21. Pathology of the Central Nervous System Part Two Flashcards

1
Q

CEREBROVASCULAR DISEASE (1)

A

Leading cause of mortality and morbidity
Incorporates strokes, TIAs, intracerebral haemorrhage

2 main pathological processes
Hypoxia, ischaemia and infarction due to impaired blood supply/oxygenation
Haemorrhage from CNS vessels

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2
Q

CEREBROVASCULAR DISEASE (2)

A

Brain requires constant supply of glucose and oxygen
Brain accounts for 1-2% body weight but receives 15% resting cardiac output and accounts for 20% blood oxygen consumption
Cerebral blood flow is autoregulated to maintain adequate perfusion over a wide range of blood pressure and ICP

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3
Q

CEREBROVASCULAR DISEASE (3)

A

Blood flow reduced to a portion of the brain, tissue survival depends on :
Collateral circulation
Duration of ischaemia
Magnitude and rapidity of flow reduction

Blood flow reduced to the whole brain ie. Global hypoperfusion (eg hypotension, cardiac arrest) can result in generalised neuronal dysfunction

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4
Q

Stroke (1)

A

130,000 patients per year have a stroke in UK

Major neurological disorder

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5
Q

F A S T

A

Face- facial drooping
Arms- person may not be able to raise both arms and keep them raised due to weakness or numbness
Speech- slurred speech
Time- is of the essence ring for ambulance urgently

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6
Q

Stroke or Transient Ischaemic Attack

A

TIAs are characterised by temporary loss of function that resolves itself within 24 hours

Sometimes called “mini-strokes”

Symptoms are similar to that of a full stroke but recovery is rapid

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7
Q

Treatment of TIAs

A

1 in 10 chance of having a full stroke within 4 weeks if left untreated

Anti-platelet therapy: aspirin or clopidogrel

Control blood pressure

Lower cholesterol

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8
Q

stroke (2)

A

Loss of function lasting greater than 24 hours

2 main pathological types:

Ischaemic

Haemorrhagic

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9
Q

STROKE – Risk Factors

A
Hypertension
Diabetes mellitus
Heart disease – ischaemic, atrial fibrillation
Previous transient ischaemic attacks
Hyperlipidaemia
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10
Q

STROKE - Causes

A

Hypoxia of brain
Blockage of blood vessel by atheroma
Blockage of blood vessel by embolus

Bleed into the brain
Hypertension related
Berry aneurysm

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11
Q

MANAGEMENT

A
NICE guidance
Thrombolysis
Aspirin/Clopidogrel
Physiotherapy
Occupational therapy
SALT
Supportive treatment
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12
Q

Causes of Haemorrhagic Events

A
Hypertension 
Vascular malformation 
Berry aneurysm 
Neoplasia 
Trauma 
Drug abuse
Iatrogenic
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13
Q

INTRACEREBRAL HAEMORRHAGE

A

‘Haemorrhagic stroke’
Presents as headache, with rapid or gradual decrease in conscious level – localizes depending on site of bleed
Usually arterial in origin
Show mass effect
In 80% of cases with hypertension bleed is ‘capsular haemorrhage’
Few survive

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14
Q

Subarachnoid Haemorrhage

A

Spontaneous
Often catastrophic
80% rupture of saccular aneurysms

‘Thunderclap headache’
‘Meningitis like’ signs
Requires neurosurgical input

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15
Q

SUBDURAL HAEMORRHAGE

A

Fluctuant conscious level
Often on anticoagulants
Bleeding from bridging veins between cortex and venous sinuses
Blood between dura and arachnoid
Often minor trauma in the elderly

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16
Q

EXTRADURAL HAEMORRHAGE

A

Post head injury, slowly falling conscious level, possibly with lucid period
Often with fractured temporal or parietal bone
Typically the middle meningeal artery

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17
Q

Dementia (1)

A

Progressive and largely irreversible clinical syndrome with widespread impairment of mental function.

Complex needs and high levels of dependency and morbidity

People should have chance to make decisions about their care in conjunction with the medical teams

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18
Q

Dementia (2)

A
80,000 people in the UK
> 65 years old increased risk
Memory loss
Speed of thought
Language
Understanding/Judgement
People can become disinterested in usual activities
Have difficulties in controlling emotions
19
Q

Dementia (3)

A
About 70% is Alzheimer’s Disease
Remaining 15% is Vascular dementia (recurrent small strokes) 
15% Dementia with Lewy bodies
Along with some very rare causes!
Eg syphilis
20
Q

Dementia (4)

A

Can be mimicked by depression or delirium

Long standing history or slow decline with possible personality change

Increasing prevalence with increasing age

21
Q

Brain area: Frontal

A
Dysfunction:
Disorders of behavior
Mood
Motivation
Judgment 
Planning
Reasoning
Appetite and continence
Disinhibition
22
Q

Brain area: Temporal

A

Dysfunction: Memory dysfunction

23
Q

Brain area: Parietal

A

Dysfunction: Dysphasia and dyspraxia

24
Q

Brain area: Subcortical

A

Dysfunction: Slowness of thought processes

25
Q

Assessment

A

Can include
TSH – ensure thyroid function is normal
CT scan (Not all cases) to check for intracranial pathology
Vitamin B12, thiamine – alcoholism

26
Q

Alzheimer’s Disease

A

Due to an accumulation of Aβ amyloid, Tau – neurofibrillary tangles and plaques, and loss of neurones and synapses

Leads to defects of visual-spatial skill (gets lost), memory loss, decreasing cognition, ansognosia (lack of awareness)

27
Q

Treatment

A

Needs multidisciplinary team approach

New treatments include cholinesterase inhibitors eg rivastigmine

Their use is closely controlled by NICE

28
Q

Epilepsy

A
‘A recurrent tendency to spontaneous, intermittent, abnormal electrical activity in part of the brain, manifest as seizures’
Seizures can take many forms
Focal twitching, trance-like, convulsions
Usually no identified cause
For example, can be due to 
Space occupying lesions
Stroke
Alcohol withdrawal
29
Q

Epilepsy - diagnosis

A

Good history taking
Exclude structural abnormality
EEG
Any triggers? Eg TV

30
Q

Epilepsy - management

A
Compliance is very important
Depending on seizure type
Have serious side effects, eg teratogenic
Examples
Sodium valproate – epilim
Carbamazepine
Phenytoin
Lamotragine
31
Q

Infection

A

Diffuse infection
Eg. Meningitis
Focal infection
Eg. Abscess

32
Q

Meningitis

A
Bacterial
Neisseria meningitidis
Pneumococcus
Meningococcus
Viral
Fungal
33
Q

Presentation

A

Early
Headache
Cold hands and feet
Pyrexial

Late
Neck stiffness
Photophobia
Kernig’s sign
Non-blanching rash
Seizures
34
Q

Brain Abscess

A

Focal infection
Can lead to focal brain damage or mass effect
Can present with headaches, seizures, temperature
Radiologically a ‘ring enhancing lesion’ – differential diagnosis is a glioblastoma
Can spread via blood, eg.
Embolus from bacterial endocarditis
IV drug users at risk
Or direct, eg.
From an infected inner ear

35
Q

Parkinson’s Disease

A

Movement disorder
Sporadic or familial
Occurs 1 in 1000, usually over 50 years
Can be drug induced!

36
Q

Parkinson’s Clinically

A

rigidity
bradykinesis
resting tremor
postural instability

37
Q

Parkinson’s Treatment

A

MDT approach
L-dopa eg Madopar
Anticholinergic drugs eg orphenadrine

Drug induced Parkinson’s (eg Haloperidol) can be helped by procyclidine

Surgery?

38
Q

TUMOURS/SPACE OCCUYPING LESIONS

A

Benign or Malignant?

Benign tumours can cause problems depending on location and mass effects

Can affect the skull, the meninges or the brain itself

39
Q

Presentation

A
Headaches
Seizures
Cognitive or behavioral change
Vomiting
Altered conciousness
40
Q

Metastasis

A

Cancers elsewhere in the body can metastasize the brain
Must be included when tumours are found on CT and MRI scans
These include:
Breast
Small cell lung cancer

41
Q

Meningiomas

A

Benign tumours
Generally well circumscribed, slow growing
Derived from meningothelial cells
Enlarge slowly, don’t often infiltrate the brain, and can be often be removed surgically
Can be found incidentally on brain imaging scans

42
Q

Astrocytomas

A

Range from WHO Grade I-IV

Grade I generally good outcome, grade 4 usually fatal

43
Q

Pituitary Tumours

A
Cause compression symptoms
For example of the optic nerve 
These can be hormonally active
Classified based on the hormone produced
For example a prolactinoma
Surgically removed transphenoidally