GCS

1. Best eye response - (max 4)2. Best verbal response - (max 5)3. Best motor response - (max 6)

GCS- 13+ mild H I9-12- moderate H I8 or less – severe H I

HI

• May result in LOC• Longer unconscious and deeper coma >likelihood that pt has suffered severe HI• 60% good recovery• Based on US, UK and Netherland figuresfor every 100 HI, 5 VS, 15 severely disabled, 20 minor problems, 60 full recovery

Nature of lesions in HI

• Non - missile- RTA• Missile

Distribution of lesions• Focal• Diffuse

TIME COURSE

Immediate

Delayed

Primary damage• scalp laceration• skull fracture• cerebral contusions• ICH• DAI

Secondary damage• ischemia• hypoxia• cerebral oedema• infection

Pattern of damage in non -missile HIPattern of damage in non -missile HI

FocalFocalScalp- contusion, lacerationSkull - fractureMeninges - haemorrhage, infectionBrain - contusions, laceration, infection

Diffuse damageDiffuse damageBrain, DAI, DVI, HIE, Cerebral oedema

ICH is a complication of 66% of cases of non-missile head injury

HaemorrhageHaemorrhage

May be

EXTRADURAL

INTRADURAL - subdural, subarachnoid intracerebral

EDH

• Found in 2% HI

• Usually associated with skull fracture

• Arterial bleed - usually meningeal vessels

Subdural Subdural haemorrhagehaemorrhage

• Usually venous

• Rupture of bridgingveins

Subdural haematoma: classification

48-72 hours – acute composed of clotted blood

3-20 dys – subacute – mixture of clotted and fluid blood

3 weeks + - chronic encapsulated haematoma

Traumatic SAH

• may result from severe contusions• Fracture of skull can rupture vessels• IVH may enter SAS

• RULE OUT ANEURYSMRULE OUT ANEURYSM

Cerebral contusionsCerebral contusions

• Superficial bruises of the brain

• Frequent but not inevitable afterhead injury

Various types of surface contusions and lacerations

~ Coup – at point of impact~ Contrecoup- diametrically opposite point

of impact~ Herniation – at point of impact between

hernia~ Fracture related to # of skull

Sites of cerebral contusionsSites of cerebral contusions

• Frontal poles• Orbital surfaces of the frontal poles• Temporal poles• lateral and inferior surfaces of occipital poles• cortex adjacent to sylvian fissure

Uncommon types of focal brain damageUncommon types of focal brain damage

• Ischaemic brain damage due to traumaticdissection and thrombosis of vertebral or carotidarteries by hyperextension of the neck• Infarction of pituitary - due to transection of pituitary stalk• pontomedullary rent

InfectionInfection

• complication of skull fracture• Open HI• Incidence is increased even after closedHI as devitalised tissue prone to infection

Diffuse damageDiffuse damage

• DAI - widespread damage to axons in theCNS due to acceleration/deceleration of the head• Pts usually unconscious from moment of impact• Lesser degrees compatible with recovey of consciousness

Brain swelling and raised ICPBrain swelling and raised ICP

Results from:• cerebral vasodilation - inc cerebral blood vol• damage to BV - escape of fluid through BBB• inc water content of neurones and glia- cytotoxiccerebral oedema

ICH herniation

SubfalcineSubfalcineherniationherniation

Tentorial herniationTentorial herniation

Tonsillar herniationTonsillar herniation

End result of herniation is compression and Duret haemorrhages as seen in the pons

The pathologist and CNS neoplasms

Clinical details of importance~ Age~ Sex~ F/X~ Site of neoplasm

INCIDENCE;

~ Second commonest form of cancer in childrenAccounts for 3.5% of all deaths in the 1-14 year age group

Sixth commonest cause of cancer deaths in adults25% of all tumors in adults are in the brain and 35% are neurectodermal and 40% are metastatic

~ Most primary tumors are sporadic andof unknown aetiology

~ Secondary tumors vary greatly between 14-40%

~ Fewer than 5% are associated with hereditary syndromes that predispose to neoplasia

CNS neoplasms present with:

~ epilepsy (focal or generalised)~ focal neurologic deficits~ symptoms and signs of raised ICP~ symptoms and signs of hydrocephalus

SSites of cerebral tumorsSites of cerebral tumors

ADULTSSupratentorial tumors account for 90%

Therefore increased incidence of epilepsy and decreased incidence of headache

Posterior fossa tumours cause headache and vomiting as early features

CHILDRENCerebellum

PonsOptic nerve/chiasm

SUPRATENTORIAL TUMORS ARE RARE

ThereforeHeadache, vomiting, visual disturbances

commonEpilepsy - unusual

DiagnosisDiagnosis

1. Clinical picture

2. CT or MRI scan

3. Biopsy ~ smear~ Frozen section~ paraffin section

Epidemiological aspects of stroke

~ In the USA stroke is the third commonest cause of death

~ Incidence increases with age

~ Major risk factors for stroke are hypertension, cardiac disease, smoking, hyperlipidemia, and diabetes

~ Other causes OCP, sickle cell, coagulation disorders

~ In USA - brain infarction 10 times commoner than haemorrhage

Blood supply to the brain

~ Human brain approx 2% of body weight~ Receives 15% of total cardiac output O2 consumption approximately 20% of whole body (i.e high metabolic rate)~ How long would the brain survive if blood flow interrupted

Terminology

~ Ischaemia - arterial stenosis or occlusionInfarction - perfusion territory of the affected vessel

~ Global brain ischaemia - < CPP below the threshold for autoregulation i.e when systemic blood pressure falls very low e.g cardiac tamponade, heroin overdose, or ICP rises to a level that compromises cerebral perfusion

Resultant brain damage or infarction is accentuated in the

WATERSHED REGIONS

CPP= SAP - ICP

CPP > 40 mmHg - necessary for autoregulation

If CPP < 40 mmHg CBF falls dramatically

Selectively vulnerable zones

~ Hippocampus - CA1

~ Laminae 3 and 5 of cortex

~ Purkinje cells cerebellum

HYPOXIA - blood flow to the CNS may be normal or increased

Damage occurs in selectively vulnerable neurones

CIRCLE OF WILLIS

Berry aneurysms

Congenital

Risk of bleeding inc;• Hypertension• AVM • systemic vascular disease• defects collagen• polcystic renal disease

ICH causesICH causes

• Hypertension• Trauma• CAA• Berry aneurysm• AVM• Bleeding diathesis• Vasculitides• Drugs • Neoplasm• Infective

CNS INFECTIONCNS INFECTION

Development and outcomeDevelopment and outcomedepends ondepends on

Organism Organism natureroute of entrydose

HostHost Anatomical defenses - skull, meninges

Physiological - immune defense mechanisms

BacteriaBacteria

Entry into the cranial cavityEntry into the cranial cavity

Haematogenous -Haematogenous - distant foci e.g lung

Local spread -Local spread - Skull - middle ear, nasal sinus, osteomyelitis

Abnormal routesAbnormal routes - Trauma -fractures Surgery - shunts

Congenital sinus

BACTERIAL INFECTIONSBACTERIAL INFECTIONS

Depending on their virulence/pathogenicity bacteria can induce:

1. Purulent lesions

2. Cellular inflammatory reactions with giant cells

3. Inflammatory oedema caused by toxins and other inflammatory substances released by bacterial secretions or lysis, in the absence

of bacterial replication

PYOGENIC INFECTIONPYOGENIC INFECTION

1. BONE – EPIDURAL – usually spinal sec to osteomyelitis

2. DURA MATER - SUB DURAL - sec to sinusitis, otitis etc.

3. ARACHNOID – SUBARACHNOID – sec to haematogenous spread of bacteria

4. PIA - INTRAPARENCHYMAL - abscess

SUBDURAL

Three organisms responsible for acute meningitis in childhood or adult life

• Meningococcus

• Haemophilus influenza

• Pneumococcus

Bacterial meningitis

Complications of acute meningitisComplications of acute meningitis in the neonatein the neonate

• Obstructive hydrocephalus

• Cavitating lesions in the white matter

CSFBacterial Viral TB

low N low glucose

v. high Slightly increased

Raised protein

neutrophils

lymphocytes

lymphocytes

cells

Complications of bacterial meningitisComplications of bacterial meningitis

• Acute inflammation of adjacent structures

• Organisation of inflammatory structures

Organisation of inflammatory exudate

Impedes flow of Impedes flow of CSF into CSF into venous sinusesvenous sinuses

Obstructs CSF outflow fromObstructs CSF outflow fromIV ventricleIV ventricle

Cerebral abscess

~ Mean age – 35.2~ P/C – headaches, pyrexia, altered mental state (depends on site, number, and +/- secondary cerebral lesion)~ Site – frontal lobe commonest~ Majority – associated with sinusitis, mastoiditis

20% no source~ Bacteria isolated from 73%. Polymicrobial – 17.7%~ Anaerobes – 13.6%~ 9.8% died~ 11% developed epilepsy

Cerebral abscess

Predisposing conditions

Local – otitis media, sinusitis, trauma

Systemic ~ chronic lung disease~ cyanotic congenital heart disease~ transplants~ immunosupression

Parenchymal abscess formation

~ Early cerebritis (days 1-3)

~ Late cerebritis (days 4-9)

~ Early capsule formation (days 10-13)

~ Late capsule formation (days 14 onward)

AIMS OF TREATMENT

~ Eliminate infectious process

~ Reduce mass effect within cranial cavity – thus reduce secondary injury

~ Treat infections

Tuberculous meningitis

Usually M Tuberculosis

More commonly associated with documented history of tuberculosis exposure in children than adults

CSF

Bacterial Viral TB

glucose low N low

protein v. high Slightly increased

Raised

cells neutrophils

lymphocytes

lymphocytes