brain disease 2 Flashcards

1
Q

epilepsy means

A

‘to seize’ having repeated seizures

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2
Q

seizure

A

abnormal, transient highly synchronous brain activity

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3
Q

types

A

partial/focal (simple and complex)

generalised

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4
Q

incidence

A

prevalence of active epilepsy about 0.5-1%

5% will expereince a non febrile seizure

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5
Q

childhood absence epilepsy

A

4-12 years

absence of seizures/ petit mal (10-30 sec episodes of unresponsivity sometimes eye rolling, lip smacking, hand shaking, several hundred per day)
characteristics 3 Hz spike-wave discharge
mutations in low threshold voltage-dependent Ca channels
resolves with pathology during puberty

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6
Q

temporal lobe epilepsy

A

late childhood and adolescence
most common epilepsy of adults
epileptogenic focus in hippocampus and or amygdala and or parahippocampal gyrus (recurrent excitatory circuits)
complex partial seizures often preceded by aura
may develop into secondary generalised tonic-clonic /grand mal seizure

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7
Q

causes of epilepsy

A
  • over 2/3 idiopathic in nature
  • reflex seizures, precipitated by a trigger e.g. flashing light…
  • genetic - mutations in Na channels
  • cerebrovascular disease
  • tumours
  • alcohol/drugs
  • trauma/hypoxia
  • infection
  • metabolic disorder
  • developmental disorders
  • degenerative disorder
  • pathological synaptic plasticity (kindling)

PRODUCING AN IMBALANCE IN EXCITATION AND INHIBITION IN THE NERVOUS SYSTEM

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8
Q

treatments acute

A
  • generalised or complex partial - recovery position
  • simple partial- reassurance, maintain safe environment
  • benzodizepenes
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9
Q

treatment for chronic

A
  • pharmacological e.g. ethosuximide (blocks/modulate Ca and Na channels) and carbamazepine (modulates Na channels potentiates GABA receptors)
  • surgical e.g. remove tumour, arteriovenous malformation or epileptogenic tissue (temporal lobe, hippocampus)
  • electrical e.g. vagal, depp brain stimulation
  • avoidance of seizure triggers
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10
Q

Sz incidnence

A

about 0.6% population worldwide

peak onset early 20s

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11
Q

Sz pathology

A

increased levels of dopamine in the mesolimbic pathway

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12
Q

negative symptoms of Sz

A

flat affect, alogia, anhedonia, asociality, avolition

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13
Q

causes of Sz

A

genetics: 50% concordence in mono zy twins - DISC-1
env: 50% in mono az twins
developmental: infection in utero, poor diet, asphyxia
social facotrs: env, stressful relationship
drug abuse: cannabis/cocaine cause or effecT?
dopamine hypothesis excessive D2R stimulation
redcued NMDAR function

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14
Q

mice with reduced expression of NMDARs exhibit

A

excessive motor activity
stereotypy
deficits in social and sexual interactions
symptoms that are ameliorated by typical and atypical antipsychotics

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15
Q

pathology depression

A

reduced hippocampal volume
vascular lesions
reduced BDNF

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16
Q

incidence of depression

A

3% japan
18% USA
average 10%
women 2x men

17
Q

stroke definition

A

neurological deficit of cerebrovascular cause that persists

beyond 24 hours or is interrupted by death within 24 hours”

18
Q

difference between stroke and transient ischameic attach

A

the latter is a syndrome with of stroke like symptoms that resolve within 24 hours

19
Q

crucial points- brain function ceases…

A

brain function ceases 60-90 seconds of an ischaemic event

irreversible brain damage if ischaemic event > 3 hours duration

20
Q

2 types of stroke

A

ischaemic

haemorrhagic

21
Q

ischaemic strokes

A

embolus (wandering clot)
thrombus (locally-formed clot)
systemic hypoperfusion e.g. heart attack

22
Q

haemorrhagic strokes

A

entry of blood into CNS via rupture of a blood vessel/sinus or an aneurysm

23
Q

types of haematomas in the brain

A

epidural
subdural
subarachoid
intracerebral

24
Q

epidural haematoma

A

traumatic damage to the meningeal artery or dural venous sinus (e.g. blow to the head)

25
Q

subdural haematoma

A

caused by rapid movement of head causing tearing of the cerebral being as it enters a dural venous sinus

26
Q

subarachnoid haemotoma

A

caused by damage (e.g. aneurysm) to a cerebral artery or vein subsequent bleeding into the subarachnoid space

27
Q

intracerebral haemotomas

A

cause by damage of a blood vessel within the brain

28
Q

incidence of stroke

A

10% deaths worldwide
2nd leading cause of death
95% occur>45 years

29
Q

risk factors for stroke

A
  • high blood pressure (?)
  • high cholesterol
  • diet
  • physical inactivity
  • drugs of abuse (alcohol, cigarettes, cocaine, amphetamine)
30
Q

treatment for stroke preventative

A

anticoagulaants ; carotid angioplasty/endarterectomy; diet/lifestyle

31
Q

treatment for acute ischamic stroke

A

thromoblysis- tissue plasminogen activators (within 3 hours); thromobectomy; angioplasty; stenting

32
Q

treatment for acute hemorrhagic stroke

A

surgery

33
Q

treatment for chronic post stroke

A

control of hypertensions; aspirin; physical and occupational therapy

34
Q

alzheimer’s disease 1907 alois alzheimer pathology

A

profound loss of neurones
plaques (amyloid)
neurofibrillary tangles (hyperphosphorlyated tau)

35
Q

incidince of alzheimers

A

1.5%-2% worldwide

36
Q

causes of alzheimers

A

• age, 10% over 65, 50% >85
•genetics but predominantly for early onset e.g. ApoE4 gene
variant
•trauma
• high blood pressure/hypercholesteremia (but statins
ineffective),
•environmental factors?

37
Q

Alzhiemrs treatmetn

A

• symptoms - acetyl cholinesterase inhibitors, NMDA
receptor antagonists e.g. memantine
• risk - NSAIDs and caffeine, intellectual stimulation, diet and
exercise