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NAS > Week 11 > Flashcards

Week 11 Flashcards

1
Q

CNS injuries- diverse group of disorders

A

Spinal cord injury SCI and traumatic brain injury TBI primarily affect young people 15-24
Stroke and brain cancer primarily affect older generation
Most common causes SCI- fall, road traffic accidents and sport

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2
Q

Repair of tissues not in CNS

A

Proliferation of cells occurs- tissue repair
Cells can be replaced
Complexity at expense of individual immortality

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3
Q

Repairing neuronal networks in CNS

A

In CNS in order for the final development and function of CNS there must be fast neuronal networks- hundreds of interconnected neurones
Taking one cell out makes entire systems fail
Can’t replace dead neurones, neurogenesis doesn’t happen- adult neurones dont proliferate so very difficult to repair
Complexity at the expense of reparability

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4
Q

Topographical organisation of CNS

A

If you damage a specific region of the brain that function will be lost
In spinal cord- loss of movement, sensation and autonomic control below level of injured segment affects functions of that spinal region

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5
Q

Functional consequences of injury

A

Depend on the site and size of the injury not the type of injury
Signs and symptoms tell you which part of the brain is injured but not the type of injury

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6
Q

Energy supply to the brain

A

2% of the total body mass
Consumes 15% of the energy generated in the body, disproportionally high energy consumer
No energy stores of its own (small amount glycogen in astrocytes)
Energy is derived exclusively from glucose metabolism, constant supply of glucose and oxygen to the brain

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7
Q

Skull fractures

A

Depression fracture- fracture of skull where fragment is depressed
Compound fracture- bone fracture that’s accompanied by breaks in skin, open wound
Temporal skull fracture- houses middle ear, inner ear, facial nerve, presence of bloody discharge from ear or ecchymosis (bruise) behind ear are signs

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8
Q

Hypertensive cerebral haemorrhage

A

Subarachnoid- bleed between arachnoid and pia mater increasing pressure inside skull
Intracerebral- bleeding into tissues of brain or its ventricles

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9
Q

Cerebral amyloid angiopathy and lobar haemorrhage

A

Amyloid- protein that’s deposited in liver, kidneys, spleen or other tissues in certain diseases
Angiopathy- disease of the blood vessels
Cerebral amyloid angiopathy- age related change in small vessels in brain, accumulation of amyloid, allow blood to leak out can lead to lobar haemorrhages
Lobar haemorrhage- bleeding into lobe of cerebrum, primary haemorrhage occur within either subcortical white matter or at junction of hemispheric grey-white matter

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10
Q

Arterio-venous malformations

A

Proliferation of dilated blood vessels where blood stagnates and doesn’t flow properly leading to bleeding into tissue

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11
Q

Aneurisms

A

Bulge that forms on thinning wall of an artery
Can have coagulated blood in it increasing pressure in CNS

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12
Q

Lacunar infarcts and white matter damage

A

Lacunes are small areas in the brain where poor blood flow has starved a group of cells of oxygen causing them to die
Tiny parts of tissue that died away
Stroke
Affecting pathways in white matter leading to specific function deficits
Typical in patients who suffer from vascular dementia or multiinfarcts dementia

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13
Q

Traumatic brain injury

A

Mechanical impact causes cerebral contusions (bruise brain tissue) and lacerations (Brain tissue is cut or torn)
Movement of the brain in the skull causes subdural hematoma (bleeding, collection of blood between inner layer of dura mater and arachnoid matter, tears in bridging veins) and diffuse axonal injury ( happens when brain rapidly shifts inside skull, axons sheared)
Consequences: hematomas (epidural and subdural) leads to compression of the brain, raised intracranial pressure.
Contusions and diffuse axonal injury- structural brain damage
Hypoxic injury, focal ischemic lesions
Multiple lesions and different types of lesions

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14
Q

Hypoxic injury, focal ischemic lesions

A

Deficient blood supply
As a consequence of the oedema and raised intracranial pressure, compression of blood vessels- decrease in oxygen supply

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15
Q

Anoxia

A

No oxygen

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16
Q

Difference between thrombosis and embolism

A

Thrombosis is the formation and presence of blood clot in any blood vessels
Embolism is the obstruction of a artery by a blood clot

17
Q

Energy crisis- demand outruns the supply

A

Drop in cerebral perfusion (blood flow in the brain) Global ischemia- cardiac arrest or severe hypotension (shock)
Hypoxia- CO poisoning
Hypoglycaemia
Severe anaemia can trigger energy crisis in brain
Generalised seizures

18
Q

Anoxic neurons

A

Differential sensitivity of different neuronal populations
-ischaemia lasting 4-5 minutes-irreversible damage:
Hippocampal and neocortical pyramidal cells
Striatal neurones
Purkinje cells- inhibitory neurons in cerebellum
-more protracted ischaemia- irreversible damage:
thalamic and brainstem neurones- need longer periods of ischaemia , less sensitive
In hypoxic patients there’s few pyramidal cells, loss shape

19
Q

Pseudolaminar and laminar necrosis

A

Death of cells in cortex of brain, layer 3 neocortex, clear band pattern
Affected by hypoxic events
Selective vulnerability of different neuronal populations

20
Q

The progressive changes following a cerebral infarct

A

1-2 days: tissue swelling, anoxic neurones, pyramidal cells lose shape
2 weeks: no neurones, tissue necrosis (cell death), lots of glial cells. Neovascularisation- proliferation of new blood vessels
2 months: glial scar, replaces dead neuronal tissue, large glial cells, no neurones

21
Q

Series of events in TBI

A

Neuronal death and tissue loss (partially due to direct impact and also the movement of brain in skull)
Blood brain barrier BBB breakdown and oedema- consequence of primary and secondary injuries, makes oedema worse perpetuating neuronal loss
Upregulation of inflammatory mediators- cytokines, as response to repair, inflammatory response.
Gliosis and cell infiltration- local proliferation of glial cells
However can make tissue damage worse in CNS: cytokines can be neurotoxic, substances released by glial cells prohibit regenerative attempts in CNS

22
Q

Consequence of CNS injury

A

Loss of cells and connections:
-functional deficit
- BBB breach
Response to injury:
-inflammatory response
-oedema
-gliosis
Reactive change of glial cells mainly astrocytes in response to damage of CNS. Proliferation or hypertrophy glial cells
Long term consequences:
-sequelae: pathological condition following injury
-repair: depends on how big original damage was and how much repair will happen in brain, regions affected

23
Q

Long term consequences of severe TBI

A

Seizures
Focal neurological deficits
Dementia
Persistent vegetative state
Increased risk of Alzheimer’s disease

24
Q

PNS: axonal regeneration present

A

Axonal injury— macrophage clear debris— no inhibitory molecules present, extending growth cone

25
Q

CNS: no axonal regeneration

A

Axonal injury— no macrophage to clear debris— myelin associated inhibitory molecules (Nogo, MAG, OGmp) and reactive astrocytes upregulate inhibitory extracellular matrix ECM molecules that inhibit regeneration

26
Q

Features of CNS injury

A

CNS axons intrinsic capacity for regeneration
Inhibitory environment:
-lack of neurotrophic stimulation
- neuronal death
-demyelination
-glial scar
-inhibitory molecules: associated with glial scar proteoglycans (CSPG), associated with damaged myelin (Nogo, MAG, OMgp). Prevent regenerative attempt
Neurotrophins are a family of proteins that induce development, function of neurones

27
Q

Treatment options for CNS injury

A

Surgery:
-remove hematoma
-repair skull fractures
-decompression: to decrease raised intracranial pressure, prevent hypoxia, prevent extension damage
Medication:
-anti seizure medication-reduce risk of seizures
-reduce oedema- diuretics (increase urine production in kidney, promoting removal salt and fluid in body)
-induced coma- reduce oxygen and nutrient requirements, prevent further damage due to high demand without appropriate supply
Rehabilitation

28
Q

Difference between hematoma and haemorrhage

A

Hematoma- accumulation of leaked blood inside body within tissue planes, localised bleeding
Haemorrhage- leaking of blood from blood vessels due to lack of integrity in the vessel wall

29
Q

Neurorehab

A

A process whereby patients who suffer from impairment following neurologic diseases regain their former abilities or, if full recovery is not possible, achieve their optimum physical, mental, social and vocational capacity

30
Q

Neurological and functional recovery

A

Neurological recovery:
-early recovery (local processes), due to rapid intervention of surgery or medication
-late recovery (Neuroplasticity) modification in structural and functional organisation. Ability of brain to form and reorganise synaptic connections, growing and evolving
Functional recovery:
-recovery in everyday function with adaptation to absence of certain functions and training in presence/absence of natural neurological recovery
-dependent on quality, intensity of therapy and patients motivation

31
Q

Neuronal plasticity signalling mechanisms involved

A

Neuronal activity increases neurotrophin synthesis, secretion and signalling
Increases postsynaptic responsiveness, synaptic morphology, presynaptic transmitter release, membrane excitability
Leading to modification of synaptic transmission and connectivity
Plasticity much quicker in development than in adult- remodelling of connections, rapid neuronal network over a long period of time ~90 days

32
Q

Neuroplasticity principles

A

Use it or lose it
Use it and improve
Specificity
Repetition matters
Intensity matters
Time matters
Salience matters- earlier process starts the better outcome for patient
Age matters- Neuroplasticity slows down as we age
Interference - plasticity on response to one training experience can impede acquisition of similar behaviours

33
Q

Experimental strategies for treatment of CNS injury

A

Trophic support: neurotrophic factors to neuronal cell bodies, that would support neuronal regeneration and survival
Inhibiting the inhibitors, changing environment: NOGO antibodies, digestion of GSPG-chondroitinase, Rho inhibitors (siRNA)
Endogenous stem cells: neurogenesis- subventricular zone, subgranular zone. Cells with neurogenic potential found in these zones. Get depleted over time with age
Cell therapy especially if local damage: replace dead cells, create favourable environment, bridge cyst cavities, autologous stem cells (Same individual)

34
Q

Multiple sclerosis MS

A

Affects CNS
Immune system attacks the myelin causes inflammation and lesions. Oligodendrocytes affected
Affect conduction of action potentials
Episodes, comes and goes. Affect different anatomical locations
Motor and sensory
Double vision and vertigo (loss of balance)
Ataxic- lack of coordinated movement
Brisk reflexes and planar reflexes were up going
Reduction in pinprick sensation, tingling and numbness on one side of body

35
Q

Guillian Barre syndrome

A

Rapid onset muscle weakness cause by immune system destroys myelin sheath of nerves in PNS
Has a preceding infection, immune response to infection starts generating antibodies that attack myelin
Motor and sensory
Numbness and tingling in limbs
LMN signs- muscle weakness, reduced tone and absent reflexes in all limbs
Plantar reflexes down going
Reduction in pinprick sensation over lower limbs
Symptoms often start in feet and hands before spreading to arms and legs

36
Q

Sensory peripheral neuropathy due to diabetes mellitus

A

Numbness and tingling
Sensory
Reduction in pinprick sensation in distal, extreme peripheries (stocking distribution)
Ankle jerks absent
Impairment of vibration and joint position sense- Proprioception
Sensory neurones affects first, smaller diameter

37
Q

Brown- Sequard syndrome

A

Caused by damage to one half of spinal cord
Numbness and tingling on one side right - sensory
Dragging leg on other side left - motor
Increased tone, brisk reflexes, up going plantar on left leg
Position and vibration sense are lost in left leg- sensory
Impairment of pin prick sensation and temperature over right leg up to level of umbilicus, sensory loss different to left
CNS reflexes- spinal cord
T10 level of umbilicus
UMN sign (cortiospinal) left leg, posterior column lost
Pain and temp (spinothalamic) right leg
Left sided T10 spinal cord
Ipsilateral weakness with loss of position and vibration sense
Contralateral loss of pain and temp

38
Q

What is the major reason why CNS neuronal axons do not regenerate after axonal transection

A

Inhibitory molecules are expressed and up-regulated on glial cells

NAS (12 decks)

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