that the patient has.
So I think that is what uh we discussed
about localization of stroke importance
of localization as a part of treatment.
Yes, we have to be aware of certain
complications that can be there when the
cranial nerves get involved. And please
remember why the cranial nerves get
involved
because the cranial nerves will only get
involved if the nucleus gets involved.
Suprauclear they do not get involved
because there is bilateral
representation. Importance of jaw jerk.
Uh again remember jaw jerk the cranial
nerve we are testing is which cranial
nerve which cranial nerve is jaw
fifth cranial nerve. So fifth cranial
nerve. Now normally the jaw jerk is not
elicitable but if the jaw jerarch is
brisk okay the jaw jerk is brisk or it
is exaggerated it means there is an
upper motor neuron leion of the fifth
nerve. We know the fifth cranial nerve
nucleus is located in the
where is the fifth cranial nerve located
pawns upper part of pawns. So um for
that means it is above the pawns. So
when the jaw jerk is exaggerated it
means we have a lesion above the pawns
either in the midbrain or the cortex or
the internal capsule. Again it also
means it is not one-sided lesion. It has
to be bilateral leions only then the
cranial nerve will get affected. So uh
jaw jerk exaggerated means bilateral umn
lesion above the pawns. The disease we
call it as pseudo bulbar paly. Pseudo
bulbar paly it's nothing but umn for the
lower cranial nerve that is what we mean
by pseudo bulbar paly. Why persistent
hiccups? because of I've told you the
nucleus that gets involved there the NTS
the nucleus ambiguous and also certain
uh theories that you have something
called as a marit triangle there that
gets involved so persistent hiccups is a
very important sign of that middle but
please remember hiccups can occur due to
various other causes you have to rule
out other things also it could occur due
to uremia hyponetriia okay those things
have to be ruled
out emotional fibers in balbar versus
pseudo fiber
uh that's because of the facial nerve.
So emotional fibers emotional component
is related to the facial nerve. So
facial nerve we say pawns has the
nucleus which controls the various parts
of the facial expression. But the
emotional fibers are located in
different parts. It could be located in
the hippocampus embdela frontal cortex.
So these emotional fibers finally have
to travel through the facial. Now but
their nucleus is not in the pawns.
Do you understand the nucleus is not in
the pawns nucleus they don't have
nucleus emotional fibers are from
multiple side but finally they travel
through the facial nerve so if you have
a facial nerve involvement ln
involvement the emotional fibers are
involved but if you have a um
involvement upper motor type of facial
nerve paly emotional fibers are spared
because they are arising from different
sources so emotional fibers are
difficult
to emotional fibers are spared in case
of um and facial palsy. That means if
you crack a joke, the patient will
laugh. But if you ask him to laugh,
he'll not be able to laugh. How do you
check propreception on the face? Prop
reception you don't check. You check
only vibration. That's what and fine
touch. That's the same pathway. There's
no propriception should be tested. What
are the features of waterershed? In
fact, now waterershed in fact they will
not fit into any of the criteria.
Depends upon where the waterershed is.
If it is in the ACA and MCA mid part,
they may have hemoplegias. If it is in
the occipital cortex, they may just have
uh visual loss or hemianopias that could
happen. Yeah. Pseudobelvar palcy this is
what I just explained. Pseudobalbar paly
is
bilateral paly whereas balbar paly means
lmn paly. So the difference is
pseudobalbar paly the patients will have
emotional incontinence. That's a very
characteristic. They'll spontaneously
cry, spontaneously laugh and very
important, jaw jerk is exaggerated, gag
is exaggerated and it is bilateral
pyramidal cortical spinal tract
involvement. So the patient will have
bilateral exaggerated reflexes,
bilateral
extens. Why is it called pseudobelvar?
Because the patient has uh symptoms
suggest you of lower cranial nerves but
it is not due to the cranial nerve
involvement. It is because of the
bilateral cortical nuclear. So it
behaves like the cranial nerve but the
cranial nerve is nucleus is not
involved. It is because of the cortical
nuclear. That's why it's called a
pseudobel. Jokic exaggerated is the
feature of pseudobelar palcy. That's the
common question they ask you in your
bas. Any other questions or doubts?
Clumsy hand clumsy hand syndrome with
disorder. Can you explain about that? Uh
there are lacunar influx. We were
talking about all this thrombosis and
emolism and hemorrhage on bigger areas
but uh small vessels can get blocked. We
call it as lacunar influx. So this
lacunar influx can occur at various
parts. So it does not involve the entire
meal. So it's a small structure like a
poster limb of the internal capsule can
get involved or basis pontis get
involved. So it's a very small structure
that is getting involved. So the entire
pyramidal tract or entire cranial nerve
will not get involved. So disarthria
clumsy hand syndrome is a type of
lacunar in fact which occurs due to the
involvement either of the basis pontis
or poster limb of internal capsule. So
they will not have uh any
u complete hemoplegia. They'll just have
some amount of disarthria facial
weakness because of that or the uh
cranial nerve involvement and they'll
have clumsiness in the hand. So it could
occur due to uh thealamus involvement.
It could occur in the nucleuses that are
located there. So this is a part of
lacunar influx. So they will not have
all the features of a full pyramidal
tract involvement. Sometimes you can get
the lacinar influx could be pure motor
or pure sensory also but disartria
clumsy hand could be either in the basis
pontis postal limb of internal capsule
or sometimes in the cerebilum
also. What about involvement of vital
centers in the medula?
If the medula you have a big lesion that
is there, it can cause death because of
respiratory
depression frontal eye field etc. I
think it's a long topic. I don't think
so I'll be able to complete it in the
small when we if at all we discuss
sometimes of theopopleas then we can
discuss
about frontal life fields anything
related to
stroke members please feel free to ask
any kind of doubts with sir it was a
indeed was a brilliant session sir
indeed one of the best sessions we had
in white army so far uh it was very nice
uh uh to listen to your explanations
questions and such sweet explanation
sir. Thank you so much. Members feel
free to ask any questions related to
stroke today. Okay. Mono versus saying
pontine hemorrhage why there is a
hyperarexia. Hyperexia pinpoint pupil.
Yeah. Pinpoint pupil is because of
horner syndrome. Okay. Pontine
hemorrhage. Horners has meiosis. So the
patient has pinpoint because of horness.
the temperature set point the
hypothalamus and the control of the
hypothalamus is at that point there
that's why they have
hypothermia venus thrombosis is a stroke
venus thrombosis is a venus stroke at
that time I told CVT is not stroke when
I talk when I was speaking about stroke
I was speaking about arterial stroke
only venus thrombosis also belongs to
stroke but does not fit into the
classical definition of a arterial
stroke mono versus diplegia again
remember monopia one arm only. Diplegia
the word diplegia means symmetrical
structure involvement on either side of
the body. Now if I say facial diplegia
means symmetrical involvement of the
face on either side or if I say diplegia
for the body classically described is
for uh your cerebral pulsy but they have
symmetrical involvement on either side
of the body that's when we mean
diplegia. Hemoplegia is one side, mono
is one, one limb only. Diplegia is
symmetrical structure involvement on
either side of the body. Okay? Due to a
cortical involvement. Diplegia is a word
used only due to cortical involvement
specifically for cerebral palsy.
So lack stroke in internal capsule and
difference between the whole internal
capsule lenticular triate artery stroke.
What is the difference?
Individual branches of the uh internal
capsule. Again remember lenticlorostry
is not one branch. Lenticlorost is
multiple branches are there in the
lenticlorostrite. So just one
lenticloride branch getting blocked will
not produce all the features. If all the
features all the features are there that
means it is multiple vessels getting
involved or it's a hemorrhage which we
discussed. These lacking or strokes
involve only one of those branches. So
they may just produce pure monoplesia
only. They may not have sensory problem.
They may not have facial or they may
have just disarthria. They may not have
other features could be there. So in the
lacina strokes you'll have only one of
the features. You will not have all the
other features that will be
there. If the patient develop giddiness
and vomiting at 5:00 p.m. then patient
is stuper by the next day. Okay. So 5:00
p.m. it's
uh okay it's hemorrhagic stroke most
often which produces this uh rapid
deterioration of things like that. Okay.
Uh most likely it could be a cerebellar
hemorrhage that could be there which
generally produces worse worst sight of
bleed is in the cerebulum because it
directly compresses on the fourth
ventricle and you have rapidly
progressive raised intraranal tension
and the patient can go into coma.
Evening occurs of stroke is most often
hemorrhagic or emolic strokes. It's
unlikely to be thrombosis. Okay. So
stroke in evolution versus progressive
stroke. Stroke in evolution both these
words are no longer there. Stroke in
evolution is nothing but thrombotic
stroke. Okay. Thrombotic stroke where
the deficit is progressing.
So in morning the in morning the stroke
and MI are more common. Is it due to the
sympathetic surge or no? Because of the
proth thrombotic state. Remember the
clot which is formed should get liced
isn't it? So that requires a
fibbrinolytic system and fibbrinolyis
starts with what? What starts
fibbrinolyis? How does fibbrinolyis
start? What should how does the
fibbrinolyis
start? What is the the first factor that
is required there?
Plasine. Plasine. Yes. plasminogen
should get activated. So the plasmogen
should get activated that will convert
into plasine and then the fibbrin
breakdown happens. So now this plasmogen
to get activated you require a factor
called as the tissue plasmogen activator
tpa you heard of it and in the stroke
also in acute strokes we give isn't it
we give what do we give for acute stroke
RTPA RTPA isn't it recominant tissue
plasmogen activator so that is the key
uh factor that is there tissue plasmogen
activator now the function of the tissue
plasmminogen activator is uh The
function of the tissue plasmogen
activator is governed by one more
factor. I think in pathology you would
have learned which is produced at the
endothelium called as P AI. What is the
full form of PI?
Protease activator inhibitor.
You're coining a new term. We're talking
about plasmogen. So it's called as
plasmogen activator inhibitor. So that
is produced at the endothelium.
Plasmogen activator inhibitor is
produced in the endothelium and the act
the function of the plasmminogen
activator inhibitor is to inhibit the
plasmminogen. So if a stroke has to
happen if the thrombosis has to happen
what should happen the plasmogen
activity should be suppressed isn't it?
Plasmogen activity has to be suppressed
only then the clot will form. So at 4:00
a.m. in the morning the plasmogen
activator inhibitor levels are high and
that is why even if you go to sleep at
10:00 there is stasis and all those
things at 4:00 a.m. in morning that is
where the plasmogen activator inhibitor
levels activity is high and as you age
why do you get MI at older age why do
you get stroke at older age it's because
of this endothelial dysfunction more the
endothelial dysfunction more is the
activity of plasmminogen activator
inhibitor and that is where the
fibbrronolyis will not happen and that's
why stroke happens early in the morning
yeah the other factors are always there
stasis is there hyperccobility is there
endothelial injury can occur any time
but uh this is The proposed mechanism
why you get strokes in early morning
hours, thrombotic
strokes. Hope that was
clear. Features of thelamic stroke.
Features of theamic stroke. They get
something called called as a gerine
syndrome. They have very severe burning
disesthesia on the side of uh on the
side of stroke. They have burning pain.
They develop. That's a classical feature
they get.
Additionally they have burning pain.
Okay. It's called as degeneri
syndrome. Any other question? How do you
check Babinsky bilateral
uh bologn amputation is there as far as
you have the amputation stump? Bologn
means amputation stump is still there.
You can stroke the amputation stump and
look for the contraction of the uh
tensoracial ata. So tensor facial ata is
still there. So you can stroke the stump
there and you can check it there. But uh
if the amputation is above knee then we
can't check it in the lower limb. We'll
have to look for beansky equivalent in
the upper limb. So you have something
called as a beansky equivalent in the
upper limb. You have your uh hoffman
sign. You have the tromus sign. So those
are the uh things that you see in case
of you can check if the lower limbs is
amputated above only. If below you can
still stroke the stump and look for the
ilotrial tract.
Venus system thrombosis. How do you
differentiate? Again, uh the stroke
producing due to again remember the
Venus thrombosis CVT etc. generally
produces a diffuse uh focal deficits are
little rare in there. They've come with
encphilitis sort of features. They have
headache, they have seizures etc. And it
does not fit into a vascular territory.
The deficit does not fit into vascular
territory. So that's why I told Venus
stroke is a total different feature
compared to an arterial thrombosis.
So they will not have all the features
like a particular arterial territory
which is getting
blocked. Any other
questions? So if a patient comes with
well controlled hypertension with hemi
parisis then what would be the uh
location of the stroke? Well only
hemiparis. Yes sir. Only hemiparasis.
The most common location is internal
capsule
itself. Okay. The most common location
is internal capsule itself. Either the
facial nerve has recovered or the facial
nas will occur later. Most common
location is always internal capsule.
Okay. Uh hypertension longstanding you
have something called as lipohilyinosis
that happens there. The small vessels
get involved and any structure where
there is a small vessels. So most common
location would still be the internal
capsule. Okay.
So could we consider it as a lacer
stroke? Then if pure motor it's it is
lacunar. Yeah. Again please remember
lacunar is based on the size when we do
an MRI or you get the size. Okay. If on
the CT or an MR you get a big inact we
can't say it is lacun. Lacunar is uh uh
lacunar is based on the size that we get
on the imaging. Okay.
So what is the difference between rend
and uh tia? Rend is a term please
remember is a term is outdated way back
in 2003 that word was removed. Okay r is
no longer there but yes you should know
rind means the deficit is progressing
for a week whereas TIA recovers within
24 hours and the latest definition that
we have November 2020 TIA the definition
says it has to recover within 1 hour.
Okay, the deficit should recover within
one hour and more importantly on imaging
of the brain spinal cord or retina you
should not find any
infin TIA there should be a focal
deficit which completely recovers within
earlier we were calling it as 24 hours
now we say it's 1 hour but the imaging
should be totally normal there should
not be an in fact if you find an inact
it is stroke okay now all the
definitions have been revised and they
uh define it anatomically based on the
MRI or a scans. If there is an infact
that becomes stroke even if it is 1 hour
recovered it becomes stroke. So TIA is
within 24 hours the traditional
definition new definition says 1 hour
but there should not be any infact on
MR was the deficit which was progressing
up to 7 days. That term is no longer
used
about the CT city scan and MRI
difference. Now recently it is said that
diffusion weighted MR should be done.
Diffusion weighted MR is the gold
standard test that we have. Yes, that is
the but we normally do but we normally
do CT scan and CT scan is not that
applicable. CT scan is done very fast.
CT scan you can get it done within 5
minutes. Why do we do a CT scan is to
rule out a bleed because the basic
difference in treatment of stroke is
between a hemorrhagic stroke and an
infact. Hemorrhagic stroke we'll have to
start on anti-adma measures etc. Whereas
an infact we'll have to start on
antiplatelets, anticogulants and we'll
have to thrombolize. So CT is done very
rapidly very important CT gets done
within five minutes and you can get the
report and rule out a bleed. But in fact
look on a CT a plain CT would take 6 to
8 hours for it to appear. So if you wait
for a CT change to happen it will the
golden period that is the 3 hours that
you have for thrombolyis is gone. So MR
is best and still best MRA is what we
call it as a diffusion weighted MR.
Again that would take a minimum of 30 to
45 minutes. Okay. Okay. So if the
patient comes really early we can do a
diffusion weighted MRI and within 3
hours we can
thrombolize target. Yeah. Tell me. So
hemorrhagic stroke patient will say
complain about headache or not is
differential. Yeah. Most often they'll
have headache. Yes. Headache as a
feature prior to the stroke and
afterwards is a very important sign of
hemorrhagic strokes. Yes.
Agreed. Target BP in es schemic stroke.
Please remember in eskeemia we should
not lower the BP even if it is above 200
you should not lower it in eskeemic
strokes because that is the region
surrounding the eskeemic area what we
call it as eskeemic penumbra the blood
supply to that the vascularity to that
is maintained by a pressure head so if
inveradently if you lower the BP you're
going to cause more damage for the
eskeemic area so unless we are planning
thrombolyis thrombolysis we have a cutff
of 80 you have to have a blood pressure
less than 180 otherwise you can't have
thrombolyis because otherwise
hemorrhagic conversion is high only then
we'll give them a anti-hypertensive
otherwise in an acute stroke even the BP
is more than 200 you will not correct it
at least for the first 12 hours because
this hypertension is called as a
reactionary hypertension to preserve the
eskeemic penumbra this BP is raised so
unless it is a you're planning for
thrombolyis you don't have to get it
down but yes there are certain absolute
indications like a intraceral hemorrhage
we'll have to get it down immediately if
the patient has renal failure or he has
an iotic dissection or a pulmonary edema
then we'll have to decrease it
immediately stroke mimics again uh a
very common question they ask you in
your viva is what are the stroke mimics
you have structural stroke mimics and
functional stroke mimics structural
means there is some problem but it is
not stroke and functional is where there
is no problem And it is. So common
functional ones are like migraine. You
have hemoplegic migraine,
hypoglycemia and sometimes
hyperglycemia. Hyperglycemia can also
produce stroke. Uh other electrolyte
disturbances can also produce
stroke. Epilepsy or a seizure can
produce something called as a todd
paralysis after uh it may last for 48
hours. Sometimes a week also it might
last. So you can have todds paralysis.
You can have tumors which can manifest
acutely as a stroke or you can have a
space occupying lesion coming as a
stroke. So these are the mimics of
strokes. Okay, common ones you have to
roll out them and you have psychoggenic
patient can mimic that feels that he
wants to gain something so he might
mimic stroke. So that's called as a
functional
hemiplegia. Stuttering hemiplegia again
uh this was a term used we do not have
it anymore. uh stuttering hemoplegia is
where it uh it's a uh frequent TIA is
coming supposedly you have different
different TAs coming within a span of a
few hours it comes and goes comes and
goes comes and goes it herald stroke in
the next 24 hours the patient will go
into a completed stroke in the next 24
hours again these words are all obsolete
stuttering hemoplegia stroke in
evolution all those things are nothing
uh now presently you have all functional
definitions that are there But yes, this
can be asked in your exam. So you should
be able to answer
that. Any other
questions? You have this nothing about
stroke then maybe if you have time you
can ask otherwise I think you already
crossed to
us. Yeah. What do you want to ask about
lia?
Yeah you can ask.
Uh Mr. MacBook you can unmute yourself
and ask. Okay sir
directly instead of typing.
Sir, they will keep asking the whole
night sir because if you keep explaining
so nicely it's a good opportunity for
them sir to clear their doubts but yeah
we'll have a separate session on
important topics of gastro as well by
sir week by week uh s agreed to take us
classes on important topics anyway so I
think today we had an very extensive
discussion on stroke. I think it was
very like very sort of explained in a
very simplified manner in a very
understandable manner. Even like you
know a student like me very average
every student like me could understand
the most of it. So sir thank you so much
we are really delighted to have a class
like this sir. Um in fact I on behalf of
all the white army members I should say
admit that this is one of the best class
we had in the white army so far. Thank
you really sir. Really and we are really
grateful to you for taking such valuable
classes for us and making the studies
more and more interesting.
Sir, we are worried if every like
everyone will be taking up medicine only
next listening to your class. It would
be nice. I would not mind more
cardiologists rather than cardiothoracic
people. Why sir? No, I'm saying more
medical people. That would be always
nice. Yeah. Anyways, medicine is needed
for all the subjects. And yeah
definitely they will carry forward your
legacy sir your knowledge whatever
you're sharing they'll carry for carry
it forward yeah and uh thank you I don't
know sir how to thank you really you
have been a constant source of
motivation for us and also a constant
source of energy for our white army you
have been the one of the best mentors we
have so we don't have words you are our
own sir so no problem I don't I don't
think we should thank you in fact okay
it's yours is yours all yours So sir uh
sir you take this platform to teach the
students uh the best of yours sir and we
are really indeed honored privileged and
grateful to you for all all your
teachings and valuable time you spend on
the weekends for us thank you so much
sir if possible sir we'll have a
medicine I'll let you know I'll let you
know because I'll let you know the
schedules whatever it is okay yes sir
yes right okay thank you so much for all
the activ today the participation was
also very good. The students were very
enthusiastically participated
and cleared most of their doubts. Yeah.
Hopefully their doubts are clear. They
will be able to localize disease better
when they see the next patient in the
Yeah. And yeah request is members use
this video to revise. Okay. As and when
you require you can use these videos to
revise for yourself and uh like remember
better. Okay. So thank you one and all
for all your for all the participation.
Thanks. A special thanks to sir for
making the best use of this evening.
Thank you so much. Okay. Thank you. Bye.