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HLTH3200 > CNS Pathology > Flashcards

CNS Pathology Flashcards

1
Q

Provide an overview of PNS and CNS disorders

A
  • PNS: Axonal injury and neuropathies
  • CNS: Trauma, demyelinating disorders, neurodegenerative disorders, neoplasia, infectious disorders and CV related stress
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2
Q

What is the PNS and structures involved

A
  • Structures: Nerves, ganglia, neuronal cell bodies and nerve endings, ascending tracts (sensory information) and descending tracts (muscle action)
  • Peripheral Nerves: Epineurium surrounds nerve, perineurium surrounds fascicles, endoneurium surrounds peripheral (myelinated) nerve fibre, myelin sheath formed by schwann cells surrounds axon
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3
Q

List the different types of nerve injuries

A
  • Neurapraxia
  • Axonal degeneration
  • Axonotmesis
  • Neurotmesis
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4
Q

What is neurapraxia

A
  • Injury to a myelinated nerve by pressure that interrupts conduction
  • Causes temporary paralysis and loss of function but not degeneration
  • Followed by a complete and rapid recovery
  • Relatively mild type of nerve injury, often result of trauma to the body
  • Endoneurium intact, axon intact and no nerve degradation
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5
Q

What is axonal degeneration

A
  • Direct injury to axon leading to axon transection / crushing leads to Wallerian degeneration (axotomy, swelling, granulation)
  • Controlled event leading to distal axon death
  • Preventing neuronal death, promoting nerve regeneration
  • Sensory / motor axons cannot effectively communicate between PNS and CNS
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6
Q

What is axonotmesis

A
  • Nerve injury where axons and myelin sheath are damaged
  • Endoneurium, perineurium and epineurium remain intact
  • Mainly follows a stretch injury
  • Break down of axon at distal end causes Wallerian degeneration (axotomy, swelling, granulation)
  • Optimal circumstances for regeneration and functional recovery possible
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7
Q

What is neurotmesis

A
  • Nerve injury involving complete severance or crushing of nerve
  • Different degrees of severity
  • Mostly spontaneous recovery not expected
  • In all forms distal end will undergo Wallerian degeneration (axotomy, swelling, granulation)
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8
Q

Differentiate between CNS and PNS nerve regeneration

A
  • CNS: Most CNS fibres cannot regenerate
  • PNS: If soma is damaged peripheral nerve cannot regenerate (cell body / nucleus) but if axon is damaged the cell can regenerate (axonal degeneration / demyelination)
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9
Q

Describe the events following injury and mechanisms of repair

A
  • Nerve injury and nerve will begin to degrade
  • Axon surrounding myelin break down, myelin degenerates simultaneously
  • Phagocytic macrophages interact with schwann cells to remove injured tissue debris
  • Connection with target muscle lost, leading to muscle atrophy and fibrosis
  • Axon sprouts with a fingerlike growth cone advance using schwann cells as guides (align in bungner bands and express surface molecules)
  • Newly connect axon matures and the pre-injury cytoarchitecture and function are restored
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10
Q

What are peripheral neuropathies and symptoms

A
  • Heterogeneous group of diseases
  • Result from inflammatory, toxic and metabolic conditions in addition to genetic defects
  • Symptoms vary depending on the type of nerves affected
  • Movement, sensory and autonomic nerve impairment (control of organs)
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11
Q

What are the causes of peripheral neuropathies

A
  • Altered metabolism, covalent modification
  • Altered organelle function and reactive oxygen species formation
  • Altered intracellular and inflammatory signalling
  • Slowed axonal transport and altered ion channel dynamics and expression
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12
Q

What are the types of peripheral neuropathies

A
  • Trauma (car accidents, sports injuries)
  • Diabetic neuropathy
  • Chemotherapy induced peripheral neurotoxicity
  • Viruses
  • Autoimmune (Guillain-Barre Syndrome)
  • Genetic (Charcot-Marie-Tooth disease)
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13
Q

What is Guillain-Barre syndrome (acute peripheral)

A
  • Acute peripheral neuropathy
  • Demyelinating disorder
  • Very rare (1:100,000)
  • Can lead to death from failure of respiratory muscles within days of onset of symptoms
  • Autoimmune disease (against myelin or axon)
  • Antibodies and lymphocytes attack and damage peripheral nerves
  • Symptoms appear suddenly, progress rapidly, and resolve slowly as damaged nerves heal
  • Cause unknown, usually follows viral / bacterial infection
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14
Q

What is Charcot-Marie-Tooth disease (chronic peripheral)

A
  • Chronic peripheral neuropathy
  • Symptoms begin subtly and progress slowly
  • More common (1:2,500)
  • Both motor and sensory abnormalities are common (muscle weakness & pain)
  • Decreased reflexes, difficulty heel walking, calf atrophy
  • Follows a chronic relapsing-remitting or progressive course
  • Caused by duplication / mutation of PMP22 (peripheral myelin protein) or hereditary neuropathy
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15
Q

What is trauma, a concussion and the types of trauma to the CNS

A
  • Injury or damage to living CNS tissue caused by an extrinsic agent or force by either direct or indirect mechanisms
  • Concussion: Traumatic brain injury that can lead to bruising, swelling, tearing of BV and injury to nerves
  • Types: Diffuse and focal traumatic brain injury
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16
Q

What is diffuse traumatic brain injury (DTBI)

A
  • Generalised injury to all regions of the brain
  • Axonal or hypoxic injury
  • Negatively impacts brain functioning
  • Brain can become injured whether or not the skull is fractured
  • Primary (mechanical damage) and secondary (indirect result)
17
Q

What is axonal injury (DTBI)

A
  • Caused by global disruption of axons due to severe shearing forces
  • Immediate primary axotomy, delayed secondary axotomy principally due to ischaemia
    Pathology
  • Focal accumulations of β-amyloid precursor protein (4-5h)
  • Axonal varicosities / swelling (12-24h)
  • Axonal swellings (24h-2m)
  • Microgliosis (2w-5m)
  • Loss of myelinated fibres (>2m)
18
Q

What is focal traumatic brain injury (FTBI) and cerebral contusion

A
  • Localised injury of the brain
  • Blunt forced trauma, rapid tissue displacement, bruising of brain parenchyma, brain contacts rough skull surfaces (orbital floor / petrous ridges)
19
Q

What is a hematoma (FTBI)

A
  • Brain haemorrhaging from a ruptured vein or artery
  • Increasing pressure forces brain towards foramen magnum
  • Symptoms: Headaches, agitation and drowsiness, can result in death if not treated quickly
20
Q

What are the two types of hematoma’s (FTBI)

A

Epidural:
- Between skull and dura mater
- 30% mortality rate
- Torn artery increases intracranial pressure
- Rapidly expanding with arterial blood, skull fracture, torn middle meningeal artery
- Dura pushed away by hematoma
Subdural:
- Between dura matter and arachnoid meningeal layers
- Occur more slowly (venous)
- Pushes brain away from skull across midline (including ventricles)
- Dura is attached to skull, hematoma cannot cross falx cerebri, tentorium may form

21
Q

What are neurodegenerative disorders

A
  • Characterised by the progressive loss of neurons, typically affecting groups of neurons with functional interconnections
  • Parkinsons
  • Alzheimers
  • Huntingtons
22
Q

What is Parkinson disease and Lewy bodies

A
  • Atrophy and loss of dopaminergic neurons in substantia nigra pars compacta (SNPc) in basal ganglia
  • Depigmentation of substantia nigra
  • 99% sporadic and 5% genetic causes
  • Loss of dopamine
  • Resting tremor, bradykinesia, rigidity, postural imbalance)
  • Lewy Body: Accumulation of intracellular fibrillar aggregates
23
Q

What are cerebrovascular diseases and strokes

A
  • Cerebrovascular Disease: Brain disorders caused by pathologic processes involving blood vessels
  • Stroke: Acute-onset neurologic deficits resulting from hemorrhagic or obstructive vascular lesion
24
Q

What is an ischaemic stroke

A
  • A clot blocks BF to an area of the brain due to occlusion
  • Cause: Embolism, thrombosis of cerebral artery, hypo-perfusion
  • Result: Decrease in cerebral blood flow / oxygen supply (hypoxia), widespread neuronal cell death (infarct grows and spreads), penumbra (injury of surrounding tissue)
  • Histology: Eosinophilic neurons and cytoplasm, pyknosis, cortical atrophy and gliosis develop
25
Q

What is a haermorrhagic stroke

A
  • Bleeding occurs inside or around the brain tissue due to rupture of blood vessels
  • Types: Subarachnoid and intracerebral
  • Cause: Rupture of a weakened blood vessel (atherosclerosis from hypertension), uncontrolled hypertension
  • Location: Cerebrum and bleed into the lateral ventricle
  • Result: Sudden and often lethal, poor prognosis
26
Q

What is the ischaemic cascade

A
  • Series of biochemical reactions that are started in the brain after ischaemia takes place
  • Within seconds or minutes of inadequate blood supply
27
Q

List the steps involved in the ischaemic cascade

A
  • Vascular occlusion decreases BF (ischaemia) leading to energy depletion
  • Failure of NaK pumps, depolarisation of neuronal membrane (loss of function) and AnO2 glycolysis (acidosis)
  • Neurons release glutamate into synaptic cleft leading to excitotoxin
  • Glutamate acts on channel receptors and opens NMDA and AMPA receptors leading to Ca influx
  • Ca influx causes activation of catabolic enzymes and NO synthase (formation of free radicals)
  • Free radicals and catabolic enzymes destroy structural proteins and DNA
  • Neuronal necrosis edema / lysis, lipid peroxidation and membrane disruption (all induce apoptosis)
  • Free radicals also injure mitochondria and lead to apoptosis through pro-apoptotic molecules
28
Q

What is neoplasm and neoplasia

A
  • Neoplasm: Abnormal mass of tissue, growth exceeds and is uncoordinated with that of normal tissues and persists in excessive manner after cessation of stimuli
  • Neoplasia: Cancer, new growths of cells in the body
29
Q

What are the two types of neoplasms

A
  • Glioma: Tumours that arise from the glial group of cells (supporting cells), 50% of all brain tumours, highly malignant
  • Meningioma: Non-glial tumours, slow growing, form from meninges, non-aggressive, interfere with circulation of CSF (hydrocephalus), 80% surgically removed
30
Q

What are infectious disorders

A
  • Infections of the brain can be caused by viruses, bacteria, fungi, or, occasionally, protozoa or parasites
31
Q

What are two examples of infectious disorders

A
  • Encephalitis: Infection causing inflammation of the brain, viruses are most common cause
  • Meningitis: Inflammation of meninges, bacterial and viral meningitis can develop into encephalitis

HLTH3200 (14 decks)

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