wk 6 neurology Flashcards
gliosis
- 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
common causes of raised ICP
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
acute thromboembolic infarct
- 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
long term consequences of middle cerebral artery occlusion
- Large part of middle cerebral artery territory has disappeared on left
- Liquefactive necrosis then macrophages mop up debris
- Ventricle has expanded to fill space
borderzone/ waterline infarct
- Consequence of hypotension
- Infarcts that develop at interface between anterior, middle and posterior cerebral artery territories
selective vulnerability
- 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
areas at risk during lack of blood flow
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)
extensive trauma induced subarachnoid haemmorhage
- Due to hyperextension of the neck
- Vertebral artery tearing
- = massive subarachnoid haemorrhage
fetal infections of the CNS
- Rubella
- CMV
- Toxoplasma
- Syphilis
- HIV
organisms causing meningitis
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
pathology of meningitis
pus lies within subarachnoid space
herpes simplex encephalitis
- 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
rabies
- 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
malaria effect on brain
Malaria caused by plasmodium infection
Most severe is plasmodium falciparum
Can give rise cerebral malaria
Acute brain swelling and widespread haemorrhage
fungal infections effect on brain
Fungal infections
Rare
Seen in neonatal, infants, immunosuppressed
Cause purulent meningitis
Or abscess
Caused mainly by – candida, aspergillus, cryptococcus
prion infection effect on brain
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
2 different types of neuromuscular disorders
neurogenic
myopathies
muscular dystrophies
- genetically determined destructive myopathies
- usually progressive
- all proteins in muscle can be defective and cause dystrophy
- eg abnormalities of dystrophin cause dystrophinopathies…
types of dystrophinopathies
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
myelinating cells in PNS vs CNS
1 schwann cell will myelinated one axon in the PNS
1 oligodendrocyte can myelinate many axons in the CNS
tumours of peripheral nerves
- 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
definition of a seizure
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
definition of epilepsy
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
causes of seizures
- Hypoglycaemia
- Electrolyte imbalance
- Acute head injury
- Drug abuse
- Alcohol withdrawal
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
whats the most common type of epilepsy
temporal lobe
tests/ diagnosis of epilepsy
a thorough history
- often including an eyewitness
MRI
EEG
paroxysmal LOV “blackouts”
- Syncope (heart event) vs primary brain event (eg seizure)
- Pallor, posture, precipitants
- ECG, BP, echocardiograms
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
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
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
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
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
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
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
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
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
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
acute contusions in TBI
- Bruises on surface of brain
- Bleeding
- Mostly seen in frontal and temporal region
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
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
diffuse axonal injury
- Widespread axonal damage – rotational injury to the brain
- No requirement for blunt force impact
- Involves corpus collusum, internal capsule, cerebellar peduncles
why low grade brain tumours aren’t necessarily curable
Local invasion, angiogenesis, anatomical location
common brain tumour types
- Metastatic tumours
- Gliomas (astrocytes including glioblastoma, oligodendrogliomas)
- meningiomas
- in children -> medulloblastoma
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
cornea problems
• Inflammatory (keratitis) – infective/non-infective • Degenerations – corneal dystrophies (epithelium, stroma, endothelium) • Neoplasms – very rare; epithelial/ melanocytic
iris, ciliary body and choroid problems
• Inflammatory (uveitis) – often non-infective (RA, Behcets) • Neoplasms – melanocytic – soft tissue
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
orbital lesions
• Inflammatory
• Neoplastic
– soft tissue; rhabdomyosarcoma, osteosarcoma
– lymphoid
