CNS PATHOLOGY

Cerebral infarction
• Ischaemic stroke characterized by sudden loss
of blood circulation to an area of the
brain,resulting to corresponding loss of
neurologic function
• Caused by thrombotic or embolic occlusion of
a cerebral artery and is more common than
hemorrhagic stroke.

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 presentation
• Suspicion to any patient with acute neurologic deficit
ar any alteration in level of consciousness
• Abrupt hemiparesis,monoparesis,quadriparesis
• Hemisensory deficits
• Monocular or binocular visual loss
• Dysarthria
• Ataxia
• Aphasia
• Decreased level of consciousness
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 pathology
• Vascular occlusion results to ischaemia causing cell hypoxia
and depletion of cell adenosine triphosphate (ATP),
• Without ATP no energy to maintain ionic gradient across
cell membrane,Na+ -K+ pumps and cell depolarization.
• Influx ofsodium and calcium ions and passive inflow of
water in to the cell lead to cytotoxic edema,calcium
activate degraditive enzymes
• Disruption of blood brain barrier results with in 4-6 hrs
• There is release of free radicals,nitric oxide,arachidonic acid
leading to neuronal damage

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 Cerebral haemorrhage
• Bleeding occurs directly into brain parenchyma –mechanism
thought to be leakage from small intracerebral arteries
damaged by chronic hypertention
• Intracerebral haemorrhage and hemorragic stroke used
interchangeably
• S+S
• Depends on area affected
• Right hemiparesis
• Right hemisensory loss
• Visual field affected
• Aphasia

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 Intracranial hemorrage CONTI...
• Accumalation of blood with in the cranial vault
• May occur with in brain parencyma or
sorrounding meningeal spaces
• Accounts for 8-13% of all strokes
• Displacement of brain parenchymal may cause
ICP and potentialy fatal herniation

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 Nontraumatic
Hypertensive Damage to blood vessels
o Hypertention
o Eclampsia
o Drug abuse
Auto regulation dysfunction and so excessive blood flow
o Reperfusion injury
o Cold exposure
Rupture aneurysm
o Moyamoya
o Amyloid angiography
Altered homeostasis
o Thrombolysis
o Anticoagulation
o Bleeding diathesis
Hemorrhagic necrosis
o Tumour
o Infection
Venous outflow obstruction
o Cerebral venous thrombosis
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 Contin..
• Hypertention associated with small vessel
vasculopathy with areas of necrosis and
development of charcot-bourchard aneurysm
affecting penetrating arteries throughout the
brain

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 traumatic
• Blunt head indury and more so if treated with clopidogrel,warfarin
• Penetrating injuries
Gunshot injuries etc

Predilection sites
o Basal ganglia 40-50%
o Lobar regions 20-50%
o Thalamus 10-15 %
o Pons 5-12%
o Cerebellum 5-10%
o Other brain stem sites 1-5%

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• Intraventricular hemorrage occurs in one third
of intracerebral hemorrage from extention of
thalamic ganglionic bleeding into ventricular
space

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 Intraparenchymal hemorrage
subarachnoid
• Subarachnoid hemorrage (SAH) –extravasation of blood into the subarachnoid space-between pia
and arachnoid membranes
• Commonest in head trauma but SAH has been used widely with nontraumatic (spontaneous)
hemorrage
• Seen in ruptured aneurysm,arteriovenous malformation
S+S
Prodromal signs usualy due to effect of aneurysm,leaks,emboli these are sensory of motor distabance
Seizure
Ptosis
Dysphasia
Lassic presentation are:
Headach of sudden onset
Diziness,menigeal irritation,loss of consciousness,seizures
Orbital pain photophobia
Visual loss,retinal haemorrhage
Mild to moderate BP elevation,temp elevation

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• Hydrochephalus
• Rebleeding
• Vasospasm
• Seizures
• Cardiac dysfunction

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 Vascular malformations
Vascular anomalies divided into
• Vascular tumours(hemangioma,spindle cell angioma,lobular capilary hemangioma,hemangioendothelioma,kaposis
sarcoma,angiosarrcoma)
Vascular malformations
• Capillary malformatiom (CM)
• Nevus simplex “angel kiss”
• Reticulate CM
• Cutis marmorata telangiectatica congenita
Lymphatic malformation (LM)
Acuired progressive lymphagioma
Primary lymphoedema
Chanel type LM
Venous malformation (VM)
• Common vm
• Cerebral cavernous malformation (CCM)
• Familial vm cutaneomucosa
others
• Arteriovenous fistula
Combined vascular malformations
Vascular malformations associated with other anomalies
Maffucci sydrome
Macrocephaly-cm
Stuge-weber syndrome

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 pathology
• Not well understood
• But thought to involve vasculogenesis eg errors
in vesel remodeling ,excess angiogenesis
• AVMs never regress
• Morbidity and mortality depend on
o location and size
o Accessibility for surgery
o Presence or absence congestive heart failure
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• Commonly misdiagnosed
• May become more clinically evident in 2 or 3rd
decade
• intracranial more common than extracranial lesions
• Palpable thrill,bruit
• Facial assymetry
• Secondary infections
• bleeding

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• Intracranial pressure (ICP)
pressure inside the skull and thus in
the brain tissue and cerebrospinal fluid (CSF).
ICP is measured mmHg and, at rest, is normally
7–15 mmHg for a supine adult
Monro-kellie hypothesis
The pressure–volume relationship between ICP,
volume of CSF, blood, and brain tissue,
and cerebral perfusion pressure (CPP) is known
as the Monro–Kellie doctrine or hypothesis

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 Increased intracranial pressure
• An increase in pressure, most commonly due
to head injury leading to intracranial
hematoma or cerebral edema, can crush brain
tissue, shift brain structures, contribute
to hydrocephalus, cause brain herniation, and
restrict blood supply to the brain.It is a cause
of reflex bradycardia

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 causes
• Mass effect such as brain tumor, infarction
with oedema, contusions, subdural or epidural hematoma,
or abscesses all tend to deform the adjacent brain.
• Generalized brain swelling can occur in ischemic-anoxia
states, acute liver failure hypertensive encephalopathy, .
These conditions tend to decrease the cerebral perfusion
pressure but with minimal tissue shifts.
• Increase in venous pressure can be due to venous sinus
thrombosis, heart failure, or obstruction of superior
mediastinal or jugular veins.

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 Cont....
• Obstruction to CSF flow and/or absorption can occur
in hydrocephalus (blockage in ventricles or subarachnoid space
at base of brain, e.g., by Arnold-Chiari malformation),
extensive meningeal disease (e.g., infection, carcinoma,
granuloma, or haemorrhage), or obstruction in cerebral
convexities and superior sagittal sinus (decreased absorption).
• Increased CSF production can occur in meningitis,
subarachnoid hemorrhage, or choroid plexus tumor.
• Idiopathic or unknown cause (idiopathic intracranial
hypertension, a common cause in otherwise well people
especially younger obese women)

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•  CSF pressure has been shown to be
influenced by abrupt changes in intrathoracic
pressure during coughing (intra-abdominal
pressure), valsalva manoeuvre, and
communication with
the vasculature (venous and arterial systems)

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 pathology
• if caused by a unilateral space-occupying
lesion (e.g. a hematoma) can result in midline
shift, a dangerous sequela in which the brain
moves toward one side as the result of
massive swelling in a cerebral hemisphere.
Midline shift can compress the ventricles and
lead to hydrocephalus.

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 Cont...
• Once the ICP approaches the level of the
mean systemic pressure, cerebral perfusion
falls. The body’s response to a fall in CPP is to
raise systemic blood pressure and dilate
cerebral blood vessels. This results in
increased cerebral blood volume, which
increases ICP, lowering CPP further 

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 symptoms and signs
 headache, vomiting without nausea, The headache is
classically a morning headache which may wake them from
sleep.
The headache is worse on coughing, sneezing or bending and
progressively worsens over time. There may also be
personality or behavioral changes
ocular palsies,
altered level of consciousness,
back pain
 papilledema.
In children, a low heart rate is especially suggestive of high
ICP.
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 Cerebral oedema
• accumulation of fluid in the brain's
intracellular and extracellular spaces. There
are four fluid compartments in the brain-
blood (cerebral vessels), cerebrospinal fluid
(CSF) (ventricular system), interstitial fluid
(brain parenchyma) and intracellular fluid
(neurons and glial cells). These compartments
are interlinked and under normal physiological
conditions
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