CNS Path Flashcards
Describe Neurones
- Functional and structural unit of CNS
- Transmit electrical impulses
- Excitable cells
Describe Neuroglia
- Non-excitable cells
- Outnumber neurones 5:1
- There are 2 types:
Describe macroglia
- Macroglia are a Type of Neuroglia
-There are 3 types of macroglia
—> Oligodendrocytes, Astrocytes, Ependymal cells
Describe Oligodendrocytes
Produce Myelin
Type of macroglial cell
Describe astrocytes
Type of macroglial, neuroglial cell
Role:
- Scar formation
- Metabolism
- Barrier function
- Repair
- Nutrients
Describe Ependymal cells
Line the brain ventricles
Type of macroglial neuroglial cells
Describe Microglia
CNS Macrophages
Fixed
Type of neuroglial cell
List the control centres in the brainstem
1. Cardiac 2 Pulmonary 3. Urinary 4. Vomitting 5. Swallowing
What is the normal volume of CSF?
120 ml
Replaced 3-5 x/d
Causes of obstructive hydrocephalus
Tumours:
- Of brainstem or posterior fossa
- Papilloma of choroid plexus
- Colloid cyst in 3rd ventricle
Blood: - SAH
Infection: - Meningitis
Congenital:
- Chiari Malformalion
- Dandy Walker syndrome
Describe Chiari malformation
- Part of the cerebellum is pushed through the foramen magnum
- Blocks flow of CSF through the foramen magnum
Describe Dandy Walker syndrome
- Cerebellar hyperplasia and/or cyst formation
- Causes obstruction of CSF flow through the Foramen Magnum
Describe Hydrocephalus Ex Vacuo
- Compensatory dilatation of the ventricles in dementia
- Due to loss of brain parenchyma
Normal composition of intracranial contents
Brain = 70%
CSF = 15%
Blood = 15%
At what level of CSF does compensation cease and ICP starts to increase?
15mmHg
200ml CSF
Causes of increased ICP
Tumour
Abscess
Infarction
Haemorrhage
Clinical features of Raised ICP
HA Vomitting Confusion FNS (Paralysis, Hemianopia, Dysphasia) Depressed consciousness Seizure Papilloedema
Define papilloedema
Bilateral swollen optic discs
3 FNS
Hemianopia
Dysphasia
Paralysis
4 stages of raised ICP
- Spatial compensation
- Spatial compensation exhausted
- ICP increases
- SAP increases (Cushing response) - Rapid increased ICP, decreased cerebral perfusion
- ICP=SAP (vasomotor paralysis)
What type of patients cope best with raised ICP?
Elderly
Mechanisms of spatial compensation in raised ICP
- Flattening of gyri
- Compression of ventricles
- Lateral shift in midline structures
- Internal herniation
Types of internal herniation
Supracallosal/ subfalcine
- Cingulate gyrus through Falx cerebri
Uncal Herniation
- Unci through tentorial incisure
Tonsillar Herniation
- Cerebellar tonsils through foramen magnum
Complications of uncal herniation and signs
CN3 compression
- Ptosis
- Eye deviated down and out
- Abnormally dilated pupils
Posterior cerebral A aneurysm
Haemorrhage in midbrain and pons
Complications of Tonsillar herniation
Brainstem compression (leads to death)
Types of cerebral oedema
Vasogenic Oedema
Cytotoxic Oedema
Interstitial Oedema
Definition and cause of Vasogenic oedema
Definition:
- Fluid leaks into brain parenchyma because BBB is disrupted
Cause:
- Localised: Abscess, tumour, infarct
- Generalised: Sepsis
Definition and cause of Cytotoxic oedema
Increased fluid as result of ischaemic injury
Cause: Generalised ischaemia
Definition and cause of Interstitial oedema
Increased fluid in peri ventricular tissues
Cause: Acute hydrocephalus
Rx of cerebral oedema
- Steroids if tumour related
- Surgical removal if haemorrhage
Type of infarcts in the circle of willis
Wedge shaped watershed infarcts
Place in brain most susceptible to infarction
Area between anterior and middle cerebral artery
Define stroke
Focal and/or global loss of cerebral function
Lasting >24hrs
Define TIA
Transient Ischaemia Attack
Focal loss of cerebral or ocular function lasting <24hrs
Timeline of macroscopic features of infarction (brain)
0-6hrs = nothing
6-48hrs
- Tissue pale and swollen
- Loss of margin between grey and white matter
2-10d
- Tissue is gelatinous and friable
10-14d
- Liquefactive necrosis
Timeline of microscopic features of infarction (brain)
0-12hrs
- Red neurones
- Oedema
12-48hrs
- Inflammatory response
- Neutrophil polymorphs
2-3w
- Lots of microglia
> 3w
- Reactive astrocytosis surrounding the infarction
Causes of Intracerebral haemorrhage
6
HTN Amyloid angiography Anticoagulants Tumours Vasculitis AV Malformation
Causes of Subarachnoid Haemorrhage
2
Berry aneurysm
AV malformation
Causes of HTN which cause Intracerebral Haemorrhage
5
Large vessel atherosclerosis
Small vessel hyaline arteriolosclerosis
Charcot-Bouchard Microaneurysms
Lacunar Infarcts
Slit Haemorrhages
Complications of lacunar infarcts
Accumulative effect to cause Multi-infarct dementia
What would cause bleeding into the ventricular system?
Intracerebral haemorrhage of the basal ganglia
Pathogenesis of amyloid angiography
Media of small penetrating vessels is replaced with amyloid
This causes vessel wall weakening
And increases the risk of rupture
In what diseases/aspects of life do you see amyloid angiography?
3
Alzheimer’s
Down’s Syndrome
Aging
Ix for amyloid angiography
2
Amyloid Immunological stain
OR
Congo-red stain (goes apple green under polarised light)
What is AV malformation?
Abnormal connections between arteries and veins
Instead of joining via the capillary system, they just join up
Epi AV malformation
3rd-4th decade
M>F
Complication of AV malformation
Rupture
Intracerebral Haemorrhage
SAH
Where do berry aneurysms occur?
Circle of Willis
RF for Berry aneursym
3
PCKD
Neurofibromatosis
Marfan’s
Causes of cardiac mural thrombi
3
MI
Valve disease
AF
Causes of embolic stroke
Cardiac mural thrombi
Carotid atherosclerotic thromboembolism
Ventricular septal defects (structural abnormality)
Cardiac surgery
Tumour, Fat, Gas, Atherosclerosis, foreign body, Infection, amniotic fluid
What % of brain tumours are mets?
50%
Most common origins of brain mets
4
Breast
Prostate
Lung
GIT
Brain Tumour should be a differential Dx in …
5
New onset epilepsy
Hydrocephalus
FNS
Balance/Gait abnormalities
Visual field defects
Complications of Brain tumours
Epillepsy, Hydrocephalus, FNS, Balance/gait abnormalities, Visual Field Defects
Raised ICP
Brainstem compression
Ix of SOL
- CT or MRI
Confirm:
- Brain biopsy (send to histology)
- Brain smear (send to cytology)
How are brain tumours named?
According to the cells from which they are derived
Define Neuroblastoma
Tumour of neurones
Define Meningioma
Tumour of the meninges
Tumours of the Cranial Nerves
Schwannoma
Neurofibroma
Define Gliomas
Tumours of Neuroglia:
Astrocytoma
Oligodendrocytoma
Ependymoma
How are brain biopsies/smears graded?
- Degree of nuclear atypia
- Necrosis
- Endothelial hyperplasia
Rx Brain tumour
- Surgical Excision
- Chemoradio
- Proton beam
Weight of female adult brain
1250g
Weight of male adult brain
1400g
Gross features of cerebral atrophy
Narrowing (flattening) of gyri
Widening of the sulci
Compensatory enlargement of the centricular system
Which area of the brain suffers most neurodegeneration in Alzheimer’s disease?
Hippocampus
Which area of the brain suffers most neurodegeneration in parkinson’s disease?
Substantia Niagra
Epi Alzheimer’s
F>M
47% >85yo
Define neurodegeneration
Progressive neuronal degeneration and death
Define dementia
An acquired global impairment of intellect, reason and personality , without impaired consciousness
Gross appearance of an alzheimers brain
6
Cerebral atrophy:
- Brain weight <1000g
- Atrophy is mostly in the frontal and parietal lobes
- Hippocampal atrophy
- Compensatory enlargement of ventricular system (Hydrocephalus ex vacuo)
- Widening of sulci
- Flattening of the gyri
Microscopic features of Alzheimers disease
4
Tau-2 +ve Neurofibrillary tangles
BA4-Amyloid Plaques
- Senile (Neuritic) plaques
Amyloid angiopathy
Neuronal loss and reactive astrocytosis
Stain and colour of BA4- Amyloid Plaques
Sliver stain
OR
Congo-red stain —> apple green colour under polarised light
Where are BA4-Amyloid plaques deposited in alzheimers disease?
Mainly:
- Hippocampus
- Neocortex
- But can be anywhere in the brain parenchyma
What cause the formation of BA4-Amyloid plaques?
Breakdown of the normal membrane protein APP (B-amyloid pre-cursor protein)
Stain used for Tau-2 +ve neurofibrillary tangles
Silver stain
Where are Tau-2 +ve neurofibrillary tangles deposited?
Cytoplasm of neurones
What do Tau-2 +ve neurofibrillary tangles look like?
- Bundles of filaments
- Elongated
- flame shaped
Pathogenesis of multi-infarct dementia
Chronic HTN causing:
Lacunar infarcts
- Presentation gets progressively worse with the accumulation of more infarcts
What disease is associated with Lewy Body Dementia?
Parkinsons
Epi of Vascular Muti-Infarct dementia
M>F
What parts of the brain are mainly involved in Vascular (Multi-infarct) dementia?
Cortex and basal ganglia
Epi of Pick’s Disease
Any age between 21-90
Gross features of Pick’s Disease
- Brain <1000g
- Selective atrophy of the temporal lobes and medial surface of the frontal lobes
What parts of the brain are involved in Pick’s disease
Temporal lobes
Medial aspect of frontal lobes
Microscopic features of Pick’s disease
Neuronal Loss (in outer 3 layers of the cortex)
Pick cells (swollen neurones)
Presentation of Pick’s Disease
Early onset of:
- Fontal lobes: Behaviour and personality change
- Temporal lobe: Language disturbance
Pathogenesis of Creutzfeldt Jakob Disease (CJD)
Prion disease usually acquired from beef resulting in transmissible spongiform encephalopathy
What is a Prion Disease?
Abnormal forms of normal neuronal cell proteins
They are produced following a mutation
They replicate and can be passed on by infection or inheritance
Gross features of CJD
Brain usually looks normal
Microscopic features of CJD
- Spongiform transformation of the cerebral cortex
- small vacuoles through the parenchyma
- Numerous
