Lecture 13 Flashcards

(69 cards)

1
Q

what are some Diseases types in the Nervous System?

A
  • Cerebrovascular diseases
  • Nerve damage
  • Neurodegenerative diseases
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2
Q

What are the main components of the nervous system (NS) parenchyma and support cells?

A

Parenchyma = neurons; Support cells = glia.

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3
Q

What is cerebral blood flow (CBF) in terms of brain tissue?

A

CBF is 45-55 ml per 100 g of brain tissue per minute.

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4
Q

What is cerebral autoregulation, and what mechanisms does it involve?

A

Autoregulation maintains stable CBF within a wide MAP range using metabolic and myogenic mechanisms.

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5
Q

What are the two types of cerebrovascular accidents (strokes) and their prevalence?

A

Ischaemic (80-85%) and Haemorrhagic (15-20%).

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6
Q

How long can neurons survive without oxygen (hypoxia) before cell death occurs?

A

Neuronal death occurs after 5-7 minutes of hypoxia.

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7
Q

What is the prevalence of strokes in Australia?

A

Stroke is the third most common cause of death in Australia, with about 55,000 Australians having a stroke annually, 73% of which are first-ever strokes.

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8
Q

What is the survival and recovery rate of stroke patients in Australia?

A

Of 100 stroke patients:

  • About 30 will die within the first year.
  • About 70 will survive, with 35 remaining permanently disabled after one year, 10 of whom may need long-term care.
  • Around 35 may recover independence, with 25 still unable to perform all previous activities but able to live independently.
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9
Q

What percentage of stroke patients have ischaemic vs haemorrhagic strokes?

A

85% have ischaemic strokes, and 50% of haemorrhagic strokes lead to survival.

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10
Q

What is the Circle of Willis?

A

The Circle of Willis is a circulatory anastomosis that supplies blood to the brain and surrounding structures.

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11
Q

How does the cerebral blood supply affect clinical outcomes after a stroke?

A

The vessel affected in a stroke determines the area of brain damage, which leads to varied clinical effects based on the specific cerebral region impacted.

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12
Q

What is an ischaemic thrombotic stroke?

A

A stroke often involving the carotid distribution rather than vertebrobasilar, typically preceded by transient ischaemic attacks (TIAs) and may occur during mild blood pressure depression.

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13
Q

What is a TIA?

A

Transient Ischaemic Attack, also known as a “mini-stroke,” which is a temporary period of ischaemia without permanent damage.

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14
Q

What is an ischaemic embolic stroke?

A

A stroke that often involves the middle cerebral artery and leads to global ischaemia due to an embolus blocking blood flow.

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15
Q

What areas are commonly affected by an intracerebral haemorrhage?

A

Basal ganglia, thalamus, cerebellum, and pons (in that order).

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16
Q

What is a subarachnoid haemorrhage?

A

A type of haemorrhagic stroke often related to an aneurysm, which increases intracranial pressure (ICP) and causes bleeding in the subarachnoid space.

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17
Q

What are the main types of cerebrovascular accidents and their associated percentages?

A

Cerebral infarction (80%), Intracerebral haemorrhage (15%), and Subarachnoid haemorrhage (3%).

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18
Q

What is the clinical presentation and 30-day mortality rate for a cerebral infarction?

A

Slow evolving symptoms with a 15-45% 30-day mortality rate.

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19
Q

What are the causes and risk factors for cerebral infarction?

A

Causes include thrombus, embolism, and atheroma. Risk factors include heart disease, hypertension, atheroma, and diabetes.

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20
Q

Describe the pathogenesis of subarachnoid haemorrhage.

A

Rupture of a saccular aneurysm (often in the circle of Willis) can lead to subarachnoid haemorrhage, sometimes accompanied by a vascular spasm.

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21
Q

What is the classic triad of symptoms for meningism?

A

Neck stiffness, photophobia, and headache.

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22
Q

What are some key risk factors for cerebrovascular accidents?

A

Hypertension, atrial fibrillation, diabetes, and smoking.

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23
Q

Describe the process of cerebral infarction.

A
  • 24 hrs after: Local softening and oedema.

-4 days after: Liquefactive necrosis, macrophage infiltration, and reactive astrocytes at the periphery.
- Final stage: Phagocytosis of necrotic tissue with cystic cavitation.

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24
Q

What is the pathogenesis summary for cerebrovascular accidents?

A

“THE SCAR OF Vessels”
T - Thrombosis: Arterial thrombosis due to atheroma in intracranial or extracranial arteries.
H - Head Injury: May lead to cerebral ischaemia, vascular occlusion, or rupture.
E - Embolism: Embolic arterial occlusion from atheroma in extracranial vessels.
S - Subarachnoid Haemorrhage: Rupture of a saccular aneurysm causing vascular spasm.
C - Critical Blood Flow Reduction: Reduction in cerebral blood flow (e.g., cardiac arrest).
A - Arterial Disease: Generalized arterial disease (e.g., vasculitis) affecting vessels.
R - Respiratory Arrest: Critical reduction in arterial oxygenation due to hypoxia.
O - Oral Contraceptives: Venous thrombosis due to local sepsis or drug effects (e.g., oral contraceptives).
V - Vasculitis: Generalized arterial disease affecting both intracranial and extracranial vessels.

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25
What is liquefactive necrosis?
A type of tissue necrosis where tissue transforms into a liquid viscous mass, often seen in brain infarcts.
26
How does normal cortex tissue compare to liquefactive necrosis?
Normal cortex tissue is structured and intact, while liquefactive necrosis shows a disorganized, liquid-like area.
27
Name the three types of aneurysms.
Berry (saccular), fusiform, and dissecting aneurysms.
28
What is a berry (saccular) aneurysm?
A round, sac-like aneurysm that typically occurs at arterial branch points in the Circle of Willis.
29
What are common sites for berry aneurysms in the brain?
- Anterior communicating artery (40%) - Middle cerebral artery (34%) - Posterior communicating artery (20%) - Internal carotid artery (4%).
30
What are the potential effects of an aneurysm?
Motor, sensory, perceptual, cognitive, and affective effects, depending on the injury's location.
31
How does the location of an aneurysm impact its effects?
The effects relate to functional brain anatomy, as different brain areas control different functions.
32
What structures make up a peripheral nerve?
Axon, myelin sheath, endoneurium, perineurium, epineurium, fascicles, and blood vessels.
33
What are the types of peripheral nerve injuries?
Complete (neurotmesis) Compression (neuropraxia) Stretch (axonotmesis)
34
What is neurotmesis?
A complete peripheral nerve injury where the nerve is entirely severed.
35
What is neuropraxia?
A type of peripheral nerve injury due to compression, causing temporary loss of function without permanent damage.
36
What is axonotmesis?
A peripheral nerve injury due to stretch, causing damage to the axons but preserving some of the surrounding structures.
37
What are the effects of nerve compression?
Fibre deformation, ischaemia, trauma to epineurial vessels, oedema, demyelination, epineurial haemorrhage, neural fibrosis, scarring, and chronic irritation.
38
What factors affect the extent of a compression injury?
- Amount of epineurium (less epineurium increases susceptibility) - Position of fibre within fascicle (surface fibres are more susceptible) - Size of fascicle (larger fascicles are more susceptible) - Relationship with unyielding surfaces (e.g., common peroneal nerve around the head of the fibula)
39
What are the key responses involved in neural degeneration and repair?
Axonal degeneration, Schwann cell response, nerve cell body response, proximal axon response, and axonal regeneration.
40
What are the stages involved in axonal degeneration?
Protease activation, proteolysis of the distal segment, myelin breakdown, debris removal, and the development of an amorphous interior in the nerve fibre.
41
What responses are part of Schwann cell reaction to nerve injury?
- Mitosis and proliferation in the distal segment - Formation of cytoplasmic extensions and interdigitation - Release of Nerve Growth Factor (NGF) - Atrophy of axons that do not route down the new tube
42
What changes occur in the nerve cell body in response to injury?
- Shift in metabolic activity from neurotransmitter production to synthesis of proteins for axonal growth and repair - Increased reaction if the lesion is closer to the cell body - Increased cell body volume - Enhanced production of cytoskeletal proteins
43
What occurs in the proximal axon response to injury?
- Axonal degeneration over a few internodes, leaving Schwann cells intact - Degeneration if the cell body degenerates - If the cell body survives, the axon diameter and myelin thickness decrease, which can increase after functional contact is re-established - Collateral and terminal sprouting, which will degenerate if functional contact is not made
44
Why do crush injuries recover better than complete lesions?
Because the basement membrane and endoneurium remain intact, providing a pathway for nerve regeneration.
45
What are some consequences of inappropriate innervation?
It can affect motor control, increase motor unit size, leave some fibers denervated, and may lead to muscle atrophy that cannot be reversed.
46
List neurodegenerative disorders of interest mentioned in the slide.
- Neurodegenerative dementias - Huntington's Disease - Parkinson's Disease
47
What are the key pathological features of Alzheimer's Disease?
- Amyloid Beta extracellular plaques - Hyper-phosphorylated intracellular tangles - Inflammation
48
List common symptoms of Alzheimer's Disease.
Memory loss/changes Forgetting words or inappropriate words Problems in speaking, reading, understanding Disorientation to time and place Poor or decreased judgment Problems with abstract thinking Misplacing things in inappropriate places Drastic changes in personality Difficulty performing familiar tasks
49
What are the treatment options for Alzheimer's Disease?
- Cholinesterase inhibitors (block acetylcholinesterase to preserve acetylcholine for memory) - Memantine (blocks excitotoxicity from glutamate)
50
What is the main limitation of current treatments for Alzheimer's Disease?
They only treat symptoms and have minimal effectiveness.
51
What new Alzheimer's treatment was approved by the FDA in June 2021?
Aducanumab (Aduhelm), a monoclonal antibody.
52
What is Lecanemab, and what is its significance in Alzheimer's treatment?
Lecanemab is an Alzheimer's treatment that showed a 27% reduction in cognitive decline in a phase 3 clinical trial. It is currently under FDA review.
53
What are potential future treatment options for Alzheimer's Disease?
- Anti-inflammatory compounds - NSAIDs/CSAIDs - The Bredesen protocol (diet-based therapy focusing on low animal fat and no sugar)
54
What type of disease is Huntington's Disease, and how does it progress?
Huntington's Disease is a rapid progressive neurodegenerative disease.
55
What are the symptoms of Huntington's Disease in the early stages?
Mood, character, memory, and attention disruptions.
56
What symptom is characteristic of late-stage Huntington's Disease?
Involuntary rapid movements.
57
At what age does Huntington's Disease typically present?
in the 30s.
58
What is the genetic inheritance pattern of Huntington's Disease?
It is an autosomal dominant disorder.
59
Is there a cure for Huntington's Disease?
No, there is no cure.
60
How is Huntington's Disease managed?
By treating and reducing symptoms, as there is no treatment for the disease itself.
61
What is Parkinson's Disease also known as?
Shaking palsy.
62
Describe Parkinson's Disease.
It is a progressive, degenerative brain disease that causes trembling, stiffness, slowness of movement, and loss of fine motor control.
63
What are common symptoms of Parkinson's Disease?
Tremor at rest, rigidity, akinesia (absence of spontaneous movement), or bradykinesia (slowed movement).
64
What is a common protein aggregate found in Parkinson's Disease?
Lewy bodies, which are associated with alpha-synuclein accumulation.
65
What are the known causes of Parkinson's Disease?
Some genetic factors are involved, but the exact cause is largely unknown.
66
: Is there a cure for Parkinson's Disease?
No, there is currently no cure.
67
What treatments are available for Parkinson's Disease?
- Levodopa: Promotes dopamine in the brain. -Dopamine agonists: Mimic dopamine effects in the brain. -Anticholinergics: Control tremor.
68
What are potential future treatment options for Parkinson's Disease?
Possible options include deep brain stimulation, stem cell therapy, or transplantation.
69