CENTRAL NERVOUS SYSTEM

TRAUMA

G. Roman MD.,FPSP 2009

TRAUMA
 Considerations:
 Anatomic location
 Capacity for repair
 Factors:
 Shaped of the object causing the trauma.
 Force of impact
 Head in motion
 Penetrating or blunt

G. Roman MD.,FPSP 2009

Three types of injury
 Skull fractures
 Parenchymal injury
 Vascular injury

*Usually there is a combination of the

three.

G. Roman MD.,FPSP 2009

Skull Fracture
 Diastatic fracture – crosses suture
lines.
 Displaced skull fracture.

G. Roman MD.,FPSP 2009

PARENCHYMAL INJURIES
 CONCUSSION vs. CONTUSSIONS.
 EFFECTS OF TRAUMA
 Rapid tissue displacement.
 Disruption of vascular channels.
 Hemorrhage
 Tissue injury
 Edema
 COUP AND CONTRECOUP INJURY

G. Roman MD.,FPSP 2009

G. Roman MD.,FPSP 2009
G. Roman MD.,FPSP 2009
G. Roman MD.,FPSP 2009
G. Roman MD.,FPSP 2009
G. Roman MD.,FPSP 2009
G. Roman MD.,FPSP 2009
G. Roman MD.,FPSP 2009
G. Roman MD.,FPSP 2009
TRAUMATIC VASCULAR INJURY
 EPIDURAL
 SUBDURAL
 SUBARACHNOID
 INTRAPARENCHYMAL

G. Roman MD.,FPSP 2009

G. Roman MD.,FPSP 2009
G. Roman MD.,FPSP 2009
G. Roman MD.,FPSP 2009
G. Roman MD.,FPSP 2009
G. Roman MD.,FPSP 2009
G. Roman MD.,FPSP 2009
G. Roman MD.,FPSP 2009
G. Roman MD.,FPSP 2009
G. Roman MD.,FPSP 2009
CEREBROVASCULAR
DISEASES
 THROMBOSIS
 EMBOLISM
 HEMORRHAGE

G. Roman MD.,FPSP 2009

HYPOXIA
 Functional
 low inspired partial pressure of oxygen.
 Impaired oxygen carrying capacity
 Inhibition of oxygen use by tissues
 Ischemia
 Transient
 permanent

G. Roman MD.,FPSP 2009

ISCHEMIA
 Modifying factors:
 Collateral circulation
 Duration of ischemia
 Magnitude and rapidity of reduction of
flow
 Types of Ischemia:
 Global cerebral ischemia
 Focal cerebral ischemia

G. Roman MD.,FPSP 2009

GLOBAL CEREBRAL ISCHEMIA
 Cardiac arrest, shock , severe
hypotension
 Confusional state to irreversible
tissue damage.
 Selective vulnerability
 Pyramidal cells of the Sommer sector of
the hippocampus
 Purkinje cells of the cerebellum
 Pyramidal neurons in the neocortex

G. Roman MD.,FPSP 2009

Brain Death
 Persistent evidence of diffuse
cortical injury (isoelectric – “flat” –
EEG)
 Brain stem damage
 Absent reflexes
 Absent respiratory drive
 Absent perfusion

G. Roman MD.,FPSP 2009

FOCAL CEREBRAL ISCHEMIA
 Thrombosis or embolism
 Thrombosis usually atherosclerotic in
nature. Common sites:
 Carotid bifurcation
 Origin of middle cerebral artery
 Either end of basilar artery
 Arteritis usually seen in syphilis & TB
in the setting of immunosuppression

G. Roman MD.,FPSP 2009

FOCAL CEREBRAL ISCHEMIA
 Embolism usually from cardiac
mural thrombi, plaque from carotid
arteries
 Territory of distribution of middle
cerebral artery is most frequently
involved.
 Emboli tend to lodge where blood
vessels branch or in areas of
preexisting stenosis
 Shower embolization (fat embolism)
usually after bone fractures
G. Roman MD.,FPSP 2009
G. Roman MD.,FPSP 2009
BRAIN INFARCTS
 HEMORRHAGIC (RED) INFARCTS
 Usually embolic

 NONHEMORRHAGIC (PALE, BLAND,

ANEMIC) INFARCTS
 Usually thrombotic

G. Roman MD.,FPSP 2009

G. Roman MD.,FPSP 2009
G. Roman MD.,FPSP 2009
G. Roman MD.,FPSP 2009
INTRACRANIAL HEMORRHAGE
 INTRACEREBRAL
(INTRAPARENCHYMAL)

 SUBARACHNOID HEMORRHAGE &

RUPTURED BERRY ANEURYSMS

 VASCULAR MALFORMATIONS

G. Roman MD.,FPSP 2009

INTRACEREBRAL (INTRAPARENCHYMAL)
HEMORRHAGE

 Mid to late adult life (peak 60 yrs)

 Most due to rupture of intraparenchymal
vessel.
 Hypertension is most common cause.
 Chronic hypertension causes Charcot-
Bouchard microaneurysms
 Ganglionic hemorrhages – basal ganglia
and thalamus
 Lobar hemorrhages – cerebral
hemisphere

G. Roman MD.,FPSP 2009

G. Roman MD.,FPSP 2009
G. Roman MD.,FPSP 2009
G. Roman MD.,FPSP 2009
G. Roman MD.,FPSP 2009
G. Roman MD.,FPSP 2009
SUBARACHNOID HEMORRHAGE
 Rupture of berry aneurysm
 Other causes:
 Extension of a traumatic hematoma
 Rupture of hypertensive intracerebral
hemorrhage
 Vascular malformation
 Hematologic problems
 Tumors

G. Roman MD.,FPSP 2009

G. Roman MD.,FPSP 2009
G. Roman MD.,FPSP 2009
G. Roman MD.,FPSP 2009
G. Roman MD.,FPSP 2009
G. Roman MD.,FPSP 2009
G. Roman MD.,FPSP 2009
G. Roman MD.,FPSP 2009
 VASCULAR MALFORMATION

 ARTERIOVENOUS MALFORMATIONS

 CAVERNOUS ANGIOMAS

 CAPILLARY TELANGIECTASIAS

G. Roman MD.,FPSP 2009

ARTERIOVENOUS MALFORMATIONS

 Tangle mass of numerous abnormally

tortuous, misshaped vessels.
 Males are more affected.
 Between 10 & 30 yrs old.
 Clinical presentation:
 Seizure disorder,
 intracerebral hemorrhage
 Subarachnoid hemorrhage
 Common site – middle cerebral artery

G. Roman MD.,FPSP 2009

G. Roman MD.,FPSP 2009
CAVERNOUS HEMANGIOMAS
 Greatly distended vascular channels
 Devoid of intervening nervous
tissue
 Cerebellum, pons and subcortical
region

G. Roman MD.,FPSP 2009

CAPILLARY TELANGIECTASIA
 Dilated thin wall channels separated
by normal brain tissue
 Most frequently in the pons

G. Roman MD.,FPSP 2009

HYPERTENSIVE CEREBROVASCULAR
DISEASE
 Most important effects:
 Massive intracerebral hemorrhage
 Lacunar infarcts
 Slit hemorrhages

G. Roman MD.,FPSP 2009

G. Roman MD.,FPSP 2009
LACUNAR INFARCTS
 Arteriolar sclerosis  small cavitary
infarcts – lacunes
 Lenticular nucleus, thalamus,
internal capsule, deep white matter,
caudate nucleus and pons

G. Roman MD.,FPSP 2009

G. Roman MD.,FPSP 2009
HYPERTENSIVE ENCEPHALOPATHY
 Diffuse cerebral dysfunction
 Headache, confusion, vomiting,
convulsions , coma.
 Brain edema  herniation

G. Roman MD.,FPSP 2009