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Year 3 core conditions > neurological > Flashcards

neurological Flashcards

1
Q

who gets strokes/TIAs

A

people >65

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2
Q

two main types of stroke

A

ischaemic stroke

haemorrhagic stroke

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3
Q

what causes ischaemic stroke

A

blood vessel blocked by something - fatty material/clot

thrombotic - blood clot spontaneously forms in artery in brain, complication of atherosclerosis

embolic - part of athersclerotic plauqe or clot breaks off and travels until trapped by narrow artery in brain - e.g. in AF

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4
Q

causes of haemorrhagic stroke

A

intracerebral haemorrhagic stroke - bleeding from blood vessel within brain. high blood pressure is biggest cause

subarachnoid haemorrhage - bleeding between brain and arachnoid matter

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5
Q

risk factors for TIA/stroke

A

thromboembolic stroke - hypertension, diabetes, smoking, hyperlipidaemia

also obesity, COCP, excessive alcohol consumption, polycythemia

AF - big risk factor

migraine, vascultitis and cocaine cause stroke by vasoconstriction

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6
Q

presentation of TIA/stroke

A

carotid territory symptoms - amaurosis fugax: transient loss of vision, aphasia, hemiparesis, hemisensory loss, hemianopic loss

vertebrobasilar territory symptoms: diplopia, vertigo, vomiting, choking, dysarthria, ataxia, hemisensory loss, menianopic or bilateral vision loss, tetraperesis, loss of consciousness

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7
Q

investigations for TIA/stroke

A

blood - glucose, FBC, ESR, creatinine, electrolytes, cholesterol, INR

brain imaging - MRI, CT

carotid artery imaging - doppler to look for atheroma and stenosis, MR angiography or CT angiography if US suggests carotid stenosis to determine degree of stenosis

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8
Q

treatment of ischaemic stroke

A

aspirin 300mg initially
continued long term 75g aspirin with 200mg TDS modified dipyridamole

clopidogrel instead of aspirin if needed

lifestyle changes for secondary prevention

carotid endarterectomy in patients with carotid artery stenosis

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9
Q

treatment of haemorrhagic stroke

A

anticoagulants should be stopped and their effects reversed by prothrombin complex concentrates

neurosurgical refferal to those with large intracerebral haematoma (deepening coma or brainstem compression etc)

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10
Q

who gets subarachnoid haemorrhage

A

mean age 50 yo

5% of strokes

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11
Q

causes of subarachnoid haemorrhage

A

spontaneous arterial bleeding into subarachnoid space caused by:
- saccular berry aneurysms (70%)- acquired lesions at branching points of major arteries coursing through subarachnoid space at circle of willis

congenital arteriovenous malformations - 10%

unknown cause

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12
Q

risk factors for subarachnoid haemorrhage

A

high blood pressure risk factors

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13
Q

presentation of subarachnoid haemorrhage

A

sudden onset severe headache
often occipital
maximum intensity within minutes (worst ever)
accompanied by nausea and vomiting and sometimes LOC

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14
Q

signs on examination of subarachnoid haemorrhage

A

signs of meningeal irritation - neck stiffness and positive kernings sign

focal neurological signs and subhyaloid haemorrhages (between retina and virteous membrane) with or without papilloedema.

some patients experience a warning headahce a few days before

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15
Q

investigation of subarachnoid haemorrhage

A

immediate CT - shows subarachnoid or intravascular blood in 24 hrs
lumbar puncture indicated if strong clinical suspician of SAH but CT is normal

increase in pigments (bilirubin and/or oxyhaemaglobin released from lysis and phagocytosis of RBC) = key finding. 12hrs after onset to 2 weeks

MR angiography to establish source for potential surgical patients

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16
Q

treatment of subarachnoid haemorrhage

A

cautious control of hypertension, bed rest and supportive management

nimodipine (calcium channel blocker) to reduce cerebral artery spasm

obliteration of aneurysms by surgical clipping or insertion of fine wire coil under radiological guidance prevents re-bleeding

lifestyle changes

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17
Q

causes of peripheral neuropathy

A

result of damage to nerves located outside brain and spinal cord. 6 core principles causing nerves to malfunction:

  • demyelination
  • axonal degeneration (toxin)
  • wallerian degeneration following nerve section
  • compression
  • infarction (arteritis)
  • infiltration by inflammatory cells (sarcoid)

health conditions that can cause: autoimmune diseases, diabetes, infections, inherited disorders, tumours, bone marrow disorder, also alcoholism, poisons, medications, truama/injury, vitamin deficiency

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18
Q

risk factors for peripheral neuropathy

A

DAMIT BITCH

Drugs and chemicals
Alcohol
Metabolic - diabetes, hypoglycaemia, uraemia
Infection
Tumour (paraneoplastic phenomenon)
B12 and other vitamin deficiencies
Idiopathic and infiltrative (amyloidosis)
Toxins
Connective tissue diseases and congenital
Hypothyroidism

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19
Q

presentation of peripheral neuropathy

A

sensory - gradual onset of numbness, prickling or tingling spreading upwards into legs and arms. extreme sensitivity to touch,

motor - lack of coordination and muscle weakness

autonomic nevres - heat intolerance, excessive sweating or nil sweat, bowel, bladder or digestive problems, postural hypotension, erectile dysfunction, arrythmias

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20
Q

investigations of peripheral neuropathy

A

blood tests - vitamin deficiences, diabetes, immune function

imaging - CT or MRI for herniated discs, pinched nerves etc

nerve function tests - EMG, thin needle electrodes, nerve conduction study

nerve or skin biopsy

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21
Q

treatment of peripheral neuropathy

A

manage underlying conditions
healthy lifestyle choices

medications - pain releivers, antiseizure meds (gabapentin+ pregabalin), topical treatments (capsaicin, lidocaine patches) and antidepressants

therapies - TENS, palsam exchange and IV immuen globulin, physical therapy, surgery

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22
Q

who gets epilepsy/seizures

A

bimodal incidence - children or >60yo
learning disabilities
often falsely diagnosed

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23
Q

causes of epilepsy/seizures

A 
alcohol
stroke
intracranial haemorrhage
space occupying lesion
metabolic disturbance
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24
Q

risk factors of epilepsy/seizures

A 
FH
genetic conditions
previous febrile seizures
previous intracranial infections
brain trauma
surgery
comorbid conditions - CVD or cerebral tumours
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25
Q

tonic seizure presentation

A

impairment of consciousness and stiffening (trunk straight or flexed at waist)

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26
Q

clonic seizure presentation

A

jerking and impairment of consciousness

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27
Q

typical absense seizures

A

begin in childhood
sharp onset and no residual symptoms
normal activity interrupted and child stares for few seconds
eyelids may twitch and some v small jerking movements of the hands may occur
lasts 5-10 seconds and less than 30 sec

can occur hundreds of times a day in children

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28
Q

myoclonic seizures

A

brief shock like contraction of limbs without the apparent impairment in consciousness

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29
Q

atonic seizures

A

sudden brief attacks of loss of tone associated with falls and retained consicousness

30
Q

features of focal seizures

A

Temporal lobe - Automatisms (eg. lip-smacking); déjà vu or jamais vu, emotional disturbance (eg. sudden terror); olfactory, gustatory, or auditory hallucinations.

Frontal lobe - Motor features such as Jacksonian features, dysphasia, or Todd’s palsy.

Parietal lobe - Sensory symptoms such as tingling and numbness; motor symptoms - due to spread of electrical activity to the pre-central gyrus in the frontal lobe.

Occipital lobe - Visual symptoms such as spots and lines in the visual field.

31
Q

investigaition of seizures

A

cardiac, neurological mental state and development assessment if possible

baseline tests for adults - FBC, U+Es, LFTs, glucose and calcium

12 lead ECG

32
Q

treatment of seizures

A

prolonged seizure or repeated seizure (>3min) = rectal or IV diazepam or lorazepam

status epilepticus = rectal diazepam or buccal midazolam

prevent attacks drugs are specific to type of seizure: tonic clonic = sodium volproate, lamotrigine, carbamazepine, topiramate, penytoin

33
Q

causes of meningitis

A

inflammation of the meninges as a reuslt of bacterial infection

  • neisseria meningitides = meningococcal disease
  • streptococcus pneumoniae = pneumococcal disease
  • haemophilus influenza type B (most common children <3months)
34
Q

risk factors of meningitis

A 
young age
winter season
absent or non functioning spleen
>65
immunocompromised
organ dysfunction 
smoking
crowded housing
basal skull fractures with leakage of CSF
cochlear implants 
otitis media
sinusitis
sickle cell disease
35
Q

presentation of meningitis

A 
non blanching rash
fever
vomiting/nausea
lethargy
irritability/unsettled behaviour
ill appearance
refusing food/drink
headache
msucle ache/joint pain
respiratory symptoms/signs or breathing difficulty
36
Q

signs on examination of meningitis

A 
non blanching rash
stiff neck
cap refill >6 sec +cold hands and feet
unusual skin colour
shock and hypotension
leg pain
back ridigity
bulging fontanelle
photophobia
kernings sign (unable to fully extend at knee when hip flexed)
brudzinskis sign (persons knee and hip flex when neck flexed)
unconscious or toxic moribund state
paresis
seizures
37
Q

investigations for meningitis

A

head CT if suspicion of intracranial mass lesion such as focal neurological signs, papilloedema, LOC, seizures

lumbar puncture

  • urgent CSF microscopy
  • white cell count and differential and analysis for protein and glucose concentration

blood cultures, glucose, CXR, viral and syphillis serology

38
Q

treatment of meningitis

A

admit to hospital as emergency 999
administer parenteral benzyl penicillin at earliest opportunity
cefotaxime 2g 6 hourly IV for initial treatment

add ampicillin 2g 4 hourly if immunosuppressed

follow sensitivity results

39
Q

who gets migraines?

A

18% prevalence

mean age of onset = 18yo

40
Q

causes of migraines

A

unknown
genetic and environmental factors
changes in brainstem and interactions with trigeminal nerve may be involved

41
Q

risk factors of migraines

A

genetic - first degree relative
sex
age - peak at 30yo
hormonal changes

42
Q

3 types of migraine

A

with aura
without aura
migraine variants (unilateral motor or sensory symptoms resembling a stroke)

43
Q

typical migraine headache

A

unilateral
throbbing
build up over minutes to hours

44
Q

presentation of migraine

A 
heaches
nausea
vomiting
photophobia
irritable and prefers dark
fatigue, nausea etc may occur hours to days before
auras 
aphasia, tingling, numbness, weakness on one side of body
45
Q

treatment of migraine

A

mild attacks = simple analgesia + antimetic such as metoclopramide

moderate/severe attacks = triptans are serotonin agonists (inhibit release of vasoconstirctive peptides)
- contraindicated in vascular disease

prophylactically (if >2 attacks per month) = pizotifen, beta blockers

46
Q

causes of parkinsons disease

A

progressive depletion of dopamine secreting cells in substantia nigra

other causes of parkinsonism: drug induced, CVD, lewy body dementia, multiple system atrophy, progressive supranuclear palsy

47
Q

parkinsonism

A

bradykinesa+

ridgity, tremor, postural instability

48
Q

risk factors for parkinsons

A

clustering of early onset PD in some families

linked to mutations in a synuclein

49
Q

presentation of parkinsons

A

unilaterally initially but becomes bilateral as disease progresses

slow progression

bradykinesia, hypokinesia, sitffness and ridigity, resting tremor, postural instability,

depression, anxiety, fatigue, reduced sense of smell, cognitive impairment, sleep disturbance, constipation

50
Q

treatment of parkinson’s disease

A

levodopa + peipheral decarboxylase inhibitor (carbidopa or beserazide) = control peripheral side effects

dopamine agonists

monoamine oxidase B inhibitor = inhibit catabolism of dopamine in brain

51
Q

what is proximal myopathy

A

symmetrical weakness of te proximal upper and/or lower limbs

52
Q

causes of proximal myopathy

A 
drugs
alcohol
thyroid disease
osteomalacia
idiopathic inflammatory myopathies
hereditary myopathies
malignancy
infections 
sarcoidosis
53
Q

aim of clinical assessment of proximal myopathy

A

distinguish proximal myopathy from other conditions that can present similarly

identify patients who need prompt attention - cardiac, resp or pharyngeal muscle involvement

determine underlying cause

54
Q

investigations for proximal myopathy

A

creatine kinase, thyroid function and OH vitamin D levels

further evaluation - neurological studies, muscle imaging and muscle biopsy in those whom no toxic, metabolic or endocrine cause is found and those with clinical features suggestive of inflammatory or hereditary myopathy

55
Q

treatment of proximal myopathy

A

depends on underlying cause

remove offending agent, correction of endocrine or metabolic problem, corticosteroids and immunosuppressive therapy for IIM and physical therapy and genetic counselling for muscular dystrophies

56
Q

who gets multiple sclerosis

A

begins in early adulthood

more common in women

57
Q

what causes multiple sclerosis

A

multiple plaques of demyelination within the brain and spinal cord

inflammatory process

thought that exposure to infectious agent in childhood EBV may predispose

58
Q

what is MS

A

inflammation, demyelination and axonal loss

59
Q

presentation of MS

A

young adult with 2 or more clinically distinct episodes of CNS dysfunction followed by remission

relapsing/remitting MS = optic neuropathy, brainstem demyelination and spinal cord lesions

60
Q

investigations of MS

A

MRI of brain and spinal cord is definitive test

61
Q

treatment of MS

A

short courses of steroids
subcut beta-interferon reduces relapse rate by 1/3 in relapsing/remitting disease

physio + other drug options to consider

62
Q

3 catagories of focal seizures

A

complex = impairment of consciousness
simple = no LOC
secondary generalised = focal evolves to generalised

63
Q

4 types of general seizure

A

absence
tonic-clonic
myoclonic
atonic

64
Q

treatment of absence seizure

A

valproate or ethosuximide

65
Q

what not to give in absence seizure

A

carbamazepine

66
Q

treatment of tonic clonic seizure

A

volproate or lamotrigine

67
Q

treatment of myoclonic seizure

A

valproate

or levitiraetam or topiramide if preg

68
Q

what not to give myoclonic seizures

A

carbamazepine

69
Q

atonic seizure treatment

A

valproate or lamotrigine

70
Q

treatment of focal seizures

A

carbamazepine or lamotrigine

71
Q

complications of seizures

A

status epilepticus
depression
suicide
SUDEP (due to cardiac arrhithmia)

72
Q

treatment of status epilepticus

A

iv lorazepam
buccal midazolam
if not work - phenytoin and call anaesthetist

Year 3 core conditions (15 decks)

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