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S7) Pathology of the brain Flashcards

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1
Q

The normal intracranial pressure is 0-10 mmHg. With coughing and straining (e.g. toilet), it can increased to 20 mmHg.

It is significant if increase maintained for several minutes.

What compensatory mechanisms are there to maintain normal pressures?

A

– reduce venous blood volume

– reduce CSF volume

– brain atrophy

(Note: Remember the brain is enclosed in the skull. Also only limited compensation, and after this point, decompensation can occur)

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2
Q

What is the value for normal intracranial pressure?

A

0 - 10mmHg

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3
Q

Which physiological mechanisms increase ICP?

A

Coughing and straining increase ICP to 20 mmHG

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4
Q

Identify the three compensation mechanisms that maintain normal pressure

A
  • Reduced blood volume
  • Reduced CSF volume
  • Spatial – brain atrophy
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5
Q

Identify some causes of raised ICP and what you might see as a result of it?

A
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6
Q

How are vascular mechanisms affected by ICP?

A

Vascular mechanisms maintain cerebral blood flow as long as ICP < 60mmHg

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7
Q

State the three effects of an expanding lesion in the brain

A
  • Deformation/destruction of the brain around the lesion
  • Displacement of midline structures – loss of symmetry
  • Brain shift resulting in internal herniation

- Cerebral oedema

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8
Q

Identify the 3 different types of intracranial herniation.

A

– Subfalcine herniation

– Transtentorial herniation

– Tonsillar herniation

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9
Q

What occurs in a subfalcine herniation?

A
  • In a subfalcine herniation, the cingulate gyrus is pushed under the free edge of the falx cerebri
  • Ischaemia of medial parts of frontal lobe, parietal lobe and corpus callosum due to compression of anterior cerebral artery → infarction
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10
Q

What occurs in a tentorial herniation?

A
  • In a tentorial herniation, the uncus / medial part of the parahippocampal gyrus herniates through the tentorial notch
  • Ipsilateral occulomotor nerve damage and occlusion of posterior cerebral and superior cerebellar arteries.: resulting in ischaemia.
  • COMMON mode of death (tumours and ICH)
  • Often fatal due to secondary haemorrhage into the brainstem (duret haemorrhage)
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11
Q

What is a ‘duret’ haemorrhage?

A

Secondary haemorrhage into the brainstem due to the downward displacement of the brain parenchyma.

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12
Q

What occurs in a tonsillar herniation?

A

In a tonsillar herniation, the cerebellar tonsils are pushed into the foramen magnum compressing the brainstem

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13
Q

Identify the different types of intracranial haemorrhages.

A
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14
Q

Identify how extradural (epidural) haematoma/ haemorrhage arises.

A

Associated with trauma: Usually a blow to the side of the head → hitting the pterion - where the bone is thin – skull fractures, scalp bruises

.: damage to the middle meningeal artery.: accumulation of blood between potential space between the dura mater and skull

>40-50 mls needed to cause pressure effects on the brain

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15
Q

How does extradural haemorrhage present?

A

Presents with: Lucid interval (hrs) then signs: Drowsiness and neurological deficits.

Takes time to get signs because usually the dura is tightly adhered to the skull .: takes time for blood to accumulate and split the dura from the skull - hence lucid period – eventually dura will split and blood can accumulate v rapidly .: getting pressure effects on brain .: neurological signs

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16
Q

How does a subdural haematoma arise?

A

Shearing of bridging veins → Accumulation of blood in the potential space between the dura mater and arachnoid mater (subdural space)

• Pressure effect on brain >40mls, 80-100mls fatal – raised ICP

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17
Q

For a subdural haematoma, what are the causes?

A

ACUTE –traumatic, rapid blood accumulation.

CHRONIC – elderly and chronic alcoholics (brain atrophy - causing tension on the bridging veins → vulnerable to rupture)

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18
Q

In a subdural haematoma. a lot of blood can accumulate before clinical signs develop. What is it commonly associated with?

A

Assaults

falls

RTCs

minor head injuries (elderly etc)

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19
Q

What are some drug interactions or contraindications we should consider in a patient with subdural haematoma?

A

Anticoagulant therapy – can potentiate the effects of haemorrhage or liver cirrhosis (coagulopathies)

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20
Q

What occurs in subarachnoid haemorrhage?

A

• Shearing of meningeal blood vessels → Film of blood over the brain surface

Can occur when there is an acute rise in ICP (straining on the toilet, sexual intercourse) .: blood forced into subarachnoid space and ruptures (e.g. ruptured berry aneurysm)

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21
Q

What can cause a subarachnoid haemorrhage?

A

Traumatic – basal skulls fractures, contusions

Spontaneous:
Ruptured berry aneurysm – common!!!

Amyloid angiopathy

Vertebral artery dissection

Arteriovenous malformations

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22
Q

What is the presentation of a subarachnoid haemorrhage?

A

Sx: sudden onset headache (worst ever), rapid neurological deterioration, sudden collapse.

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23
Q

Ruptured berry aneurysm is a common cause of subarachnoid haemorrhage. Identify where berry aneurysm can be formed?

A
  • Majority - occur at the Circle of Willis
  • commonly at the anterior circulation area.
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24
Q

What is a stroke?

A

Sudden event producing a disturbance of CNS function due to vascular disease.

Clinical signs and symptoms dependent on vascular territory occluded and then on its size.

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25
What are the 2 types of stroke?
1. Ischaemic (cerebral infarct) - 85% 2. Haemorrhagic stroke - 15%
26
What 2 broad causes can cause ischaemic/ cerebral infarct stroke?
– Thrombotic occlusion – Embolic occlusion
27
What 2 broad causes can cause haemorrhagic stroke?
10% ICH (intracranial haemorrhage) 5% SAH (subarachnoid haemorrhage)
28
Identify three risk factors for stroke
- Hyperlipidaemia - Hypertension - Diabetes mellitus
29
What is the pathophysiology of ischaemic stroke/ cerebral infarction?
– **Obstruction of blood supply** leads to **ischaemia.** – If there’s **collateral blood supply** (COW- Circle of Willis) then some overlap and limits damage. – **Obstruction of deep penetrating arteries** (which supply basal ganglia, thalamus, deep white matter) .: no collateral supply. – these are end arteries .: will cause sig damage.
30
What are water shed areas of the brain?
Watershed areas – **areas that lie** at **most distal portion of artery territory** (border MCA and ACA high risk) – **wedge shaped necrosis.** This the area that is particularly prone to getting ischaemic damage in transient hypotensive episode. Seen after hypotensive episode.
31
Embolic occlusions are **most common**. Where can they come from?
– Cardiac mural thrombus (MI, valvular heart disease, atrial fibrillation) – Atherosclerosis (carotid arteries, COW) – Other emboli – via DVT and patent foramen ovale (rare) -but can happen, fat and bone marrow emboli, septic emboli (vegetations)
32
In embolic occlusions, which artery gets affected?
**MIDDLE CEREBRAL ARTERY** – **most affected** direct extension of **internal carotid artery**. **Emboli lodge** in **branches** and **areas** where there’s **underlying atherosclerosis.**
33
How can thrombotic occlusions arise?
Superimposed thrombi overlying atherosclerotic plaque. Fragments can fall off and embolise to distal sites
34
What are the common sites of thrombotic occlusions?
carotid bifurcation, origin of MCA, basilar A
35
How can lacunar infarcts arise?
**small penetrating arteries occluded** (HTN) resulting in **small mm infarcts**
36
Cerebral infarct …
37
Histology of cerebral ischaemia …
38
What commonly causes spontaneous intracerebral haemorrhage (Stroke)?
**Hypertension – 60yrs +, rupture of small intraparenchymal blood vessels.** Cerebral amyloid angiopathy Arteriovenous and cavernous malformations Tumours Traumatic ICH
39
Which common sites are affected in a spontaneous intracerebral haemorrhage stroke?
Basal ganglia, thalamus, pons and cerebellum.
40
What are the complications of spontaneous intracerebral haemorrhage?
Silent to **accumulation of haemorrhage catastrophic** (+/- cerebral oedema) resulting in **raised ICP,** **midline shift** and **compression of adjacent brain parenchyma.**
41
Hypertension has systemic effects - on the brain, heart, vessels, kidney etc. How can it arise?
due to **arteriosclerosis** (thickened walls) → can lead to weakness
42
Which arteries are at risk in the brain during hypertension and which structures will be affected?
* *Deep penetrating arteries and arterioles:** (1) **Basal ganglia and thalamus** (2) **White matter** (3) **Brainstem**
43
What is cerebral amyloid angiopathy?
seen in advancing age can lead to lobar hemorrhage involving the cerebral cortices and tiny microhemorrhages.
44
What can cause cerebral amyloid angiopathy?
**due to amyloid deposition** in the **walls of small and medium sized meningeal and cortical vessels** (congo red stain) They become rigid and inflexible which weakens the wall .: at risk of haemorrhage. Different distribution to Hypertensive ICH
45
Describe some features of the arteriovenous malformations.
– most common, M\>F 10-30 yrs age – subarachnoid vessels to brain / vessels within the brain. – can lead to wormlike (tangled) vascular channels (Risk of rupture)
46
Describe features of cavernous malformations.
– loose vascular channels, distended, thin walled – can be seen in cerebellum and pons
47
What are capillary telangiectasia?
microscopic foci of dilated thin walled vessels
48
What is venous angioma?
dilated venous channels
49
Identify symptoms of CNS tumours.
– Seizures – Headaches – Focal neurological deficits – CNS Tumours – Raised ICP – Vomiting and nausea
50
Identify the CNS tumours and categorise them into primary and secondary.
51
Describe features of gliomas.
Malignant Graded 1-5
52
What is the most common type of glioma?
Most common is **astrocytic tumours**: **Astrocytomas** – low to high grade, **80%** Glioblastoma multiforme (GBM) – high grade (4-5) - can be v aggressive Oligodendrogliomas – 20% gliomas, grade 2-4 **Ependymoma** – ventricular system, often **disseminated into CSF**
53
Identify other CNS tumours.
– Lymphomas – Germ cell tumours – Medulloblastoma – Meningiomas
54
Describe some features of the following CNS tumours: – Lymphomas – Germ cell tumours – Medulloblastoma – Meningiomas
55
What is meningiomas?
**benign**, derived from **arachnoid meningothelial cells**, can **cause problems if compress important structure / enlarge.**
56
The CNS is normally sterile. However, microorganisms gain entry by 4 possible routes. Identify them
- **Direct spread** *e.g. middle ear infection, base of skull fracture, air sinuses, skull fractures, osteomyelititis, infected teeth.* - **Haematogenous/ Blood-borne** *e.g. arterial blood (I.En), retrograde venous through anastomoses veins of face and venous sinuses of the skull. sepsis, infective endocarditis* - **Iatrogenic** *e.g. ventricular-peritoneal shunt, surgery, lumbar puncture/ spinal anaesthesia* * -* **Peripheral nerves** *e.g. HSV, viruses*
57
Infections of the CNS can affect …
– Meninges (lining of the brain) – Aggregates of acute inflammation – Brain parenchyma
58
What is meningitis?
- **Meningitis** is the inflammation of the leptomeninges, with/without septicaemia - Prompt diagnosis and treatment is life saving
59
What are the different types of meningitis?
Types: – Acute pyogenic (bacterial) – Aseptic (viral) ?immunocompromised – Chronic (myco tuberculosis, fungi) – Carcinomastosis (disseminated tumour from the original site and can lead to lots of little tumour deposits occurring in the meninges)
60
What are the symptoms of meningitis?
– headache – photophobia – irritability – altered consciousness – stiff neck ***due to meningeal irritation*** – focal neurological impairment
61
What are the causative organisms of meningitis in patients of various ages?
- **Neonates** – E. Coli, L. monocytogenes - **2 - 5 years** – H. influenzae type B (HiB) - **5 - 30 years** – N. Meningitides (types) - **Over 30 years** – S. pneumoniae
62
What investigations would do for meningitis?
CT scans lumbar puncture (look for increased pressure, Neutrophils, increased proteins, less glucose etc).
63
Identify complications of meningitis.
– cerebral oedema – cerebral infarction – cerebral abscess / empyema – epilepsy – meningoencephalitis – septicaemia. (even death)
64
What is a common organism that can cause cerebral abscess?
Streptococci and staphylococci
65
What is encephalitis?
- **Encephalitis** is the classically **viral inflammation of the brain parenchyma due to infection** - **Neuronal cell death by virus occurs**, with the **inclusion bodies** - Prominent lymphocytes
66
Identify the causative organisms for encephalitis in the following areas: - Temporal lobe - Spinal cord motor neurons - Brain stem
- Temporal lobe *e.g. herpes virus* - Spinal cord motor neurons *e.g. polio* - Brain stem *e.g. rabies*
67
What are prion diseases?
– Diseases involving **abnormal cellular protein accumulation** leading to **cell injury both inside or outside of the cell.** – ‘infective’
68
Prion diseases can lead to cell injury. Identify how?
Neuron cell death Synapse loss Microvacuolations (gives this spongiform appearance) Lack of inflammation
69
Identify some examples of prion diseases.
– Creutzfeldt- Jakob disease (CJD), variant CJD – Scrapies (sheep) – Bovine spongiform encephalopathy BSE (‘Mad cow disease’)
70
We have different forms of prion diseases. What are the three?
- Sporadic - Familial - Iatrogenic (contaminated equipment / bld transfusions or ingested)
71
What is the effect of the mutated PrP on the body?
**Mutated PrP** interacts with normal PrP to undergo a post translational conformational change
72
What occurs in prion disease?
**PrPSC aggregates** leading to neuronal death and holes in grey matter
73
How is prion disease said to be ‘infective’ - even though no microorganism is involved?
Usually, we have a normal protein configuration which is rich in alpha helices. If there is a sporadic mutation → can get a conformational change to the protein - abnormal protein now This conformational change results in a change from alpha rich helix to beta pleated sheet - this causes a problem because the abnormal protein is now more resistant to protein lysis and breakdown - difficult to get rid of. If this abnormal protein is adjacent to a normal protein of the same type, it forces that protein to undergo a conformational change causing both to have the abnormal cellular configuration - this is why it classes as ‘infective’. (causes other cells to under conformational change to become like itself)
74
Compare Creutzfeld Jakob disease (CJD) and Variant Creutzfeld Jakob disease (Variant CJD).
75
What are neurodegenerative diseases?
* Loss of neurons * Accumulation of protein aggregates
76
Neurodegenerative diseases can affect the hippocampus, basal ganglia, cerebellum and motor neurons. What does this result in?
Hippocampus and cerebral cortices → cognitive changes, alteration in memory, behaviours, language. Basal Ganglia → movement disorders (hypo /hyperkinetic) Cerebellum → ataxias Motor neurons → motor neuron disease
77
What is dementia?
**Dementia** is the acquired global impairment of intellect, reason and personality without impairment of consciousnes
78
Identify four common forms of dementia
- Alzheimer’s (50%) - Vascular dementia (20%) - Lewy body - Picks disease
79
How does Alzheimer's disease arise?
– 3% 65-74yrs of age – Sporadic (~90%) – Familial (earlier onset) – 5-10%
80
Describe some defining features of Alzheimer's Disease
Exaggerated aging process due to: - **Loss of cortical neurones** – ↓ brain weight/ shrunken brain, ↓ cortical atrophy - ↑ **neuronal damage** – neurofibrillary tangles (tau), senile beta plaques
81
In AD, which lobes are particularly affected?
Frontal, temporal and parietal lobes.
82
In three steps, describe how neuronal damage occurs in AD due to neurofibrillary tangles
⇒ Intracellular twisted filaments of **Tau protein** ⇒ Tau normally binds and **stabilises microtubules** ⇒ Tau becomes **hyperphosphorylated** in AD
83
In two steps, describe how neuronal damage occurs in AD due to senile plaques
⇒ Foci of **enlarged axons**, synaptic terminals and dendrites ⇒ **Amyloid deposition** in vessels in centre of plaque
84
What signs and symptoms can be seen in Alzheimer's disease?
– Impaired intellectual function – Impaired memory – Altered mood and behavior – Disorientated • Ch21 Trisomy and Down link
85
In Down’s syndrome, there is early onset AD. Explain why
- Mutations of 3 genes on chromosome 21: I. Amyloid precusor protein (APP) gene, II. Presenilin (PS) genes 1 and 2 code for components of secretase enzyme - Leads to incomplete breakdown of APP and amyloid is deposited
86
What is Parkinson disease?
**Loss of dopaminergic neurons** from the **substantia nigra** due to **accumulation of Alpha synuclein** neuronal inclusion (Lewy body).
87
What symptoms and signs can diagnose Parkinson disease?
Hypokinesia (rigid, bradykinesia, instability, tremor)
88
What is Huntington disease?
It is an auto **dominant condition.** It is due to **CAG trinucleate repeat expansion** resulting in **mutant protein broken down**(ubiquitination and proteolysis) to intranuclear aggregates of ubiquitinated **huntington protein**) This results in **cell injury and death, gliosis.** Characterised by **hyperkinesia - involuntary jerky movements**
89
Other protein inclusions in neurodegenerative diseases …

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