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Scientific Basis of Clinical Practice > CNS Pathology > Flashcards

CNS Pathology Flashcards

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1
Q

describe the function of neurones

A

cells specialised for rapid communication

connected to one another by a series of synapses through the transfer of neurotransmitters

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2
Q

describe the function of neuroglia

A

form the scaffolding of the nervous system

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3
Q

describe macroglia and their subtypes

A

a subtype of neuroglia
oligodendrocytes; form myelin and aid impulse transport down the axon
astrocytes; metabolic buffers, detoxifiers, supply nutrients, electrical insulators, involved in repair and scar formation
ependymal cells; line the ventricle system

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4
Q

describe microglia and their function

A

another subtype of neuroglia

a fixed macrophage system within the CNS and respond to injury

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5
Q

describe the pathway of CSF

A

produced b the choroid plexus of the lateral 3rd and 4th ventricles
exits through the foramina of luschka and magendie into the subarachnoid space between the arachnoid and Pia mater
descends into the spine or ascends to the cerebellum and cerebral hemispheres
absorbed in the superior sagittal sinus

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6
Q

what are the causes of hydrocephalus?

A

posterior fossa/brain stem tumours
colloid cysts
resolving arachnoid haemorrhage
chiari malformations; defect in the posterior fossa or cerebellum
dandy-walker syndrome; cerebellar hypoxia and cyst formation
choroid plexus papilloma; excess CSF production

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7
Q

describe hydrocephalus ex vacuo

A

compensatory CSF seen in certain dementias

ventricular enlargement due to loss of brain parenchyma

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8
Q

what are the normal cranial contents?

A

brain; 70%
CSF; 15%
blood; 15%

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9
Q

what are the main causes of raised intracranial pressure?

A

tumours
abscesses
areas of infarction
haemorrhage

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10
Q

what are the symptoms and signs of raised intracranial pressure?

A 
headache
vomiting
confusion
focal neurological signs; paralysis, hemianopia, dysphagia
depressed conscious level
respiratory depression
bradycardia
seizures
papilloedema
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11
Q

what are the stages of raised intracranial pressure?

A

spatial compensation; one of the cranial contents expands
ICP rises slowly; systemic arterial pressure rises to maintain cerebral perfusion (Cushing’s response)
ICP rises rapidly as cerebral perfusion drops
cerebral vasomotor paralysis; cerebral circulation ceases

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12
Q

what re the consequences of raised ICP?

A

flattening of the gyral pattern of the cerebral hemispheres
unilateral lesion; compression of the ventricular system and a shift of the midline structures
herniation of the brain matter; through the foramen magnum, flax cerebri and tentorial incisura

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13
Q

what re the types of internal herniation?

A

supracallosa/subfalcine; cingulate gyrus herniates under falx cerebri

uncal herniation; 3rd CN or posterior cerebral artery compression, haemorrhage of midbrain and pons

tonsillar herniation; cerebellar tonsils displaced down foramen magnum, brain stem compression (life threatening)

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14
Q

what are the signs of 3rd CN compression?

A

dilated pupils

loss of eye movements

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15
Q

what are the consequences of posterior cerebral artery compression?

A

infarction of its supplied territory

secondary haemorrhage into the brain stem

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16
Q

what are the types of cerebral oedema?

A

vasogenic; disruption of the brain barrier, adjacent to a tumour, haemorrhage or abscess or due to sepsis
cytotoxic; increase in intracellular fluid secondary to an insult (hypoxia or ischaemia)
interstitial; increase in water content with in the periventricular tissue (acute hydrocephalus)

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17
Q

what is the treatment of cerebral oedema?

A

based on the cause
steroids; tumours
surgery; haemorrhage

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18
Q

describe the types of cerebral ischaemia

A

focal; involvement of a territorial artery

global/diffuse; ischaemia due to decreased cerebral perfusion across the entire brain (cardiac arrest, severe shock)

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19
Q

define stroke

A

rapidly progressive clinical symptoms of focal/global los of cerebral function
>24hrs or leading to death
no apparent cause other than vascular origin

TIA; <24hrs

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20
Q

describe the macroscopic brain changes in a stroke

A

6hrs; minimal change
48hrs; tissue becomes pale, soft and swollen, less of a sharp margin between grey and white matter
2-10 days; area becomes gelatinous and friable
3 weeks; tissue liquifies into a cavity

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21
Q

describe the microscopic brain changes in a stroke

A

12hrs; red neurones and oedema
48hrs; inflammatory response, compromising neutrophil polymorphs
2-3 weeks; increasing numbers of microglia or macrophages, reactive astrocytosis surround area of infarction

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22
Q

what conditions are associated with mural thrombosis?

A

previous MI; blood stasis and thrombus formation
valve disease; turbulent flow
AF

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23
Q

what are the causes of emboli?

A 
ventricular septal defects
AF
previous MI
valve disease
cardiac surgery
tumour
air
debris from infected valves in acute bacterial endocarditis
trauma; multiple fractures
aggressive cardiopulmonary resuscitation
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24
Q

describe intracerebral haemorrhage

A

haemorrhage into the parenchyma or tissue
usually from rupture of the small intraparenchymal blood vessels
most common cause; hypertension
second most common cause; amyloid angiopathy
can be caused by trauma
diffuse axonal injury; acceleration and deceleration forces on the head
>2hrs; stain for beta-APP on histology

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25
describe Charcot Bouchard aneurysms
caused by weakening by hyaline arteriosclerosis | predisposing lesion to vessel rupture
26
what are the effects of hypertension on the CNS?
``` large vessel disease small vessel disease charcot Bouchard aneurysms lacunar infarcts slit haemorrhages ```
27
describe the pathophysiology of amyloid angiopathy
the media of the small penetrating vessels is replaced by amyloid staining; amyloid immunological stain, Congo red stain (shows up apple green) causes weakening in the vessel walls increases the likelihood of rupture
28
what are the causes of non-traumatic intracerebral haermorrhage?
``` hypertension amyloid angiopathy anticoagulant therapies; warfarin tumours vasculitic diseases AV malformation ```
29
describe AV malformations
can cause intracerebral and subarachnoid haemorrhages most common in the 3rd/4th decade more common in males
30
what are the types of non-traumatic intracranial haemorrhage?
intracerebral | subarachnoid
31
what are the causes of non-traumatic subarachnoid haemorrhages?
berry aneurysms | AV malformations
32
describe berry aneurysms
most commonly found near the major arterial branch points of the cerebral arteries 40%; between the anterior communication and anterior cerebral arteries associated with PKD, neurofibromatosis, marfan's syndrome
33
name the types of haemorrhage
extradural subdural subarachnoid intracerebral
34
describe extradural haemorrhages
blood collects between the skull and the dura a squamous temporal fracture tearing the middle meningeal artery slow accumulation of blood compensatory mechanisms can slow the rise of ICP; lucid interval between injury and death death; cerebral compression and herniation
35
describe subdural haemorrhages
resulting from the tearing of bridging veins; typically during a fall where the brain moves relative to the dura haemorrhage between the dura mater and the arachnoid mater increased risk in patients with cerebral atrophy; elderly, alcoholics presentation; minor injury, headache, confusion developing over 48hr, abrasion of the back of the scalp
36
describe subarachnoid haemorrhages
bleeding beneath the arachnoid matter most commonly caused by a ruptured berry aneurysm associated with severe contusions, fractured skull, blood from an intraventricular haemorrhage, neck blows rapid loss of conscious and death
37
name some of the symptoms and signs of brain tumours
``` new onset epilepsy hydrocephalus focal neurological deficit balance and gait problems visual field defects in pituitary tumours ```
38
what are the first line investigations to diagnose a brain tumour?
radiological; CT or MRI | confirm diagnosis; brain biopsy or brain smear
39
what is the treatment of brain tumours?
surgery; depends on whether the deficit is worth it chemoradiotherapy; blood brain barrier makes this difficult, affects cognitive ability and vision proton beam therapy; precisely targeted and reduces damage to surrounding tissues and organs
40
what are the causes of a black eye/orbital contusion?
direct blow; punch injury to the front of the scalp; bruising basal skull fracture; racoon eyes
41
describe scalp lacerations
the skin is crushed onto the rigid skull during a blunt impact can be located on the back of the scalp following backwards falls stellate laceration just above the occipital protuberance
42
what are the types of scalp surface injury?
``` bruises/contusions abrasions/grazes lacerations/cuts incisions/slashes stab/penetrating wounds ```
43
what are the types of skull fracture?
``` linear comminuted depressed contra-coup hinge ring pond; ripple/spider web diastatic ```
44
what are the common areas of cerebral contusion?
frontal poles orbital surfaces of the frontal poles temporal poles cortex adjacent to the Sylvian fissure
45
define coup and contrecoup
coup; cerebral injury at the point of contact | contrecoup; injury to the surface opposite the point of contact, after sudden deceleration
46
describe traumatic subarachnoid haemorrhage
a rare cause of death following a single blow causes a tear within the vertebral basilar arterial system may chronically cause hydrocephalus due to CSF blockage
47
describe diffuse axonal injury
blunt impact or severe acceleration/deceleration forces may cause tearing of tiny blood vessels widespread axonal damage immediately unconscious and remain in a vegetative state
48
describe the histology of diffuse axonal injury
widespread axonal swelling duet B-APP | highlighted by silver impregnation techniques
49
what are the effects of raised ICP?
flattening of the gyro pattern compression of the ventricular system internal herniations if caused by a space-occupying lesion (extradural/subdural haemorrhage); lateral shift of the midline structures
50
what are the features of age-related cerebral atrophy?
flattening of the general pattern across the cerebral hemispheres widening of the sulk compensatory enlargement of the ventricular system hippocampus affected in Alzheimer's disease substantia nigra affected in Parkinson's disease
51
what are the characteristics of neurodegeneration?
progressive neuronal dysfunction and death degeneration often affects specific systems implying some form of selective vulnerability incidence tends to increase with age
52
describe dementia
a global impairment of higher intellectual function; intellect, reason and personality, through alterations in mood and behaviour increases with age affects more females
53
describe the gross changes of Alzheimer's disease
brain weight <1000g global atrophy; particularly the frontal and parietal lobes compensatory enlargement of the ventricular system widening of the sulci due to cortical atrophy
54
describe the microscopic changes of Alzheimer's disease
neurofibrillary tangles senile (neuritic) plaques amyloid angiopathy varying degrees of neuronal loss and reactive astrocytosis
55
what are the histological findings of Alzheimer's disease?
deposition of amyloid beta subtype protein within the brain parenchyma concentrated in the hippocampus and neocortex stained suing conga red stain; apple green neurofibrillary tangles; largely composed of protein tau which can be highlighted by silver staining amyloid enruopathy varying degrees of neuronal loss and reaction; astroycytosis
56
describe vascular/multi-infarct dementia
``` stepwise progression corresponding to the episodes of infarction hypertension-driven arteriosclerosis more common in males characterised by lacunar infarcts cortex and basal ganglia involvement ```
57
what are the types of dementia?
``` alzheimer's disease vascular dementia Lewy body dementina pick's disease CJD ```
58
describe pick's disease
rare presents between 25-90 <1000g brain early onset behavioural and personality changes; selective frontal lobe atrophy language disturbances; temporal lobe atrophy neuronal loos most severe in the outer 3 layers of the cortex; neuronal swelling (Pick cells)
59
define Creutzfeldt jakob disease
rapid progression dementia recently accompanied by myoclonus and clinical evident cerebellar degeneration
60
describe creutzfeldt Jakob disease
transmissible spongiform encephalopathy (prion disease) prions; abnormal form of a normal cell protein, capable of replication and causing infection can be sporadic or familial rapidly progressive associated with myoclonus and ataxia death; usually 3-12 months after onset
61
describe the gross and histological findings of Creutzfeldt Jakob disease
gross; brain may be normal | histology; vacuoles/spongiosis in grey matter
62
what are the clinical features of Parkinson's disease?
``` diminished facial expressions stooped posture pill rolling tremor rigidity bradykinesia festinating gait ```
63
describe Parkinson's disease
degeneration fo the dopaminergic neurones of the substantia nigra severity proportional to the drop in dopamine early symptoms can be managed by L-dopa microscopy; pallor of the substantia nigra and locus cereleus lewy bodies; alpha synuclein and ubiquitin
64
what are the clinical features of Huntington's disease?
chorea rigidity cognitive decline often associated with cognitive impairment
65
what are the gross and histological features of Huntington's disease?
gross; cerebral atrophy and striking atrophy in caudate nucleus and putamen microscopically; loss of striata neurones, reactive astrocytosis
66
describe multiple sclerosis
characterised by plaque formation within the CNS clinically; fluctuates with periods of relapse and remission affects more females peak onset; 22-40yrs
67
what are the causes of multiple sclerosis?
more frequent in northern geographical regions genetic link immunological; possibly precipitated by a viral infection
68
what are the clinical features of multiple sclerosis?
unilateral visual impairment due to optic nerve impairment brain stem involvement; ataxia, nystagmus, diplopia spinal cord involvement; parasthesia, sensory impairment, muscle spasms, incontinence
69
what are the CSF findings in multiple sclerosis>
60%; increased protein concentration 40%; IgG increase oligoclonal bands on electrophoresis
70
what are the gross and microscopic features of multiple sclerosis?
gross; grey-tan irregular plaques in white matter microscopy; perivascular inflammation and macrophage reaction in association with myelin breakdown reduction in oligodendrocytes with relative preservation of axons

Scientific Basis of Clinical Practice (10 decks)

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