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SBCP Pathology > CNS Pathology > Flashcards

CNS Pathology Flashcards

1
Q

Describe the cellular makeup of the CNS.

A

Neurones - structural and functional unit of the nervous system. Specialised for rapid communication and connected by a series of synapses. .

Neuroglia - non neuronal and non excitable cells - supporting cells. Divided into macroglia and microglia. Outnumber neurones 5:1.

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2
Q

Name and describe the function of the different types of macroglia.

A
  • Oligodendrocytes: form myelin which aids impulse transport down the axon. (Comparable to Schwann cells of PNS).
  • Astrocytes: star shaped cells tat take on various complementary roles - metabolic, electrical insulation, barrier function, repair and scar formation.
  • Ependymal cells: line the ventricular system.
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3
Q

What is the function of the microglia?

A

Serve as a fixed macrophage system in response to injury.

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4
Q

Draw the basic anatomy of the brain.

A

(Please draw)

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5
Q

Name the layers of the meninges.

A

Dura mater
Arachnoid mater (underneath which is the subarachnoid space with CSF)
Pia mater

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6
Q

Describe the anatomy of the brainstem. What is its purpose?

A

The brainstem comprises the midbrain, the pons and the medulla oblongata.

Functions: vital control centres - hypothalamus and pituitary gland, vomiting centre, swallowing centre, respiratory centre etc.

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7
Q

Describe the flow of Cerebrospinal Fluid.

A

Produced by the choroid plexus of the lateral, 3rd and 4th ventricles.
Exits the lateral ventricles through the foramen of Monro into the third ventricle.
Passes via the aqueduct of Sylvuis into the 4th ventricle.
Exits the ventricler system through the foramen of Luschka and Magendie into the subarachnoid space. From here it either descends into the spine or ascends to bathe the cerebral hemispheres and cerebellum.
CSF is finally absorbed in superior sagittal sinus via arachnoid granulations.

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8
Q

What is hydrocephalus?

A

Increased volume of CSF. (Normal volume is 120ml).

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9
Q

What are the causes of Hydrocephalus?

A

Obstructive hydrocephalus is the most common cause - obstruction to the flow of CSF.

  • Previous meningitis or SAH (obstruction of flow or decreased absorption of CSF)
  • Colloid cyst in third ventricle (cause of sudden death)
  • Lesions in the infratentorial department of the skull e.g. expanding lesions, tumour. Lesions in this department block aqueduct or 4th ventricle
  • Congenital: Chiara malformations (defect in posterior fossa or cerebellum causing blockage of CSF flow) or Dandy Walker syndrome (cerebellar hyperplasia and cyst formation causing obstruction).

Papilloma of the choroid plexus causing excess CSF production.

Hydrocephalus ex vacuo - compensatory dilation of ventricles in dementia.

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10
Q

Describe the gross changes seen with hydrocephalus.

A

Dilation of the ventricular system and corresponding decrease in the volume of white mater.

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11
Q

What pressure constitutes a raised ICP?

A

An increase in mean CSF above 15mmHg.

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12
Q

Describe the makeup of the intracranial contents.

A
  • Brain 70%
  • CSF 15%
  • Blood 15%

An increase in any one of these will cause a compensatory decrease of the other two until mechanisms are exhausted an raised ICP ensues.

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13
Q

What are the causes of a raised ICP?

A

Mass effect:

  • Tumours
  • Abscesses
  • Haemorrhage
  • Infarction
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14
Q

What are the clinical features of raised ICP?

A
  • Headache
  • Vomiting
  • Confusion
  • Focal neurological signs - paralysis, hemianopia, dysphagia
  • Depressed consciousness (drowsiness –> stupor –> come –> coning with respiratory depression, bradycardia and death)
  • Seizure
  • Papilloedema.
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15
Q

Describe in detail the four stages of Raised Intracranial Pressure.

A
  1. Spatial compensation: increase in one of the components is compensated by a decrease in the other components.
  2. Raised ICP as compensatory mechanism exhausted: ICP increases slowly and systemic arterial pressure may correspondingly increase (Cushing response) to maintain perfusion)
  3. ICP increases rapidly as cerebral perfusion starts to decrease
  4. Cerebral vasomotor paralysis: ICP=SAP and cerebral circulation ceases leading to brain stem death.
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16
Q

Which factors are important in the development of raised ICP?

A
  • Speed - rapid increase in ICP exhausts compensatory measures more rapidly
  • Age (related to brain size) - older patients with a degree of cerebral atrophy and increased CSF compensate better than the young.
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17
Q

What effects does a raised ICP have on the brain?

A
  • Flattening of the gyral pattern.
  • Compression of the ventricle on the same side as any lesion
  • Lateral shift of the midline structures (if lesion unilateral)
  • Internal herniation (3 types - supracallosal/subfalcine, uncal and tonsillar).
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18
Q

Describe the types of herniation.

A
  1. Supracallosal/subfalcine: cingulate gyrus herniates under the falx cerebri.
  2. Uncal herniation: through the tentorial incisura. This causes third nerve compression (dilated pupil and loss of eye ROM), posterior cerebral artery compression and haemorrhage in the midbrain and pons).
  3. Tonsillar herniation: cerebellar tonsils displaced down the foramen magnum, causing brain stem compression, a life threatening event.
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19
Q

What is cerebral oedema?

A

An increase in the water content of the brain tissue.

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20
Q

What are the causes of cerebral oedema?

A
  1. Vasogenic oedema when integrity of the normal blood brain barrier is disrupted. This can be localised e.g. adjacent to an abscess, tumour, infarct, or generalised in sepsis.
  2. Cytotoxic oedema - increase in intracellular fluid secondary to injury - generalised hypoxic/ischaemic insult.
  3. Interstitial oedema - increase in water content in peri-ventricular tissues in acute hydrocephalus.
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21
Q

What is the clinical treatment of cerebral oedema?

A

Steroids if related to swelling around a tumour.

Surgical removal e.g. haemorrhage.

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22
Q

How is cerebrovascular disease categorised?

A

Clinically:

  • Thrombus or embolism causing anaemic infarction (impairment of blood supply results in hypoxic ischaemia).
  • Haemorrhage leading to haemorrhagic infarction due to loss of blood flow to brain tissue.
23
Q

How is acute ischaemia classified?

A
  • Global cerebral ischaemia with cardiac arrest, shock and severe hypotension.
  • Focal cerebral ischaemia, either large vessel disease or small vessel disease e.g. vasculitis.
24
Q

Which areas of the brain are vulnerable to infarction?

A

The borders between the individual vessel regions, and this is known as watershed infarcts.
Frequently seen as wedge-shaped infarcts.

25
Q

What is stroke?

A

Stroke is rapidly progressive clinical symptoms of focal, and at times global, loss of cerebral function lasting more than 24 hours or leading to death with no apparent cause other than that of vascular origin?

26
Q

What is a Transient Ischaemic Attack?

A

An acute loss of focal cerebral or ocular function with symptoms lasting less than 24 hours.

27
Q

Describe the gross changes seen in the brain after a stroke?

A

Minimal change in the first 6 hours.

By 48 hours the tissue will become soft, pale and swollen with loss of the sharp margin between grey and white mater.

Within 2-10 days the affected area becomes gelatinous and friable.

Over the next 10 days - 3 weeks the tissue will liquify to leave a cavity.

28
Q

Describe the microscopic changes seen in the brain following a stroke.

A

After 12 hours microscopy shows early ischaemic changes including red neurones and oedema.

Within 48 hours an inflammatory response is seen involving neutrophil polymorphs.

Over the next 2-3 weeks numbers of microglia/macrophages increase. A reactive astrocytosis surrounds the area of infarction.

29
Q

What are the causes of embolic stroke?

A
  • Cardiac mural thrombi: post MI (impaired contractility –> stasis –> thrombus), valve disease, Atrial fibrillation.
  • Atheromatous plaques in carotid arteries
  • Emboli associated with ventricular septal defects/ cardiac anomalies.
  • Cardiac surgery
  • Tumour emboli
  • Fat emboli (trauma patients - multiple fractures or aggressive CPR with rib fractures)
  • Air emboli
  • Acute bacterial endocarditis.
30
Q

What are the causes of Nontraumatic Intracranial Haemorrhage?

A

Can be divided into Intracerebral and Subarachnoid.

Intracerebral:

  • Hypertension leading to large or small vessel disease, Charcot-Bouchard microaneurysms, lacunar infarcts and slit haemorrhages.
  • Amyloid angiopathy
  • Anticoagulant therapy
  • Tumours
  • Vasculitis
  • AV malformations.

Subarachnoid:

  • Berry aneurysm
  • AV malformation
31
Q

Describe how hypertension is associated with non traumatic intracranial haemorrhage.

A

Hypertension can cause intracerebral haemorrhage via:

  • Large vessel disease - accelerated atherosclerosis
  • Small vessel disease - hyaline arteriosclerosis. Hyaline deposition causes weakening of the arterial wall and increased likelihood of rupture.
  • Charcot-Bouchard micro aneurysms - minute aneurysms caused by hyaline arteriosclerosis and weakening of the arterial wall.
  • Lacunar infarcts and slit haemorrhages - lacunar infarcts are small (<15mm) caveatting infarcts which are often multiple and are caused by arteriosclerosis of deep cerebral arteries and arterioles. Slit haemorrhages are the remains of micro haemorrhages as a result of rupture of small penetrating vessels).
32
Q

What is amyloid angiopathy?

A

In amyloid angiopathy the media of the small penetrating vessels is replaced by the protein amyloid. This causes weakening of the vessel wall and increases the likelihood of rupture.

33
Q

How do you test for the presence of amyloid e.g. in amyloid angiopathy?

A
  • Immunology amyloid stain

- Congo Red stain. Under polarised light amyloid shows up as an apple green colour.

34
Q

Describe the presentation of an AV malformation.

A
  • Most commonly present in 3rd and 4th decade of life.
  • More common in males
  • Can cause both intracerebral and subarachnoid haemorrhage.
35
Q

Where can one find a berry aneurysm in the cerebral circulation? What causes these?

A

Major arterial branch points of the cerebral arteries

  • 40% at the join between the anterior communicating and anterior cerebral arteries.
  • Middle cerebral arteries.

Majority are sporadic but there is an increased incidence with genetic systemic disorders e.g. Polycystic Kidney Disease, neurofibromatosis and Marfan’s Syndrome.

36
Q

How is traumatic head injury assessed in clinical practice?

A

Glasgow Coma Score:
Best ocular response
Best verbal response
Best motor response.

37
Q

What are the different types of head injury

A

Blunt injury caused by acceleration/deceleration forces.

Missile - penetrating injures

38
Q

Describe the distribution of a traumatic head injury?

A
  • Focal

- Diffuse: diffuse axonal injury, diffuse vascular injury, hypoxic ischaemic damage, diffuse brain swelling.

39
Q

What is cerebral contusion?

A

A traumatic brain injury that causes superficial bruising of the brain tissue.

40
Q

What areas are commonly affected by cerebral contusion?

A

Areas of brain closely related to boney protuberances.

  • Frontal poles
  • Orbital surfaces of the frontal poles
  • Temporal poles
  • Cortex adjacent to Sylvian fissure.
41
Q

What are the types of Cerebral Contusion?

A

Coup injury:
Cerebral inert at point of contact.

Contrecoup injury: Occurs after sudden deceleration when the surface opposite the point of contact becomes injured.

42
Q

Who presents with cerebral contusion?

A

Those at risk of falls - alcoholics and the elderly.

43
Q

What factors influence risk of laceration following cerebral contusion?

A

Increased force of injury increases the risk of laceration.

44
Q

What is extradural haemorrhage? How does it happen? What are the risks?

A

Haemorrhage between the skull and the dura. It results from torn vessels in the meninges in association with skull fracture.
There is a risk of death due to cerebral compression and herniation.

45
Q

What is the lucid interval of extradural haemorrhage?

A

The accumulation of blood between the skull and the dura mater is slow and this allows compensatory mechanisms to slow the rise of ICP. This provides a period of time between injury and death - the interval before the exhaustion of the compensatory mechanisms.

46
Q

What is subdural haemorrhage? Who is at risk? How does it present?

A

Subdural haemorrhage is between the dura mater and the arachnoid mater and results from tearing of bridging veins which empty into the superior sagittal sinus.
At risk are those with cerebral atrophy as they have an increased subdural space - the elderly and alcoholics.
Clinical presentation within 48 hours - headache +/- confusion.

47
Q

What is a traumatic subarachnoid haemorrhage? What are the clinical manifestations?

A

Haemorrhage in the subarachnoid space. Possible sources include:

  • Severe contusions +/- lacerations
  • Skull fracture can tear vessels at the base of the brain
  • Rupture if dissection of vertebral arteries
  • Blood from intraventricular haemorrhage.

Causes hydrocephalus due to blockage of CSF and symptoms of this are similar to those of increased ICP.

48
Q

What is diffuse axonal injury?
What is the clinical presentation?
What are the histological manifestations?

A

Widespread traumatic axonal damage.
Clinically the patient is typically unconscious from the moment of impact. There is no lucid interval. They remain unconscious, in a vegetative state or severely disabled.
On histology there is widespread axonal swelling due to B-APP which can be highlighted by silver impregnation techniques if patient survives >2 hours. May be useful in timing death.

49
Q

How are brain tumours classified?

A

Secondary are the most common. Metastases from breast, lung, prostate, GIT. Presentation varies depending on site of the lesion and rate of growth.

Primary brain tumours:
- Majority are GLIOMAS arising from neuroglia.
Astrocytes –> Astrocytoma/glioblastoma
Oligodendrocytes –> oligodendrioma
Ependymal cells –> ependymoma
- Neuronal tumours called NEUROBLASTOMAS
- Poorly differentiated MEDULLOBLASTOMA
- Tumour of the meninges called MENINGIOMA
- LYMPHOMA
- Cranial nerve tumours called SCHWANNOMA/NEUROFIBROMA

50
Q 
FIBRILLARY ASTROCYTOMA
Describe: 
- When in life it presents
- Location 
- Histological factors influencing grading 
- Treatment
- Prognosis 
- Gross appearance
A
  • Presents in 4th to 6th decades
  • Usually located in cerebral hemispheres but may also be found in cerebellum, brain stem or spinal cord.
  • Histological grading based on nuclear atypia, mitosis, endothelial proliferation and necrosis.
  • If resectable then surgery otherwise chemoradiotherapy.
  • The mean survival of a grade 4 astrocytoma/glioblastoma is 8-10 months.
  • Grossly the size of the tumour may be increased by surrounding oedema and haemorrhage.
51
Q 
OLIGODENDROGLIOMA
Describe: 
- When in life it presents
- Location 
- Gross appearance
- Prognosis
A
  • Presents in 4th - 5th decade
  • Usually in cerebral hemispheres
  • Tend to be more sharply defined than astrocytomas. Also associated with Ca++(90%) so may be seen on Xray
  • Better prognosis than astrocytoma/glioblastoma.
52
Q 
EPENDYMOMA
Describe: 
- When in life it presents
- Location 
- Prognosis
A
  • More common in children and adolescents
  • Occur in relation to the ventricular system inc the spinal cord. Commonly occur in the 4th ventricle and can cause hydrocephalus. CSF dissemination is common causing meningeal gliomatosis.
  • Average survival approx 4 years after surgery and therapy.
53
Q 
MENINGIOMA
Describe: 
- When in life it presents
- Location 
- Treatment
- Prognosis 
- Gross appearance
- Associations
A
  • Presents usually as benign tumours of adults
  • Attached to the dura. Mainly occur above the tentorium but 10% occur in posterior fossa and vertebral canal. They are slow growing and can attain a remarkable size before symptoms occur. They compress the underlying brain, causing cortical loss, but are easily separated from it.
  • Treated with surgical resection
  • High rate of recurrence after surgical resection.
  • Tumour of the meninges compressing on underlying brain which can cause shift of the midline structures.
  • Associated with; previous radiotherapy, neurofibromatosis type 2, breast and endometrial carcinoma due to oestrogen drive.

SBCP Pathology (4 decks)

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