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Neurology > Plasticity and Pathology > Flashcards

Plasticity and Pathology Flashcards

1
Q

What is neuroplasticity?

A

The adaptive capacity of the CNS and its ability to modify its own structural organisation and functioning

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2
Q

Why is neuroplasticity in the CNS important?

A

The CNS cannot undergo Wallerian regneneration like the PNS can
Only the hippocampus and the olfactory bulb can undergo neurogenesis

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3
Q

How is neuroplasticity done?

A

There are many pathways which lie dormant, having minimal effect
After removal of a primary pathway, dormant pathways become more effective and become stronger with increased use
Collateral sprouting occuts, the main axon is lost so an outgrowth develops from the shaft of another axon

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4
Q

How is neuroplasticity and therefore neuro-rehabillitation encouraged?

A 
Practice and repetition
Active participation
Meaningful activity
Feedback
Attention
Instructions
Motivation
Perception of ability
Sleep
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5
Q

What is meningitis?

A

Inflammation of the leptomeninges (pia and arachnoid mater)

Can be acute or chronic

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6
Q

Why is prompt diagnosis and treatment of meningitis vital?

A

The meninges become completely destroyed by the pathogen and resultant acute inflammatory response

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7
Q

Presentation of acute meningitis?

A 
Headache
Neck stiffness
Fever
Photophobia
Vomiting 
Rigors
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8
Q 
What are the main causative organisms of meningitis in
-neonates
-2-5 years
5-30 years
30+ years
A

Neonates: E. coli, Listeria monocytogenes, Streptococcus agalactiae

2-5: H influenzae type B

5-30: Neisseria meningitidis

Over 30: Strep pneumoniae

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9
Q

What can cause chronic meningitis?

A

Post-primary non-pulmonary M tuberculosis

Cryptococcus

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10
Q

How does chronic meningitis present?

A

Chronic headache

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11
Q

What is seen in chronic meningitis?

A

Granulomatous formations
Fibrosis of meninges
Nerve entrapment, can cause CN palsies

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12
Q

Main complications of meningitis?

A 
RICP due to inflammation and swelling
Cerebral infarctions
Cerebral abscesses
Subdural empyema
Epilepsy
All can result in death
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13
Q

What is encephalitits?

A

An infection of the neural parenchyma, mainly grey matter, which normally has a viral cause

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14
Q

Presentation of a patient with encephalitis?

A 
Headache
Fever
Confusion
Drowsiness
Fatigue
Seizures or tremors
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15
Q

Causative organisms of encephalitis?

A 
Herpes simplex virus
Cytomegalovirus
HIV
Toxplasmosis
Polio
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16
Q

What are prions?

A

Constituents of the neuronal synapse, function there

17
Q

How can you get mutated prion proteins (PrP)?

A

Familial or sporadic mutation

Ingesting mutated PrPs which interact with normal PrPs, allowing them to undergo post-translational conformational changes

18
Q

What happens with mutated PrPs?

A

They aggregate causing neuronal death and holes in grey matter
Produce spongiform encephalopathies

19
Q

What is prion disease seen in?

A

Creutzfeldt–Jakob disease

Kuru

20
Q

When is ICP increased physiologically?

A

Coughing or sneezing

21
Q

What are the adaptive mechanims to maintain are normal ICP?

A

Reduced bloodflow
Reduced CSF volume
Spatial - brain atrophy/shrinkage

22
Q

What are the most common benign and malignant tumours of the CNS?

A

Benign: Meningeal origin - meningioma

Malignant: Astrocytoma

23
Q

What is the difference between primary and secondary damage in a head injury?

A

Primary - the damage caused by the force of the injury, normally caused by movement of the brain as it hits the front and back of the skull

Secondary - reaction to the primary damage, which worsens the injury

24
Q

What are the types of primary damage?

A

Focal damage: where there is bruising and laceration of the brain (cerebral contusion). Can be coup or contrecoup

Diffuse damage: tearing of axons from cell bodies as a result of the injury - known as diffuse axonal injury

25
Q

How does diffuse damage/axonal tearing heal?

A

By gliotic scarring

26
Q

What can diffuse damage lead to?

A

Vegetative state
Dementia
Gliotic scarring causing epilepsy

27
Q

What is coup and contrecoup injury?

A

Coup: Focal damage at the site of impact

Contrecoup: damage on the opposite side of the brain to impact

28
Q

Where are pain receptors located in the head?

A 
In arteries and veins in the base of the brain
Meninges
Extracranial vessels
Scalp
Facial muscles
Paranasal sinuses
Brain itself has no pain fibres
29
Q

What are tension headaches?

A

Neurovascular irritation from excessive tension in the scalp muscles

30
Q

How do tension headaches present?

A

Tight band sensations
Pressure behind eyes
Throbbing and bursting sensations
Depression can accompany them

31
Q

Management of tension headaches?

A

Reassurance to the patient
Avoid precipitating causes
Analgesic withdrawal

32
Q

What is a migraine?

A

A recurrent headache associated with visual and GI disturbances

33
Q

Pathophysiology of migraines?

A

Not fully understood..

-get vasodilation or oedema in blood vessels, stimulating nearby nerve endings

34
Q

What are the phases of a migraine?

A
  1. Well-being before the attack
  2. Prodromal symptoms
  3. Main attack (hemicranial splitting headache, begins locally and becomes generalised)
  4. Sleep and feeling drained
35
Q

What can be some prodromal symptoms?

A

Usually related to visual function
Aphasia
Sensory changes
Last for a few minutes to hours

36
Q

Differential diagnosis of migraines?

A

Meningitis
Subarachnoid haemorrhage
TIA

37
Q

What is temporal arteritis?

A

A inflammatory granulomatous arteritis, presents with a severe headache especially over inflamed arterial regions

The artery becomes hard, tortuous and thickened
Scalp over the region becomes red

38
Q

What other symptoms are there of temporal arteritis?

A

Associated facial pain
Visual problems
Malaise
Tiredness

Neurology (20 decks)

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