CNS Flashcards
What causes an increased ICP and what are the symptoms
- Tumours
- Abscess
- Infarction
- Haemorrhage
Symptoms
Headache, vom , confusion , focal neurological signs (paralysis, hamianopia, dysphasia), depressed conscious level, seizure, papilloedema
Explain the 4 stages of ICP
- Spatial compensation- decrease in other components to make up for increase in 1
- Increased ICP - as compensation becomes exhausted- ICP and systemic arterial pressure (to keep perfusion) increase
- ICP rapidly increases as perfusion decreases
- Cerebral vasomotor paralysis
Old people with cerebral atrophy compensate better- more room to expand
What are the various types of internal herniation
- Supracallosal/ Subfalcine- the cingulate gyrus herniates under the fall cerebra
- Uncal Herniation- through the tectorial incisor causing 3rd cranial nerve compression (pupil dilation and loss of eye movements), posterior cerebral artery compression and haemorrhage in midbrain and pons
- Tonsilar herniation- cerebellar tonsils are displaced down the foramen magnum causing brain stem compression
Describe the different types of cerebral oedema
- Vasogenic oedema- Integrity of BBB is disrupted, can be local (beside a tumour or abscess) or generalised
- Cytotoxic oedema- increase in intracellular fluid due to injury
- Interstital oedema- increased water content in peri-ventricular tissues in acute hydrocephalus
Treat with steroids or removal surgically
Describe the various types of cerebrovascular disease
- Thrombosis and embolism- caused by anaemic infarction (upset blood supply)
- Haemorrhage- rupture of a blood vessel causing blood loss
- Acute Ischaemia- - global (due to loss of perfusion across the brain)- arrest, shock and hypotension or focal - if a specific artery is involved- large vessel disease of small vessel disease eg vasculitis
What is the difference between a stroke and a TIA
STROKE- radially progressive clinical symptoms of focal and sometimes global loss of cerebral functioning that last more than 24 hrs or lead to death with no other cause except for vascular origin
TIA- Acute loss of focal cerebral or ocular function when symptoms last less than 24 hrs
What are the causes of an embolic stroke
- MI, valve disease and AF
- Thrombi from atheroma in carotid artery
- Emboli with ventricular septal defects
- Cardiac surgery
- Acute bacterial endocarditis
Emboli can be tumour, fat (trauma etc broke bones) or air
What are the causes of the two main types of intracranial haemorrhage
- Intracerebral haemorrhage
- HTN- most common cause- atherosclerosis, hyaline arteriosclerosis, micro aneurysms
- Amyloid antipathy that weakens vessel walls
- Anticoagulant therapy
- Tumours
- Vasculitis
- Ateriovenosis malformation (40s and 50s) - Subarachnoid haemorrhage
- Berry aneurysm
- Ateriovenosis malformation (40s and 50s)
What are the risk factors for a berry aneurysm and where is it most likely to occur
50% occur between the anterior communicating and anterior cerebral arteries OR in the middle cerebral artery
Risk factors are
- Polycystic kidneys
- Marfan’s syndrome
Discuss the 3 types of traumatic haemorrhage
Based on what part of the meninges is affected
-Extradural - between skull and dura- fracture will tear the meningeal artery- slow accumulation of blood so lucid period after trauma
- Subdural- Tearing of bridging veins between dura and arachnoid mater that empty into the superior saggital sinus, higher risk in patients with cerebral atrophy due to increased subdural space- elderly and alcoholics usually due to fracture of right occipital bone
- Subarachnoid- Severe confusion, rapid unconciousness, sudden death, fractured skull and blood from intraventricular haemorrhage associated with blows to the neck, skull fracture can tear vessels at the base of the brain, may cause chronic hydrocephalus due to blockage of CSF. Can also be caused by ruptured berry aneurysm
intracerebral haemorrhage- trauma
What parts of the brain degenerate in Parkinsons and Alzhemier’s
Alzhemiers= the hippocampus
Substantia Nigra= Parkinsons
Describe the pattern or neurodegeneration in Alzhemier’s disease and the histological features
- Global cerebral atrophy particularly in the frontal and parietal lobes with compensatory enlargement of the ventricular system
- Widening of sulci
Histology
- BA4-amyloid plaques in brain parenchyma- concentrated in the hippocampus and neocortex
- Tau 2 postive neurofibillary tangles- bundles of filaments in cytoplasm of neurones- elongated shaped and made of tau protein
- Astrocytosis- varying degrees of neuronal loss
Discuss the causes of dementia
- Vascular (multi-infarct dementia)- stepwise progression- more common in males, basal ganglia involved, chronic HTN and lacunar infarcts found
- Lewy body dementia (parkinson’s)
- Pick’s disease- rare ages 21-90, atrophy of temporal lobes (language) and medial surface of frontal lobes `(personality), neural loss and swelling of pick cells
- CJD- Prion disease- abnormal proteins in neurones- rapid progressive dementia accompanied by myoclonus and cerebellar degeneration, death 3 -12 months, vacuoles in parenchyma and spongiosis in grey matter of cerebral cortex
Discuss the features and pathology behind Parkinson’s disease
- pill rolling tremor -stooped posture -rigidity -bradykinesia -festinating gait -stooped posture
- Mean age onset 61
Pathology
- Degeneration of dopaminergic neurones of the substantial nigra- severity is proportional to decrease in dopamine - early symptoms managed with L dopa
- Microscopy shows- pale substantial nigra and locus ceruleus with lower bodies
Discuss the features and pathology involved in Huntingtons disease
Features -Demetia -Chorea (involuntary movement) -Cognitive decline -Rigidity
Pathology
-Autosomal dominant condition with variable age of onset
Gene affected= short arm of chr 4 and is CAG repeat sequence
-No of repeats corresponds to age of onset and duration
-CAG repeat sequences will increased in length going down generations
Gross: Cerebral atrophy and massive atrophy in caudate nucleus and putamen
Microscope- loss of striatal neurones, cortical loss of neurones associated with astorcytosis
