Brainscape's Knowledge GenomeTM

Browse over 1 million classes created by top students, professors, publishers, and experts.


See full index

Year 2 - Semester 1 > Neuro- week 6 > Flashcards

Neuro- week 6 Flashcards

1
Q

what does the lateral spinothalamic tract do

A

pain/temperature

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
2
Q

what does the anterior spinothalamic tract do

A

crude touch/pressure

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
3
Q

how do you test sensation at the bedside

A
  • Vibration – tuning fork
  • Proprioception – joint position sense
  • Pain – neuro tip
  • Light touch – cotton wool piece rolled to a point
How well did you know this?
1
Not at all
2
3
4
5
Perfectly
4
Q

describe spinothalamic fibres

A

pain/temperature/crude touch

reticular activating system
          -  spinoreticular fibres
          -  85% of fibres
          - terminate in the brainstem
          - important in arousal
          -  first output of the spinothalamic system 
              pathways

superior colliculi

   - spinotectal fibres
   - orientating response

hypothalamus

  - spinohypothalamic fibres
  - important in autonomic response - fight or flight

thalamus –> insula –> anterior cingulate cortex –> cerebral cortex
- interoceptive cognitive model

parabrachium, amygdala
-emotional response

thalamus, S1, S2 (primary and secondary somatosensory cortex)
- localisation

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
5
Q

periaqueductal grey

A

the volume knob
• 5-HT release
• Travels downwards in CSF and triggers endogenous opioid release in dorsal horn spinal cord interneurons
• Endogenous opioids reduce incoming pain pathway activity via opioid receptors (mu, kappa, delta)

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
6
Q

sources of pain

A 
•	Peripheral pain
       o	Tissue damage, typically acute
       o	Inflammatory cascade mediators (prostanoids, 
                arachidonic acid)
       o	Treat with analgesic ladder
               	Simple analgesia – paracetamol
               	NSAIDs and aspirin
               	Opioids

• Central pain
o Chronic pain (neurogenic) – centralisation
 Drugs
• Neuropathic pain agents - gabapentin
• Anticonvulsants/ TCAs
• SSRIs
• Opioids
 Other treatments
• CBT
• Mindfulness/meditation
• Yoga/physical therapy

o Psychic pain
 Psychological therapies

o Spiritual pain
 Maybe something they’ve done or has been
done to them

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
7
Q

define seizure

A

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

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
8
Q

define epilepsy

A

epilepsy is the tendency to recurrent spontaneous seizures – a single seizure is not epilepsy

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
9
Q

what is the prevalence of epilepsy

A

Single seizure (lifetime risk) – 9%
Prevalence of epilepsy
• Under 20 – 1%
• Lifetime – 3%

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
10
Q

what are some provoking factors for epilepsy

A 
Hypoglycaemia
Electrolyte imbalance
Acute head injury
Drug abuse
Alcohol withdrawal
How well did you know this?
1
Not at all
2
3
4
5
Perfectly
11
Q

what are morbidities for epilepsy

A
  • Injuries
  • Side effects of drugs
  • Aspiration
  • Cognitive decline

Psychiatric morbidity

  • Depression
  • Psychosis

Social Morbidity

  • Employment
  • Driving
  • Embarrassment/ reduced confidence
  • Social prejudice
How well did you know this?
1
Not at all
2
3
4
5
Perfectly
12
Q

what is the mortality for epilepsy

A

Mortality overall is over twice that of the normal population
Different for different types of epilepsy

Mortality may be:

  • Seizure related
    - Status epilepticus/ burns/ drowning/ injury
    - SUDEP
  • Other
    - Chest infection/ aspiration
    - Suicide
How well did you know this?
1
Not at all
2
3
4
5
Perfectly
13
Q

what are the types of epilepsy

A

focal onset
either:

  • aware
  • impaired awareness
  • motor onset
  • non-motor onset

can progress to focal to bilateral tonic-clonic

generalised onset

can be motor

           - tonic clonic
           - other motor

or non motor
- absence seizures

unknown onset
can be motor
- tonic clonic
- other motor

or non - motor or unclassified

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
14
Q

whats important to get in a seizure history

A

two stories from the patient and an eyewitness

semiology

  • warning “aura”
  • event (ictus)
  • post event (recovery phase)

trigger - was this a provoked event

risk factors

  • family history (FHx)
  • birth
  • febrile convulsions
  • significant head injury
  • encephalitis/ meningitis
How well did you know this?
1
Not at all
2
3
4
5
Perfectly
15
Q

what are some tests for epilepsy

A

no test for epilepsy

we test for cause of seizure and classification

brain imaging - CT and MRI

EEG - for classification

for paroxysmal loss of consciousness

- was it syncope? - loss of fuel 
      - pale?  - pallor 
      - posture  - were they stood up?
      - precipitant - sweating?  - emotion or pain
      - ECG, BP monitoring, echocardiogram

-  or a primary brain event
How well did you know this?
1
Not at all
2
3
4
5
Perfectly
16
Q

how are focal symptomatic epilepsies usually described

A

by their lobe of onset

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
17
Q

what are some examples of generalised idiopathic (presumed genetic) epilepsies

A

childhood absence epilepsy

juvenile myoclonic epilepsy

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
18
Q

describe treatment for epilepsy

A 
Drugs
70% response rate with 1 AED (antiepileptic)
80& response rate with 2 AEDs
85% response rate with 3 AEDs
15% “medically refractory”

Consider suitability for epilepsy surgery
• TLE (temporal lobe epilepsy) :- 80% seizure free
• Non TLE:- 50% seizure free
• 1% risk of stroke or death
• Neuro deficits – depends on location

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
19
Q

what is gliosis

A

Astrocytes hypertrophy and increase GFAP (Glial fibrillary acidic protein) immunoreactivity in response to both acute and chronic insults. Gliotic tissue is firm and appears grey.

can stain for GFAP which is brown

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
20
Q

what are the three components in the skull and what happens if there is an increase in one of them

A

the brain, the CSF and blood.

Any increase in volume of one of these 3 components will produce an increase in ICP, unless a compensatory reduction in one of the other components occurs. This only happens for a while until the patient becomes very unwell

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
21
Q

what are common causes of ICP

A
  • Intracranial expanding lesions – tumour, haematoma, abscess
  • Hydrocephalus
  • Cerebral oedema – an increase in the water content of the brain, due to dysfunction of the blood-brain barrier. This can be localised (eg around tumours) or generalised(eg following severe head injury or in hypoxic brain damage)
22
Q

what is the cerebral flow for humans

A

– Overall- 50 ml/100g per minute
– Grey matter- >80 ml/100g per minute
– White matter- 20-25ml/100g per minute

The cerebral metabolic rate is higher for infants (and also in other species with small brains)

23
Q

what are the two types of stroke

A

thrombo-embolic or haemorrhagic

24
Q

what can develop in hypotension

A

watershed infarcts

25
Q

what can cardiac arrest lead to

A

global brain injury (hypoxic-ischaemic encephalopathy HIE)

26
Q

what are some causes of brain haemorrage

A
  • Hypertension
  • Vascular malformation
  • Neoplasia
  • Trauma
  • Cerebral amyloid angiopathy
  • Iatrogenic, other blood dyscrasias
27
Q

how are parts of the brain damaged by a lack of blood flow and what is most affected

A

When there is lack of blood flow to the brain due to heart failure, there is no oxygen and lactic acid builds up around neurons. There is selective vulnerability to this but over 20-30 mins there is global irreversible damage.

  • Hippocampus- sector CA1 is most vulnerable, sector CA2 least so.
  • Cerebral cortex- neurones of layers 3, 5 and 6 are most vulnerable. Damage is most pronounced within the depths of sulci and posteriorly within the cerebral hemispheres (triple watershed zone).
  • Basal ganglia (including thalamus)- variable.
  • Cerebellum- Purkinje cells.
  • Brainstem- Brainstem nuclei tend to be relatively preserved in adults, but when they are affected sensory nuclei are more susceptible than motor nuclei.
28
Q

what happens under the microscope to damaged neurons

A

show red cell change - cytoplasm becomes red

29
Q

what causes sub-arachnoid haemorrhage

A

Usually due to ruptured aneurysms but can be due to trauma

30
Q

what are some microorganisms which can attack the NS

A

• Viruses
o eg herpes, CMV, measles, rabies, HIV
• Bacteria
o eg meningococcus, listeria, m. tuberculosis
• Protozoa
o eg amoeba, toxoplasma, pl. falciparum (malaria)
• Metazoa
o eg echinococcus (hydatid cyst)
• Fungi
o eg aspergillus, candida, crytococcus
• Prions

31
Q

what are some foetal infections of the CNS

A
  • Rubella (deafness, blindness, microcephaly)
  • CMV (microcephaly)
  • Toxoplasma (microcephaly)
  • Syphilis (tertiary forms include GPI, tabes dorsalis and meningovascular syphilis)
  • (HIV)
32
Q

what can cause meningitis

A

• Bacteria
– Infants: Group B Streptococcus, E. coli, Listeria
– 0-4yrs: Haem. influenzae, Strep. pneumoniae,
Myco. tuberculosis (in high prevalence countries)
– 0-25 yrs: Neiss. meningitidis
– Older adults: Myco. tuberculosis (in low
prevalence countries)
– IV drug abuse: Staph. aureus

• Viruses
– Children: Enteroviruses (Coxsackie, Echo)
– Adults: Herpes viruses, Mumps

• Immunosuppressed
– Cytomegalovirus, cryptococcus

33
Q

what causes viral infections of the NS

A

• Meningitis
– eg echoviruses, coxsackie, herpes simplex, mumps

• Acute encephalitis
– eg herpes simplex, CMV, varicella zoster virus,
rabies (rubella in fetus)

• Subacute encephalitis
– HIV

• Demyelination
– JC virus (progressive multifocal
leucoencephalopathy)

• Delayed, reactivated
– Varicella zoster virus

34
Q

what are some types of prion infection

A

• Perplexing transmissible and genetic disease of
the CNS

–	Sporadic CJD
–	Familial CJD and GSS
–	Iatrogenic CJD  (infective)
–	Variant CJD (infective)
–	Kuru
35
Q

what are some neurogenic muscle diseases

A
  • Disorders of motor neurones, e.g. motor neurone disease, spinal muscular atrophy
  • Disorders of spinal motor nerve roots, e.g. disc prolapse
  • Disorders of motor nerves - peripheral neuropathies
36
Q

what are some myopathic muscle diseases

A
  • Inflammatory myopathies
  • Muscular dystrophies
  • Metabolic myopathies
  • Endocrine myopathies
  • Toxic and drug-related myopathies
  • Mitochondrial myopathies
  • Ion channel myopathies
  • Congenital myopathies
37
Q

what are some muscular dystrophies

A
  • These are genetically determined destructive myopathies.
  • They are usually progressive.
  • Duchenne Muscular Dystrophy
  • Becker Muscular Dystrophy
  • Others
    * limb-girdle muscular dystrophies
    * congenital muscular dystrophies
    * Emery-Dreifus muscular dystrophy
    * myotonic dystrophy
38
Q

describe nerve structure

A
  • Nerve trunks composed of a variable number of nerve fascicles surrounded by the epineurium
  • Individual fascicles surrounded by perineurium
  • Connective tissue within fascicles is the endoneurium - innermost
  • Intrafascicular; axons surrounded by schwann cells. Capillaries also present
  • Perineurium; flattened perineurial cells connected by tight junctions and forming concentric layers separated by collagen
  • Epineurium; collagenous tissue with some adipose and elastic tissue. Larger vessels found in the epineurium
39
Q

describe peripheral nerve disorders

A

• Trauma

• Tumour- mostly benign (schwannoma,
neurofibroma) but may be malignant (MPNST)

• Acquired neuropathies
– Nutritional- diabetes
– Neurotoxins- alcohol, drugs, industrial
chemicals
– Inflammatory- Guillain Barre syndrome
– Infective- leprosy
– systemic disorders- vasculitis, amyloidosis

• Hereditary neuropathies
– CMT(Charcot-Marie-Tooth)
– Others

40
Q

what are some types of head trauma

A 
Focal lesions
•	scalp lacerations
•	skull fractures
•	contusions
•	intracranial haemorrhages
•	lesions secondary to raised intracranial pressure

Diffuse lesions
• Global ischaemia
• Brain swelling
• Traumatic axonal injury

Tends to happen in children (toddlers and early teenage) and especially the elderly (falls)

Road traffic accidents, falls and assaults are the main causes

41
Q

what are the mechanisms of head injury

A

• Direct contact
o Object striking head/ being struck by head
• acceleration/deceleration
o unrestricted movement of the head
• Penetrating
• Blast

42
Q

describe intracranial haemorrhages

A

• Extradural
o usually associated with squamous temporal bone fractures damaging the underlying middle meningeal artery
o will strip dura away from the skull

• Subdural
o extensive, associated with cortical contusions and torn bridging veins

• Subarachnoid
o rarely extensive, usually associated with contusions

• Intracerebral
o superficial associated with contusions
o deeply seated often within the basal ganglia – often in high velocity accidents

43
Q

describe diffuse traumatic axonal injury

A

• rotational injury – no blunt force trauma needed
• damage to axons as the name suggests
• corpus callosum, internal capsule and cerebellar peduncles
• DIA can be detected by a T2* image – black dots are haemorrhage
o Susceptibility weighted image can also be used
• Macro we can see haemorrhage into the corpus callosum and pons
• Leads to unconsciousness and often coma

44
Q

what is important to remember in penetrating head injury

A

bullets produce a blast wave which can damage beyond the missile

45
Q

describe head tumours

A 
•	X-irradiation; meningiomas / sarcomas / gliomas associated with previous therapeutic irradiation (20-30 year delay).
•	Occupational exposure to herbicides?
•	Electrical and magnetic fields?
•	Oncogenic virus SV40 (introduced via polio)?
•	Hereditary tumour syndromes
o	NF; meningiomas, schwannomas, gliomas
o	VHL; haemangioblastomas
o	Tuberous sclerosis; SEGA
o	Li Fraumeni; gliomas, medulloblastomas

Things like tumours in the pons or thalamus are inoperable because of the location

Local invasion along white matter tracts also makes resection of even low grade tumours very difficult

46
Q

what are some common head tumours

A
  • Metastatic tumours
  • Gliomas (astrocytomas including glioblastoma, oligodendrogliomas etc)
  • Meningiomas
  • In children, medulloblastoma – posterior fossa of cerebellum – most common solid tumour of childhood
47
Q

what are some degenerative disorders

A
  • Tauopathies
  • Synucleinopathies
  • Trinucleotide repeat disorders
  • TDP43 proteinopathy
  • Prion disorders
  • Motor neurone disorders
  • Others

Abnormal proteins are usually ubiquitinated (ubiquitin attaches to them) and then broken down by proteosomes but in neurodegeneration this system cant keep up

48
Q

describe parkinsonism and some causes other than standard

A

Parkinson’s disease
• Commonest of the movement disorders
• Due to loss of dopaminergic neurones in substantia nigra
• Characterised by Lewy bodies

Other causes of parkinsonism
•	Multiple system atrophy
•	progressive supranuclear palsy
•	Iatrogenic (anti-psychotics)
•	vascular
•	drug induced
49
Q

what are some lesions of the cornea

A

• Inflammatory (keratitis)
– infective/non-infective

• Degenerations
– corneal dystrophies (epithelium, stroma,
endothelium)

• Neoplasms
very rare; epithelial/ melanocytic

50
Q

what are some lesions of the retina

A

• Inflammatory
– CMV, HSV, toxoplasma

• Degenerative
– retinitis pigmentosa etc.

• Neoplastic
– retinoblastoma
– lymphoid
– glial

51
Q

what are some lesions of the orbit

A

• Inflammatory

• Neoplastic
– soft tissue; rhabdomyosarcoma, osteosarcoma
– lymphoid

52
Q

what are some lesions of the iris, ciliary body and choroid

A

• Inflammatory (uveitis)
– often non-infective (RA, Behcets)

• Neoplasms
– Melanocytic
– soft tissue

Year 2 - Semester 1 (13 decks)

Brainscape helps you reach your goals faster, through stronger study habits.
© 2024 Bold Learning Solutions. Terms and Conditions