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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
classifications of seizures
``` 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
whats the most common type of epilepsy
temporal lobe
27
tests/ diagnosis of epilepsy
a thorough history - often including an eyewitness MRI EEG
28
paroxysmal LOV "blackouts"
- Syncope (heart event) vs primary brain event (eg seizure) - Pallor, posture, precipitants - ECG, BP, echocardiograms
29
epilepsy treatment
-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
epilepsy surgery
 For temporal lobe epilepsy this is 80% effective  For non TLE ~50%  1% risk of stroke or death  Neuro deficits – depends on location
31
periaqueductal grey (PAG)
- 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
the connection between the pre-frontal cortex and the amygdala
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
peripheral pain - source and treatment
- 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
central pain - source and treatment
- 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
other types of pain
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
general anaesthetic stages
- 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
mechnisn of local anaesthetics
- 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
focal vs diffuse lesions in TBI
``` - 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
acute contusions in TBI
- Bruises on surface of brain - Bleeding - Mostly seen in frontal and temporal region
40
types of intracranial haemorrhages
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
tentorial hernia
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
diffuse axonal injury
- Widespread axonal damage – rotational injury to the brain - No requirement for blunt force impact - Involves corpus collusum, internal capsule, cerebellar peduncles
43
why low grade brain tumours aren't necessarily curable
Local invasion, angiogenesis, anatomical location
44
common brain tumour types
- Metastatic tumours - Gliomas (astrocytes including glioblastoma, oligodendrogliomas) - meningiomas - in children -> medulloblastoma
45
the UPS disorders
- 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
cornea problems
``` • Inflammatory (keratitis) – infective/non-infective • Degenerations – corneal dystrophies (epithelium, stroma, endothelium) • Neoplasms – very rare; epithelial/ melanocytic ```
47
iris, ciliary body and choroid problems
``` • Inflammatory (uveitis) – often non-infective (RA, Behcets) • Neoplasms – melanocytic – soft tissue ```
48
retina problems
``` • 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
orbital lesions
• Inflammatory • Neoplastic – soft tissue; rhabdomyosarcoma, osteosarcoma – lymphoid

year 2 sem 1 (13 decks)

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