Download neuropath-for-psy-d-disorders

Document related concepts

Chickenpox wikipedia , lookup

Oesophagostomum wikipedia , lookup

Neonatal infection wikipedia , lookup

Leptospirosis wikipedia , lookup

Hospital-acquired infection wikipedia , lookup

Neisseria meningitidis wikipedia , lookup

Transcript
GCS
1. Best eye response - (max 4)
2. Best verbal response - (max 5)
3. Best motor response - (max 6)
GCS- 13+
mild H I
9-12- moderate H I
8 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 figures
for 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
Primary damage
TIME COURSE
• scalp laceration
• skull fracture
• cerebral contusions
• ICH
• DAI
Immediate
Delayed
Secondary damage
•
•
•
•
ischemia
hypoxia
cerebral oedema
infection
Pattern of damage in non -missile HI
Focal
Scalp- contusion, laceration
Skull - fracture
Meninges - haemorrhage, infection
Brain - contusions, laceration, infection
Diffuse damage
Brain, DAI, DVI, HIE, Cerebral oedema
ICH is a complication
of 66% of cases of nonmissile head injury
Haemorrhage
May be
EXTRADURAL
INTRADURAL - subdural,
subarachnoid
intracerebral
EDH
• Found in 2% HI
• Usually associated
with skull fracture
• Arterial bleed usually meningeal
vessels
Subdural
haemorrhage
• Usually venous
• Rupture of
bridging
veins
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 ANEURYSM
Cerebral contusions
• Superficial bruises of the brain
• Frequent but not inevitable after
head 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 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 damage
• Ischaemic brain damage due to traumatic
dissection and thrombosis of vertebral or carotid
arteries by hyperextension of the neck
• Infarction of pituitary - due to transection
of pituitary stalk
• pontomedullary rent
Infection
• complication of skull fracture
• Open HI
• Incidence is increased even after closed
HI as devitalised tissue prone to infection
Diffuse damage
• DAI - widespread damage to axons in the
CNS 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 ICP
Results from:
• cerebral vasodilation - inc cerebral blood vol
• damage to BV - escape of fluid through BBB
• inc water content of neurones and glia- cytotoxic
cerebral oedema
ICH herniation
Subfalcine
herniation
Tentorial herniation
Tonsillar 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 children
Accounts for 3.5% of all deaths in the 1-14
year age group
Sixth commonest cause of cancer deaths in adults
25% of all tumors in adults are in the brain and 35%
are neurectodermal and 40% are metastatic
~ Most primary tumors are sporadic and
of 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
Sites of cerebral tumors
SSites of cerebral tumors
ADULTS
Supratentorial tumors account for 90%
Therefore increased incidence of epilepsy
and decreased incidence of headache
Posterior fossa tumours cause headache
and vomiting as early features
CHILDREN
Cerebellum
Pons
Optic nerve/chiasm
SUPRATENTORIAL TUMORS ARE
RARE
Therefore
Headache, vomiting, visual disturbances
common
Epilepsy - unusual
Diagnosis
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 occlusion
Infarction - 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 causes
•
•
•
•
•
•
•
•
•
•
Hypertension
Trauma
CAA
Berry aneurysm
AVM
Bleeding diathesis
Vasculitides
Drugs
Neoplasm
Infective
CNS INFECTION
Development and outcome
depends on
Organism
Host
nature
route of entry
dose
Anatomical defenses - skull, meninges
Physiological - immune defense mechanisms
Bacteria
Entry into the cranial cavity
Haematogenous - distant foci e.g lung
Local spread - Skull - middle ear, nasal sinus,
osteomyelitis
Abnormal routes - Trauma -fractures
Surgery - shunts
Congenital sinus
BACTERIAL 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 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 meningitis
in the neonate
• Obstructive hydrocephalus
• Cavitating lesions in the white matter
CSF
Bacterial Viral
TB
low
low
v. high
N
glucose
Slightly
Raised
protein
increased
neutrophil lymphocyt lymphocyt cells
s
es
es
Complications of bacterial meningitis
• Acute inflammation of adjacent structures
• Organisation of inflammatory structures
Organisation of inflammatory
exudate
Impedes flow of
CSF into
venous sinuses
Obstructs CSF outflow from
IV 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
cells
Slightly
Raised
increased
neutrophil lymphocyt lymphocy
s
es
tes