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year 2 sem 1 > wk 6 neurology > Flashcards

wk 6 neurology Flashcards

1
Q

gliosis

A
  • common in brain
  • glial cell hypertrophy and increase GFAP immunoreactivity in response to both acute and chronic insults
  • gliotic tissue is firm and appears grey
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2
Q

common causes of raised ICP

A

o Intracranial lesions – tumours, haematoma, abscess
o Hydrocephalus
o Cerebral oedema
 Inc. in water content of brain, due to dysfunction of BBB
 Can be localised (eg around tumour) or generalised (eg following severe head injury or hypoxic brain damage

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3
Q

acute thromboembolic infarct

A
  • Tissue swollen as BBB breakdown – localised oedema
  • Raised ICP
  • Above corpus callosum – the cingulate gyrus is pushing to opposite side (under the faults)
    o Called subfalcine herniation
  • Small areas of haemorrhage at bottom due to axial displacement
  • Axial displacement is when diencephalic structures are pushed down due to brain swelling
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4
Q

long term consequences of middle cerebral artery occlusion

A
  • Large part of middle cerebral artery territory has disappeared on left
  • Liquefactive necrosis then macrophages mop up debris
  • Ventricle has expanded to fill space
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5
Q

borderzone/ waterline infarct

A
  • Consequence of hypotension

- Infarcts that develop at interface between anterior, middle and posterior cerebral artery territories

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6
Q

selective vulnerability

A
  • Cardiac arrest – complete cessation of blood to brain
  • After several mins start to see irreversible neuronal damage due to lack of oxygen and glucose
  • Also build-up of lactic acid around neurones as blood not there to remove it form perineuronal environment
  • Not all neurones act the same way to lack of blood flow
    o Some areas more at risk than others
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7
Q

areas at risk during lack of blood flow

A

o Hippocampus CA1 most vulnerable and CA2 least
o In cerebral cortex neurone layers 3, 5 and 6 are most vulnerable
 Basal ganglia(including thalamus), cerebellum, brainstem (sensory > motor)

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8
Q

extensive trauma induced subarachnoid haemmorhage

A
  • Due to hyperextension of the neck
  • Vertebral artery tearing
  • = massive subarachnoid haemorrhage
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9
Q

fetal infections of the CNS

A
  • Rubella
  • CMV
  • Toxoplasma
  • Syphilis
  • HIV
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10
Q

organisms causing meningitis

A

In infants usually – group B strep, e. coli, listeria
Older – haemophilus influenzae, strep. Pneumonias, myco. TB
All age groups – mycobacterium TB
IV drug use – staph. Aureus important
Virus meningitis less serious

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11
Q

pathology of meningitis

A

pus lies within subarachnoid space

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12
Q

herpes simplex encephalitis

A
  • Used to have high mortality
  • Aciclovir introduction – reduce mortality
  • Early intervention important to stop complications
  • Signif. Necrotising damage at bottom of brain
    o Medial temporal lobes and hippocampus
  • Survivors often have memory problems
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13
Q

rabies

A
  • Transmitted by bite from a rabid dog or bat etc
  • Virus crawls up CNS to enter CNS
  • Treatment possible when its in PNS
  • But fatal once enters CNS

NEGRI BODIES FORM IN NEURONES

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14
Q

malaria effect on brain

A

Malaria caused by plasmodium infection
Most severe is plasmodium falciparum
Can give rise cerebral malaria
Acute brain swelling and widespread haemorrhage

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15
Q

fungal infections effect on brain

A

Fungal infections
Rare
Seen in neonatal, infants, immunosuppressed
Cause purulent meningitis
Or abscess
Caused mainly by – candida, aspergillus, cryptococcus

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16
Q

prion infection effect on brain

A

Prion infection
Rare
Perplexing transmissible and genetic disease of CNS
Can be transmissible without possessing DNA or RNA
Gives rise to CJD (Creutzfeldt–Jakob disease), can be…
-Sporadic, familial, iatrogenic, variant, kuru

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17
Q

2 different types of neuromuscular disorders

A

neurogenic

myopathies

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18
Q

muscular dystrophies

A
  • genetically determined destructive myopathies
  • usually progressive
  • all proteins in muscle can be defective and cause dystrophy
  • eg abnormalities of dystrophin cause dystrophinopathies…
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19
Q

types of dystrophinopathies

A

o Duchenne muscular dystrophy
 Progressive muscle weakness leading to death in teenage years
o Becker Muscular Dystrophies
 Partial expression of dystrophin protein
 Presents at later age – early 20s or so
o Congenital muscular dystrophy– present at young age
o Limb-girdle muscular dystrophy – at old age

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20
Q

myelinating cells in PNS vs CNS

A

1 schwann cell will myelinated one axon in the PNS

1 oligodendrocyte can myelinate many axons in the CNS

21
Q

tumours of peripheral nerves

A
  • Tumour – mostly benign (eg schwannoma, neurofibroma) but may be malignant
    o Schwannoma – develop at periphery of nerve and push nerve to one side
    o Neurofibroma – intrinsic to nerve so expand nerve from inside out
    o These 2 can become malignant peripheral nerve sheath tumour
     Particularly in setting of neurofibril mitosis
22
Q

definition of a seizure

A

The manifestation of abnormal paroxysmal neuronal discharges in part(s) of the brain

  • Abnormal excess of firing of brain cells
  • neurones all firing off at same time, in same phase – coordination of this
  • failure of brain function – seizure is manifestation of this
  • part or all of the brain going into synchronise firing
23
Q

definition of epilepsy

A

tendency to recurrent spontaneous seizures

  • The thing that differs between us – how difficult it is to provoke a seizure
  • A single seizure is not epilepsy
24
Q

causes of seizures

A
  • Hypoglycaemia
  • Electrolyte imbalance
  • Acute head injury
  • Drug abuse
  • Alcohol withdrawal
25
Q

classifications of seizures

A 
Focal Onset / partial seizure
occurs in one area
- aware OR impaired awareness
- motor onset OR non-motor onset
- may progress to - focal OR bilateral tonic-clonic
Generalised Onset
both sides of brain
- Motor
o	Tonic clonic or other motor
- Non-motor
o	Absence of seizure

Unknown Onset
- Motor
o Tonic clonic or other motor
- unclassified

26
Q

whats the most common type of epilepsy

A

temporal lobe

27
Q

tests/ diagnosis of epilepsy

A

a thorough history
- often including an eyewitness

MRI
EEG

28
Q

paroxysmal LOV “blackouts”

A
  • Syncope (heart event) vs primary brain event (eg seizure)
  • Pallor, posture, precipitants
  • ECG, BP, echocardiograms
29
Q

epilepsy treatment

A

-Many of drugs used in epilepsy are used for pain and vice versa
o 70% response rate with 1 AED (anticonvulsant drugs)
o 80% response rate with 2 AED
o 85% response rate with 3 AED
-15% “medically refractory” epilepsy
o Focal epilepsy
o This is usually due to a structural lesion causing specific part of brain to be irritable

30
Q

epilepsy surgery

A

 For temporal lobe epilepsy this is 80% effective
 For non TLE ~50%
 1% risk of stroke or death
 Neuro deficits – depends on location

31
Q

periaqueductal grey (PAG)

A
  • Volume nob of how much info is coming into the CNS
  • Cells in PAG release 5-HT (serotonin)
  • Built around cerebral aqueduct (feature not a problem)
  • 5-HT has to diffuse in the CSF downwards to the spinal cord
    o Here it interacts with dorsal horn spinal cord interneuron
    o These are triggered to release endogenous opioids
    o These opioids then reduce incoming pain via opioid receptors
    o This can be utilised clinically with opioid drugs
32
Q

the connection between the pre-frontal cortex and the amygdala

A

Both of these can adjust the volume of the periaqueductal grey

  • Prefrontal cortex trying to model whether the pain is worthwhile in a given cortex
  • Amygdala says pain is just bad move in opposite direction
33
Q

peripheral pain - source and treatment

A
  • Typically, acute pain
  • Tissue damage
  • Treat the fundamental cause if you can
  • Triggered by inflammatory cascade mediators (proteinoids, arachidonic acid)
  • Treat with ‘analgesia ladder’
    o ‘simple analgesia’ – paracetamol
    o NSAIDs and aspirin
    o Opioids
34
Q

central pain - source and treatment

A
  • Chronic pain
  • Neurogenic
  • Centralisation
  • Periaqueductal pain has been turned right up leading to constant pain
  • Treat with…
    o Neuropathic pain agents
     Anticonvulsants/ TCAs
     SSRIs
     Opioids
    o Top down influenced treatment
     CBT (cognitive behavioural therapy)
     Mindfulness/ Mediation
     Yoga, physical therapy
35
Q

other types of pain

A

psychic pain

  • eg grief
  • treat with CBT, therapy

Spiritual pain
- the pain you feel when you feel like you’ve been subject to moral wronging or that you’ve done something morally wrong

36
Q

general anaesthetic stages

A
  • induction
  • excitement - depression of inhibitory movement in CNS
  • surgical anaesthesia - gradual loss of muscle tone and reflexes
  • medullary paralysis/ overdose - resp. and cardio failure
37
Q

mechnisn of local anaesthetics

A
  • Loss of sensory/ pain perception without inducing unconsciousness
  • Pass through neuronal membrane and bind to receptor at sodium gated channel
  • Stops sodium influx – stops initiation and conduction of AP
  • Leads to loss of sensory in area nerve supplies
    Some examples are…
  • Bupivacaine, lidocaine, procaine, mepivacaine, ropivacaine, tetrevacaine
38
Q

focal vs diffuse lesions in TBI

A 
-	Focal lesions
o	Scalp lacerations
o	Skull fractures
o	Contusions (bruising)
o	Intracranial haemorrhages
o	Lesions secondary to raised intracranial pressure
-	Diffuse lesions
o	Global ischaemia
o	Brain swelling
o	Traumatic axonal injury
39
Q

acute contusions in TBI

A
  • Bruises on surface of brain
  • Bleeding
  • Mostly seen in frontal and temporal region
40
Q

types of intracranial haemorrhages

A

Extradural
- Usually associated with squamous temporal bone fractures damaging the underlying middle meningeal artery
Subdural
- Extensive, associated with cortical contusions and torn bridging veins
Subarachnoid
- Rarely extensive, usually associated with contusions
Intracerebral
- Superficial associated with contusions
- Deeply seated often within the basal ganglia

41
Q

tentorial hernia

A

as a result of occupying space lesion
when the cerebrum swells downwards towards cerebellum
- Damage to ocular motor nerve -> fixed dilated pupil
- Damage to post. Cerebral artery -> medial occipital cortical infarction

42
Q

diffuse axonal injury

A
  • Widespread axonal damage – rotational injury to the brain
  • No requirement for blunt force impact
  • Involves corpus collusum, internal capsule, cerebellar peduncles
43
Q

why low grade brain tumours aren’t necessarily curable

A

Local invasion, angiogenesis, anatomical location

44
Q

common brain tumour types

A
  • Metastatic tumours
  • Gliomas (astrocytes including glioblastoma, oligodendrogliomas)
  • meningiomas
  • in children -> medulloblastoma
45
Q

the UPS disorders

A
  • Ubiquitin proteasome systems
  • Used for handling dysfunctional proteins
  • These bad proteins are ubiquitinated and digested by proteasome
  • In disorders of this system these bad proteins accumulate
  • This damages function of nerve cells
46
Q

cornea problems

A 
•	Inflammatory (keratitis)
–	infective/non-infective
•	Degenerations
–	corneal dystrophies (epithelium, stroma, endothelium)
•	Neoplasms
–	very rare; epithelial/ melanocytic
47
Q

iris, ciliary body and choroid problems

A 
•	Inflammatory (uveitis)
–	often non-infective (RA, Behcets)
•	Neoplasms
–	melanocytic
–	soft tissue
48
Q

retina problems

A 
•	Inflammatory
–	CMV, HSV, toxoplasma
•	Degenerative
–	retinitis pigmentosa etc.
•	Neoplastic
–	retinoblastoma (seen in children due to flash of cameras - eyes are white not red)
–	lymphoid
49
Q

orbital lesions

A

• Inflammatory
• Neoplastic
– soft tissue; rhabdomyosarcoma, osteosarcoma
– lymphoid

year 2 sem 1 (13 decks)

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