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Phase 2a > Neuro conditions > Flashcards

Neuro conditions Flashcards

1
Q

describe a transient ischaemic attack (TIA)

A

sudden onset, brief neurological deficit due 2 temporary focal cerebral ischaemia (no infarction)
- lasts <24hrs- Sxs usually last 10-15 mins

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2
Q

what are the 2 arteries involved in a TIA

A

90%- carotid artery (anterior circulation)
10%- vertebral artery (posterior circulation)

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3
Q

list 7 risk factors for a TIA

A

HTN
AF
VSD (ventricular septal defect)
smoking
DMT2
obesity
male + black

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4
Q

what are general presentations of a TIA

A

Sxs= maximal @ onset 10-15 mins

amaurosis fugax= transient unilateral sudden vision loss, due 2 retinal artery occlusion
hemiparesis- 1sided weakness/paralysis
hemisensory loss
hemianopia vision loss
syncope + dizziness + ataxia + vertigo

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5
Q

what are area specific signs of a TIA

A

ACA- weak, numb contralateral leg

MCA-
weak, numb contralateral side of body
face drooping with forehead sparing
dysphagia

PCA- vision loss= contralateral homonymous hemianopia with macular sparing

vertebral- cerebellar syndrome
pneumonic= DANISH

Dysdiadochokinesis (can’t do rapid, alternating movements)
Ataxia
Nystagmus
Intention tremor
Slurred speech
Hypotonia

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6
Q

investigations for a TIA

A

clinical Dx

FAST- face, arms, speech, time

1st= FBC- look for polycythaemia, glucose, increased ESR, PT

GOLD= Sx last 10-15 mins + no infarction

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7
Q

management of TIA

A

1st=
aspirin 300mg (antiplatelet therapy) + referral to specialist + diffuse weighted MRI

2ndary prevention=
clopidogrel 75mg daily
atorvastatin (20-80mg 48hrs after)
control modifiable risk factors

if AF- anticoagulant eg warfarin

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8
Q

how can you differentiate between a TIA and a stroke

A

after recovery:

TIA= Sx usually resolve within mins + always <24hrs w. no infarct

Stroke= Sx last +24hrs w. infarct

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9
Q

what are the 2 types of stroke

A

ischaemic and haemorrhage

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10
Q

describe an ischaemic stroke
(what percentage of strokes)

A

rapid onset neurological deficit lasting 24hrs+
-due to blood clot blocking blood supply to brain causing ischaemia + infarction

(85% of strokes)

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11
Q

list 8 risk factors for ischaemic strokes

A

HTN (biggest)
past TIA
smoking
obesity
T2DM
heart disease (IHD, AF, valve diseases)
combined oral contraceptive oill
clotting disorder

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12
Q

what are the four areas infarcts can occur in ischaemic strokes

A

cerebral infarcts
brainstem infarcts
cerebellar infarcts
lacunar infarcts

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13
Q

presentation of cerebral infarct in an ischaemic stroke

A

contralateral sensory loss
contralateral hemiplegia (paralysis- usually flaccid then spastic)
UMN facial weakness (forehead sparing)
dysphagia (speech)
homonymous hemianopia
visuo-spatial defecit

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14
Q

presentation of a brain stem infarct in an ischaemic stroke

A

quadriplegia
facial numbness + paralysis
vision disturbances
dysarthria + speech imparement
vertigo
n+v

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15
Q

presentation of a cerebellar infarct in an ischaemic stroke

A

palatal paralysis + diminished gag reflex
incoordination
ataxia
n+v
dizziness + unsteadiness
horizontal nystagmus

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16
Q

what is a lacunar stroke/infarct and how does it present

A

blockage of blood vessels causing ischaemia to deep parts of brain (e.g basal ganglia, internal capsule, thalamus, pons)

sensory loss
unilateral weakness
ataxic hemiparesis
dysarthria

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17
Q

investigations for an ischaemic stroke

A

urgent non contrast CT scan (NCCT) of head- 2 distinguish between ischaemic + haemorrhagic & shows site of infarct

Bloods=
FBC- thrombocytopenia, polycthaemia
ESR- raised in vasculitis
PT/INR- if on warfarin
U&Es, cholesterol, lipid profile, PT

ECG- look for AF, MI

other= diffusion weighted MRI scan

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18
Q

management of an ischaemic stroke

immediate treatment + secondary prevention

A

once haemorrhagic excluded- 300mg aspirin straight after CT

thrombolysis within 4-5 hrs of Sxs using IV alteplase 2 dissolve blood clots

other option= mechanical thrombectomy (endovascular removal of thrombus)

antiplatelet therapy= aspirin 300mg for x2 weeks
THEN
clopidogrel 75mg daily, long term

prophylaxis= atorvastatin, ramipril, warfarin 4 AF

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19
Q

describe a hemorrhagic stroke

A

rapid onset neurological defect lasting 24hrs+
-caused by bleeding into brain due to ruptured blood vessel in/around vein= infarction

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20
Q

describe the 2 types of hemorrhagic stroke

A

intracerebral haemorrhage=
rupture of bv within brain- O2 deprivation + infarction- pooling of blood > raised ICP

subarachnoid haemorrhage=
spontaneous bleed into subarachnoid space between arachnoid mater and Pia mater

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21
Q

list 6 risk factors for hemorrhagic strokes

A

(mainly the same as ischaemic)
HTN (biggest)
thrombolysis
anticoagulation
arteriovenous malformations
smoking
diabetes

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22
Q

presentation of hemorrhagic strokes

A

Sxs last 24hrs+:
raised ICP Sxs
severe headache
limb+ facial weakness
visual or sensory loss
dysphagia

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23
Q

investigations for hemorrhagic strokes

A

urgent NCCT of head
- shows hyper dense blood, distinguishes ischaemic from hemorrhagic + shows site of stroke

FBC- look for polycythemia, thrombocytopenia

other = GCS

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24
Q

management of a hemorrhagic stroke

A

stop any blood thinning meds eg warfarin, aspirin
neurosurgery referral
IV mannitol 2 reduce ICP

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25
Q

name 4 spaces haemorrhages can occur in

A

extradural
subdural
subarachnoid
intra-cerebral

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26
Q

where does an extradural haemorrhage occur and how does one occur

A

extradural space between dura mate and skull

cause-
trauma 2 temple> fracture 2 temporal/parietal bone > rupture of middle meningeal artery

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27
Q

what age group do extradural haemorrhages most commonly occur in

A

young adults
-as age increases, risk decreases as dura more firmly adhered to skull

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28
Q

what is the classic presentation of an extradural hemorrhage

A

initial head trauma 2 temple/pterion >

lucid interval (‘I feel fine’- short episode of drowsiness/unconsciousness)>

sudden rapid deterioration (old blood clot becomes haemolysed)
Sxs due to increased ICP
-rapidly declining GCS
-increasingly severe headache
-vomiting
-seizures

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29
Q

what are signs of an extradural haemorrhage

A

UMN signs
ipsilateral pupil dilation
hemiparesis + bilateral limb weakness
coma

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30
Q

what does Cushing’s triad indicate and what are the signs

A

Cushing’s triad indicates raised ICP
-decreased heart rate
-wide pulse pressure
-irregular respiration

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31
Q

investigations for an extradural hemorrhage

A

NCCT head= haematoma
-biconvex lens-shaped (lemon)
-hyperdense
-doesn’t cross suture lines
-unilateral
-midline drift

skull x-ray- for fractures

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32
Q

management of an extradural hemorrhage

A

urgent surgery > clot evacuation, ligation of bleeding vessel, burr hole craniotomy

IV mannitol 2 reduce ICP

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33
Q

where does a subdural haemorrhage occur and what causes one

A

bleeding into subdural space between dura mater and arachnoid mater
-due 2 rupture of bridging vein

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34
Q

list 5 risk factors for a subdural haemorrhage

A

shaken baby syndrome
shearing deceleration injuries
dural metastases
epilepsy
brain atrophy- dementia/elderly, alcoholics

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35
Q

how does a subdural haemorrhage occur

A

bleeding from bridging vein in subdural space= haematoma

weeks/months later- haematoma autolysis= massive increase in oncotic + osmotic pressure > H20 sucked into haematoma + increase in ICP

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36
Q

presentation of a subdural haemorrhage

A

gradual onset with latent period:
headache + confusion
fluctuating consciousness
seizures
signs of raised ICP= cushing triad
focal neurology occurs later eg unequal pupils, hemiparesis
physical + intellectual slowing
personality change
memory loss

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37
Q

investigations for a subdural haemorrhage

A

NCCT head- crescent (banana) shaped haematoma
crosses suture lines
unilateral
midline shift

acute= hyper dense blood
subacute= isodense
chronic= hypodense (darker than brain)

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38
Q

management of a subdural haemorrhage

A

surgery= clot evacuation, craniotomy, Burr hole washout
IV mannitol to reduce ICP
antiepileptics- phenytoin

address cause of trauma eg childabuse

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39
Q

where does a subarachnoid hemorrhage occur and what are 2 causes

A

spontaneous bleeding into subarachnoid space

causes=
Berry aneurysm (70-80%, mc. @ ACA)
traumatic injury
arteriovenous malformations
idiopathic

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40
Q

list 7 risk factors for subarachnoid haemorrhages

A

HTN
PKD!!!!!
known/previous aneurysm @ SA
trauma
FHx
bleeding disorders
connective tissue disorders

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41
Q

symptoms of subarachnoid haemorrhages

A

occipital THUNDER CLAP HEADACHE
n+v
collapse + loss of consciousness
neck stiffness
sentinel headache (throbbing occipital pain preceding main rupture

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42
Q

signs of subarachnoid haemorrhages

A

meninges inflammation:
-kernig sign (pain on passive extension of leg when knee is flexed)
-Brudzinksi sign (when neck elevated, hip + knee automatically flex)
- (symptom= neck stiffness)

bleeds into eye eg retinol or vitreous
focal neurological signs eg 3rd nerve palsy (fixed + dilated pupil)
low GCS

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43
Q

describe the Glasgow coma scale (GCS)

A

used to measure a person’s level of consciousness

out of 15:
eye 4, verbal 5, motor 6

15= normal
8= comatose
3= unresponsive

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44
Q

investigations for a subarachnoid haemorrhage

A

urgent brain CT- looking for subarachnoid and/or intraventricular blood aka. ‘star sign’

positive star sign- CT angiography 2 see extent of rupture

negative- lumbar puncture after 12hrs - xanthochromia confirms subarachnoid (yellowish CSF filled w. breakdown products of RBCs)

PKD= U&E- hyperkalaemia + hyponatremmia

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45
Q

management of a subarachnoid haemorrhage

A

immediate neurosurgical referral
- endovascular/surgical coiling if aneurysm

IV fluids- maintain cerebral perfusion
nimodipine (CCB)- to decrease vasospasm + BP

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46
Q

describe an intra-cerebral haemorrhage and its causes

A

sudden bleeding into brain tissue due 2 rupture of a blood vessel within the brain (10% of strokes)

causes=
HTN- stiff & brittle vessels prone to rupture

2ndary to ischaemic stroke- bleeding after reperfusion

head trauma, arteriovenous malformations, brain tumours, carotid artery dissection

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47
Q

list 6 risk factors for an intra-cerebral haemorrhage

A

HTN
anticoagulation
thrombolysis
alcohol
smoking
diabetes

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48
Q

what happens in an intra-cerebral haemorrhage

A

rupture of blood vessel within brain= O2 deprivation + infarction
-pooling of blood= raised ICP

raised ICP> puts pressure on skull + brain + blood vessels= tissue death
tissue herniation (hydrocephalus) + midline shift + tentorial herniation + coning (brainstem compression)

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49
Q

presentation of an intra-cerebral haemorrhage

A

Sxs last 24hrs+:
sudden onset severe headache
facial + limb weakness
dysphagia
visual/sensory loss
increased ICP
n+v
syncope
loss of consciousness

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50
Q

investigations for an intra-cerebral haemorrhage

A

urgent NCCT of head- distinguish between haemorrhagic + ischaemic and shows site of haemorrhage
-hyperdense blood on CT

Bloods=
FBC- polycythemia, thrombocytopenia
PT/INR if on warfarin

ECG- look for AF, MI
GCS

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51
Q

management of intra-cerebral haemorrhages

A

urgent lowering of BP
IV mannitol 2 decrease ICP
urgent anticoagulation reversal- clotting factor replacement

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52
Q

what is syncope

A

temporary unconsciousness due to a disruption of blood flow to the brain- often leads to a fall

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53
Q

what are primary and secondary causes of syncope

A

primary=
dehydration, missed meals, standing for ages, vasovagal response 2 stimuli eg blood, pain, surprise

secondary=
hypoglycaemia
anaemia
infection
anaphylaxis
arrhythmias
valvular heart disease
hypertrophic cardiomyopathy

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54
Q

what happens in syncope

A

vagus nerve receives strong stimulus > stimulates parasympathetic nervous system
>vasodilation of blood vessels in brain > BP in cerebral circulation decreases = hypo perfusion of brain tissue- loss of consciousness & fainting

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55
Q

presentation of syncope

A

prodrome=
hot or clammy
sweating
dizzy/lightheaded
vision going blurry
headache

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56
Q

investigations for syncope

A

history + clinical examination
ECG (arrhythmias, long QT syndrome)
echo
bloods- FBC =anaemia
electrolytes
bad glucose

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57
Q

list 4 primary types of headaches

A

migrane
cluster
tension
drug OD

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58
Q

list 6 secondary causes of headaches

A

giant cell arteritis
infection
subarachnoid haematoma
trauma
cerebrovascular disease

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59
Q

describe a migrane

A

recurrent throbbing headache- often preceded by aura + associated with n+v and visual changes

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60
Q

triggers of migraines using CHOCOLATE

A

Chocolate
Hangovers
Orgasms
Cheese
Oral contraception
Lie ins
Alcohol
Tumult eg loud noises
Excercise

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61
Q

what are 3 stage of a migrane

A

prodrome (days)- yawning, cravings, mood/sleep changes

aura (mins b4 attack)- visual disturbances eg dots, lines, zigzags
somatosensory eg pins and needles

throbbing headache (4-72 hrs)

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62
Q

presentation + diagnostic criteria for a migrane

A

@least 2 of:
unilateral pain (4-72hrs)
throbbing pain
moderate to severe intensity
motion sensitivity

plus @ least 1 of:
n+v
photophobia/phonophobia

-must be a normal neurological exam, no other attributable cause

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63
Q

management of migraines

A

1st= oral triptans eg sumatriptan or aspirin 900mg

NSAIDs= naproxen
anti-emtic= metoclopramide

prevention= required if 2+ attacks per month or require acute meds +2 times a week
BB (propanol), tricyclic antidepressants (amitriptyline), anti-convulsant (topiramate - CI if preggo)

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64
Q

describe a cluster headache

A

clusters of episodic headaches lasting from 7 days up to 1year
-usually 2-3 weeks w. pain free periods inbetween

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65
Q

presentation of cluster headaches

A

rapid onset of excruciating pain around eye + sometimes temples and forehead
-pain rises to a crescendo over a few mins and last 15mins-3hrs, 1-2 times a day

strictly unilateral + localised to 1 area

ipsilateral autonomic:
watery, bloodshot eye
facial flushing
blocked nose
pupil constriction
ptosis

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66
Q

investigations and management of cluster headaches

A

Dx= @ least 5 similar attacks + rule out other causes (brain MRI, ESR, pituitary function tests)

Tx=
acute attack-
15L 100% O2 for 15 mins via nonrebreather mask
triptans eg sumatriptan

prevention-
verapamil (CCB)
no smoking/alcohol

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67
Q

describe a tension headache

A

bilateral generalised pain, radiates 2 neck
mc. headache

can be episodic= <15 days/month
or chronic= >15 days/month for @ least 3 months

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68
Q

list 7 triggers of tension headaches

A

STRESS
sleep deprivation
hunger
eyestrain
anxiety
noise
overexertion

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69
Q

presentation of a tension headache

A

rubber band tight round head
bilateral pain, mild/moderate intensity
+/- scalp tenderness

-no aura, vomiting, photophobia or motion sickness

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70
Q

describe trigeminal neuralagia

A

facial pain in 1 or more branches of the trigeminal nerve : ophthalmic, maxillary, mandibular
-usually unilateral

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71
Q

what are 3 risk factors for trigeminal neuralagia

A

x20 times mc. in multiple sclerosis
increasing age
female

caused by trigeminal nerve compression

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72
Q

list 7 triggers of trigeminal neuralagia

A

eating
shaving
talking
caffeine
brushing teeth
cold weather
spicy food

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73
Q

presentation and investigations for trigeminal neuralagia

A

spontaneous electric shock pain (up to 2mins) in U1/2/3

Dx= clinical- 3+ attacks with the same presentation of Sxs

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74
Q

management of trigeminal neuralagia

A

carbamazepine (anticonvulsant)
surgery 2 decompress nerve if nothing else works

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75
Q

who is the typical person presenting with giant cell arteritis and what are their symptoms

A

50 y/o Caucasian woman presents with
-unilateral tender scalp
-intermittent jaw claudication
-amaurosis fugax

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76
Q

investigations for giant cell arteritis

A

temporal artery biopsy= granulomatous + giant cells & skip lesions
+ raised ESR/CRP
+ normocytic, normochromic anaemia of chronic disease

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77
Q

management of giant cell arteritis

A

prednisolone
- if any signs of amaurosis fugal/vision changes- high dose IV methylprednisolone ASAP

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78
Q

what is a seizure

A

transient episode of abnormal brain activity

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79
Q

what are 3 things that only occur in an epileptic seizure vs non-epileptic

A

epileptic=
-eyes open
-synchronous movements
-can occur in sleep

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80
Q

list 6 risk for seizures

A

FHx
dementia- 10x more likely
alcohol withdrawl
tumours
strokes
cortical scarring

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81
Q

describe the pathology of a seizure

A

GABA= inhibitory
glutamate= excitatory

norm balance between GABA and glutamate shifts towards glutamate
- more glutamate stimulation + more GABA inhibition= more excitatory

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82
Q

criteria for diagnosis of epilepsy

A

1 of :
@ least 2 unprovoked seizures occurring more then 24hrs apart

1 unprovoked seizure + probability of future seizures (>60% risk in 10yrs)

diagnosis of an epileptic syndrome

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83
Q

describe the prodrome phase of an epileptic seizure

A

weird feeling/change in mood days or hrs b4 seizure

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84
Q

describe the aura phase of an epileptic seizure

A

minutes B4:
automatisms (lip smacking, rapid blinking)
strange feeling in gut
deja vu
strange smells

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85
Q

describe the post-ictal period of an epileptic seizure + Todd’s paralysis

A

post-ictal period= after seizure:
headache
confusion
myalgia
sore tongue- often bitten
amnesia
dysphagia (temporal lobe)

Todd’s paralysis occurs of motor cortex affected- may have temporary paralysis + musc weakness

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86
Q

what kind of seizure involves both sides of the brain and always results in unconsciousness

A

generalised seizures

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87
Q

name and describe the 6 types of generalised seizures

A

TONIC= high musc tone, rigid, stiff limbs- will fall to floor if standing

CLONIC= rhythmic muscle jerking

TONIC-CLONIC (grand-mal)= combo of tonic & clonic
+ up gazing open eyes, incontinence, tongue bitten

MYOCLONIC= isolated jerking of a limb/face/trunk, ‘disobedient limb’ or ‘thrown to the floor’

ATONIC= opp of tonic- lack of musc tone, floppy

ABSCENCE (petit Mal) = mc. in childhood, go pale + stare blankly into space for a few secs- min, then carry on where left off
++ will have a 3Hz spike on EEG

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88
Q

what are focal/partial seizures

A

seizures mainly confined to 1 region/lobe eg temporal
-may progress later 2 generalised seizures

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89
Q

how does a simple partial seizure present

A

no loss of consciousness, patient awake + aware
just uncontrollable muscle jerking
+ sensory/autonomic/physic Sxs depending on which lobe is affected

90
Q

how does a complex partial seizure present

A

loss of consciousness
post itical period positive

91
Q

what are the different presentations of focal neurologies affecting the temporal, frontal, parietal and occipital lobes

A

TEMPORAL= aura, dysphagia, memory, emotion, speech

FRONTAL= Todd’s palsy + Jacksonian march (simple partial seizure spreads from distal part of limb 2 ipsilateral side of face- seizures march up and down motor homunculus)

PARIETAL= parathesia

OCCIPITAL= visual phenomena eg spots, lines, zigzags

92
Q

investigations for epileptic seizures + GS

A

electroencephalogram (EEG)
-supportive not diagnostic, can determine type of epileptic syndrome eg 3Hz spike in absence seizure

head MRI/CT- examine hippocampus + rule out other causes eg tumour, bleeding

bloods- rule out metabollic causes + infection

GOLD= clinical diagnosis (@least 2 seizure more than 24hrs apart) + EEG (determine type of seizure

93
Q

management of generalised seizures

A

usually only started after 2nd epileptic episode

1st= sodium valporate- males + women not childbearing age as highly teratogenic

women child bearing age (15-45)= lamotrigine
if absence- enosuximide

94
Q

management of focal seizures

A

1st= lamotrigine/carbamazepine
2nd= sodium valproate/levetrivacetam

95
Q

what is status epilepticus

A

status epilepticus= comp of epilepsy, 3+ seizures in 1hr/seizure lasting longer than 5 mins

Tx= IV/rectal benzodiazepines eg lorezapam or diazepam, if not working give phenytoin

96
Q

what is Parkinson’s a loss of

A

loss of dopaminergic neurones from substantia nigra pars compacts in basal ganglia

97
Q

list 5 risk factors for parkinsons

A

FHx
males
increasing age
encephalitis
pesticide exposure

98
Q

what are the basal ganglia responsible for

A

coordination of habitual movements eg walking, controlling voluntary motions, learning specific movements patterns

99
Q

what does the substantia nigra pars compacta produce and how does it initiate movement

A

produces dopamine, essential for correct functioning of basal ganglia

2 initiate movement:
substantia nigra pars compacta signals 2 striatum to stop firing to substantia nigra pars reticula - therefore stopping inhibition of movement

if substantial nigra pars compact= degenerated- decreased dopamine production and input= harder to initiate movement

100
Q

what are the cardinal presentations of Parkinson’s

A

bradykinsesia (slowness of movement)
resting tremor
rigidity
postural instability
often asymmetrical

101
Q

signs of parkinsons

A

impaired dexterity
fixed facial expressions
foot drag
shuffling gate w. arm swing on 1 side
pill rolling thumb (rolling thumb + finger back and forth)
cogwheel/lead pipe rigidity (resistance to motion either stop or start or constant)
stooped posture + forward tilt

102
Q

symptoms of parkinsons

A

dementia
depression
urinary frequency
constipation
disturbed sleep
fatigue
loss of sense of smell

103
Q

what are the 3 steps of diagnosis for parkinsons

A
  1. Dx of Parkinsonium syndrome= bradykinesia + 1 of : rigidity, resting tremor, postural instability
  2. exclusion criteria (can’t have any)
    - Hx of stroke
    - repeat head injury
    -neuroleptic Tx
    -unilateral features after 3 yrs
  3. supportive criteria (3+ required)
    -unilateral onset
    -rest tremor present
    -progressive
    -excellent response to L-dopa
    -visual hallucinations
104
Q

management of parkinsons

A

moderatly/severely= levodopa (L-dopa) + peripheral decarboxylase inhibitor eg beneldopa

problem= body can become resistant 2 L-dopa
-therefore give COMT inhibitor alongside L-dopa to prevent wearing off eg entacapone

105
Q

what is dementia

A

neurodegenerative disorder- decrease in cognition (memory, judgement, lang) overtime

106
Q

name 4 kinds of dementia

A

alzheimers
vascular
Lewy body
fronto-temporal

107
Q

list 4 risk factors for Alzheimers

A

Down’s
ApoE4 allele homozygosity in familial alzheimers
depression/loneliness
increasing age

108
Q

describe the pathology of alzheimers

A

extracellular deposition of:
beta-amyloid plaques + tau-containing intracellular neurofibrillary tangles
- accumulation of above= reduction in information transmission and eventually death of brain cells

also occur=
damaged synapses, atrophy, cortical scarring, decreased Ash neurotransmitter

109
Q

presentation of Alzheimers (including x3 signs)

A

memory- episodic & semantic (lang difficulty, gen knowledge, fact recall)
lang- difficulty understanding/finding words + dysphagia
attention + concentration issues
physics changes eg personality change, withdrawal, delusions, apathy
disorientation (time + surroundings)

signs=
agnosia- can’t recognise things
apraxia- can’t do basic motor skills
aphasia- speech issues

110
Q

1st line + GOLD investigations for alzheimers

A

1st= MMSE (mini mental state exam)
score out of 30
>25 = normal
18-25 = impared
<18 = severely impaire

bloods= FBC, U&E- rule out other causes

GOLD= brain MRI- temporal lobe + cortical atrophy

111
Q

management of Alzheimer’s

A

supportive therapy
-carers, adapt home, help w. daily activities

meds for Sxs= anti cholinesterase inhibitors eg donepezil, rivastigme, galantamine, memantine

112
Q

describe vascular dementia

A

chronic progressive decline due 2 loss of brain parenchyma from cerebrovascular events eg infarction caused by stroke

113
Q

list 7 risk factors for vascular dementia

A

history of TIAs
AF
HTN
CHD
hyperlipidemia
smoking
obesity

114
Q

presentation of vascular dementia

A

stepwise progression
= periods of stable Sxs followed by sudden increase in severity

visual disturbances
UMN signs
difficulty solving problems
apathy
disinhibtion
poor attention
emotional disturbances
mood changes

115
Q

investigations for vascular dementia (including GOLD)

A

Hx of TIA/stroke?
bloods 2 rule out other causes
MMSE
CT/MRI to look for previous infarcts

GOLD= dementia diagnosis + sign of cerebrovascular event

116
Q

management of vascular dementia

A

1st=
antiplatelet therapy : aspirin or clopidogrel
OR
anticoagulation therapy= warfarin, rivaroxaban

supportive therapy + lifestyle changes

SSRIs or antipsychotics eg sertraline or lorazepam

117
Q

what causes Lewy body dementia

A

abnormal deposits of a protein called alpha-synuclein (Lewy bodies)
neurodegenerative w. parkinsonium

118
Q

what would Lewy body dementia 1st and then Parkinsonism be called
vs
what would Parkinsonism as presenting complaint be called

A

dementia 1st then Parkinsonism= Lewy body dementia w. parkinsonism

parkinsonism as presenting complaint= Parkinson dementia

119
Q

presentation of Lewy body dementia (+ Parkinsonism Sxs)

A

often dementia presents initially:
memory loss
spatial awareness difficulties
loss of cog fucntion
behavioural problems
visual hallucinations
sleep disorders

parkinsonism:
bradykinesia (slowness of movement)
rigidity
resting tremor
change in gait

120
Q

investigations for Lewy body dementia (+ GOLD)

A

MMSE
bloods- rule out other causes
Brain MRI- generalised atrophy

GOLD= international criteria-

  1. prescence of dementia with 2 of
    -fluctuating attention/concentration
    -recurrent visual hallucinations
    -spontaneous parkinsonism
  2. if only one core feature- Dx can be made w. SPECT or PET scan, showing decreased dopamine transporter uptake in basal ganglia
121
Q

management of Lewy body dementia

A

supportive therapy- cog. stimulation, exercise programmes, @ home care

cholinesterase inhibitors- donezepil, rivastigmine

122
Q

describe frontotemporal dementia

A

progressive dementia common in under 65s
-atrophy of frontal + temporal lobes with loss of neurones but no plaque formation

123
Q

list 2 risk factors for frontotemporal dementia

A

autodom inheritance
- change in Tau protein on chromosome 17
FHx of MND

124
Q

presentations of frontotemporal dementia

A

behavioural issues= issues w. empathy, understanding words, recognising objects/faces

progressive aphasia= slow, difficult speech w. grammatical errors

semantic dementia= issues w. vocal, understanding words, recognising objects/ phases

parkinsonism= memory impairment, disorientation

125
Q

investigations for frontotemporal dementia (including GOLD)

A

MMSE
bloods 2 rule out other causes

GS= Brain MRI (frontal + temporal atrophy)

126
Q

management of frontotemporal dementia

A

supportive therapy= carers, speech + lang therapy
SSRIs eg sertraline, citalopram 4 behavioural Sxs
levodopa 4 Parkinsonism Sxs

127
Q

what is huntington’s and what mutation causes it

A

auto dom condition causing progressive degeneration of the nervous system
-100% penetrance, all genotypes will express phenotype

caused by trinucleotide expansion repeats
- CAG repeats on Huntingtons gene on chromosome 4
>35 CAG repeats= Huntington’s

128
Q

describe anticipation in huntingtons

A

successive generations have more CAG repeats in HTT gene on chromosome 4= earlier onset + greater severity of the disease

129
Q

presentation of huntingtons

A

HYPERKINESIA
chorea (involuntary/irregular unpredictable muscle movements)
dystonia (abnormal muscle tone= musc spasm + abnormal posture)
uncoordination
depression
physch issues
cognitive imparement
behavioural difficulties
psychosis
eye movement disorders
dysarthria (diff talking due 2 weak speech muscles)
dysphagia

130
Q

investigations for huntingtons

A

clinical diagnosis + FHX + genetic testing (35+ CAG repeats on chromosome 4)
-MRI/CT brain shows loss of striatal vol

131
Q

management of Huntingtons

A

no treatment, manage Sxs
chorea= antiphychotics (olanzapine), benzodiazepines (diazepam), dopamine antagonists (tetrabenazine)

psychosis= antipsychotics (haloperidol)
depression= SSRIs (citalopram)

132
Q

ethics around Huntingtons + testing for it

A

poor prognosis= 15-20 yrs from onset
- suicide= 2nd mc cause of death
child of affected adult has 50% chance of inheriting disease

can take a genetic test when 18 yrs

133
Q

describe the 4 kinds of hypersensitivity reactions

A

T1= IgE antibodies
basophils>mast cells - release histamine
-anaphylaxis, food + drug allergies, bee stings

T2= IgG/IgM
cytoxic/antibody mediated
-haemolytic react (eg blood transfusion)
good pasture’s

T3= IgG/IgM/immune complex mediated
immune complex deposition
hypersensitivity pneuomnitis
SLE
polarteritis nodosa

T4= T cell mediated/delayed
contact dermatitis, T1DM, MS

134
Q

describe multiple sclerosis (MS)

A

Type 4 hypersensitivity autoimmune condition
-characterised by repeated episodes of inflammation of the nervous tissue of brain + spinal cord
= results in demyelination of CNS neurones (oligodendryte destruction)

135
Q

list 4 risk factors for MS

A

female 20-40yrs
FHx
autoimmune conditions
EBV

136
Q

name and describe the 3 types of MS

A

relapsing- remitting MS:
-Sxs come and go w. good health inbtwn.

2ndary progressive MS:
-flows from relapsing-remitting to gradually worsening Sxs w. fewer remissions over time

primary progressive MS:
-from the beginning- Sxs gradually develop & worsen over time w.out remission

137
Q

name and describe the most common presentation of MS

A

optic neuritis- demyelination of optic nerve causing unilateral reduced vision + loss of colour vision

relative afferent pupillary defect:
light shone in affected eye= no pupil change, light in unaffected eye- affected eye will show pupil constriction

also may have eye movement abnormalities- due 2 6th CN palsy (abducens)

138
Q

in multiple sclerosis, describe the presentation of
4 focal neurological weaknesses
&
4 focal neurological sensory Sxs

A

focal weakness=
Incontinence
Horner syndrome
Facial nerve palsy
Limb paralysis

focal sensory Sxs=
Trigeminal neuralgia
Numbness
Paraesthesia (pins and needles)
Lhermitte’s sign (UMN sign- electric shock felt down spine, into limbs due 2 flexion of neck)

139
Q

what is the classic triad associated with MS

A

Charcot’s triad:
-nystagmus
-intention tremor
-dysarthria

140
Q

investigations for MS

A

1st= (bloods should be norm)
lumbar puncture- may show oligoclonal IgG bands in CSF

GS= McDonald criteia- 2≤ attacks disseminated in time (separate events) + space (diff parts of CNS affected)

Dx tool= MRI brain + spinal cord

oligodendrytes in CNS

141
Q

describe the non-pharm management of MS + management of acute flares

A

gen managment= MDT care, supportive therapy, legal obligation to inform DVLA

acute flares= IV methylprednisolone

142
Q

describe management of the 3 different types of MS

A

relapsing-remitting MS=
interferon beta (CI preggo)
DMARDs- IV natalizumab
immunomodulator (oral fingolimod)

2ndary progressive MS=
Siponimod (DMT) or methylprednisolone

primary progressive MS=
ocrelizumab (DMT)

143
Q

what is Motor neurone disease (MND)

A

group of diseases involving progressive degeneration of UMN + LMN (sensory neurones spared)

144
Q

describe the presentations of upper VS lower motor neurone lesions

A

UMN vs LMN
-hypertonia -hypotonia
-hypereflexia -hyporeflexia
-no fasciculation -fasciculetinous
-Babinski positive -babinski negative
-powers. -gen. reduced power
arms=flexors>
extensors
legs=extensors>
flexors

MIXED UMN + LMN- THINK MND!!!

145
Q

what mutation is associated with MND

A

SOD-1 mutation

146
Q

what are 2 things MND never affects

A
  1. eye muscles (MS + myasthenia gravis do)
  2. sensory func (MS + polyneuropathies do)
147
Q

what are the four subtypes MND can be classed as

A

ALS (mc) amyotrophic lateral sclerosis
-UMN + LMN

PMA, progressive muscular atrophy
-LMN only

PLS, primary lateral sclerosis
-UMN only

PBP, progressive bulbar palsy
-CN 9-12 affected
-worst prognosis + highest chance of rest failure

148
Q

what are the key presentations of MND

A

mixed UMN + LMN presentations
onset in limb= atypical presentation
-wrist/foot drop
-gait disorders/tripping
-wasting of hands
-excessive fatigue

149
Q

investigations for MND

A

1st= nerve conduction studies- electromyogram

GOLD= clinical diagnosis- presence of UMN + LMN degeneration & absence of evidence of other diseases

150
Q

management of MND

A

MDT care
supportive therapy- speech + lang therapy + physio
riluzole (antiglutaminergic)
quinine/baclofen (cramps)

comps= aspiration pneumoniae, resp failure, swallowing failure

prognosis= 2-4 yrs

151
Q

what is meningitis

A

inflammation of the meninges lining the brain + spinal cord due 2 viral, bacterial or fungal infection
-notifiable disease

152
Q

what are the viral, bacterial and fungal causes of meningitis

A

viral= mumps, herpes, influenza, HIV, measles, enteroviruses (coxsackie)

bacterial= N.meningitidis, E.coli, listeria, haemophiliac, influenza B, s.pneumonia, klebsiella, TB

Fungal= cryptococcus, candida, histoplasma

153
Q

name 4 risk factors for meningitis

A

immunocompromised
extremes of age
not vaxed
crowded environment (uni!)

154
Q

what most commonly causes neonatal meningitis

A

group B strep- gram pos diplococcus in chains
-mc. causing neonatal jaundice bc colonises maternal vag.

155
Q

presentation of meningitis

A

stiff neck
photophobia
headache
fever
raised ICP Sxs

kernig sign- can’t extend knee when hip flexed w.out pain
Brudzinksi sign- when neck flexed, knees + hips automatically flex

meningococcus only= non-blanching purpuric rash

156
Q

what are signs of raised ICP

A

decreased GCS
Cranial nerve palsy
focal deficits
seizures

157
Q

investigations for meningitis

A

lumbar puncture (@L3/4) + CSF analysis
to ID cause of meningitis (look up table of Investigations)

158
Q

management of meningitis

A

1st= empirical Abxs
bacterial meningits:
w. rash= benzylpenicilin IV
w. out rash= cefotaxime IV
+ steroids (dexamethasone)

add vancomycin if s.pneumoniae suspected
add amoxicillin if listeria suspected

no spec Tx for viral- analgesia, antipyretics, hydration

159
Q

what prophylaxis should be given to the household/contacts of someone w meningitis ( + what are some comps of meningitis)

A

prophylaxis= 1 off dose of ciprofloxacin

comps= DIC (disseminated intravascular coagulation)
waterhouse friedrichsen syndrome

160
Q

what is encephalitis and what is it most commonly caused by

A

viral infection causing inflammation of brain parenchyma
-mc. caused by HSV-1- herpes simplex virus

others= CMV, EBV, Lyme disease, toxoplasmosis

161
Q

presentation of encephalitis

A

fever
headache
altered mental status
rash
increased ICP
focal neurology- mc. affects temporal lobe= aphasia

meningitis Sxs=
-neck stiffness
-photophobia
-vomiting
-headache
reduced consciousness

162
Q

investigations for encephalitis

A

bloods-
FBC= raised WBC
U&Es= hyponatraemia

lumbar puncture + CSF analysis- use viral PCR to detect virus

GOLD= MRI brain > swelling of brain, normally unilateral + primarily affecting temporal lobe

163
Q

management of encephalitis

A

acyclovir

non-viral encephalitis= Abxs (IV benzylpenicilin)

164
Q

what are glial cells
name the 3 kinds of glial cells
what are gliomas

A

glial cells= surround + support the neurones

3 types=
-oligodendrytes
-astrocytes
-ependymal cells

gliomas= tumours of glial cells, these are PRIMARY brain tumours

165
Q

what are the 3 types of glioma and how are they graded

A

graded 1-4 (4= most malignant)

Astrocytoma (the most common and aggressive form is glioblastoma multiforme)
Oligodendroglioma
Ependymoma

166
Q

what are meningiomas

A

tumour of meninges- usually benign but can cause raised ICP + neurological issues

167
Q

where do secondary brain tumours mc. metastasise from

A

non-small cell lung cancers (mc.)
small cell lung cancer
breast
melanoma
RCC
gastric cancer

168
Q

presentation of a brain tumour

A

raised ICP:
-cushing triad
-CN6 palsy
-papilloedema (swollen of the optic disc- Dx w. fundoscopy)

focal neurology
epileptic seizures
lethargy + wt. loss

169
Q

investigations for a brain tumour

A

MRI to locate tumour then > biopsy to determine grade (1-4, 4= worst, glioblastoma)

170
Q

what investigation must you not do If someone has raised ICP

A

raised ICP = DO NOT LUMBAR PUNCTURE
- can cause brain herniation

171
Q

management of a brain tumour

A

surgery to remove tumour if possible
+ chemo b4 after and during surgery

dexamethasone + mannitol 2 reduce ICP

palliative care

172
Q

what does hemiplegia vs paraplegia indicate

A

hemiplegia= 1 side of body > BRAIN lesion
paraplegia= both legs > CORD lesion

173
Q

list the number of vertebrae in each section of the spinal column

A

spinal column:
C1-7= cervical
T1-12= thoracic
L1-5= lumbar
S1-5= sacral

174
Q

which vertebrae does spinal cord compression (myelopathy) occur between and what are some causes

A

compression of spinal cord from C1-L1/2

causes=
-vertebral body tumours (mc. mets from lung, breast,, prostate)
-trauma
-prolapsed disc
-epidural haematoma
-infection

175
Q

what are red flag signs for spinal cord compression + other Sxs

A

RED FLAGS=
progressive limb weakness + UMN signs in lower limbs (eg contralateral hyperreflexia, Babinski sign positive, spasticity

sensory loss below lesion
loss of bladder function/control
paraplegia
back pain

176
Q

investigations for spinal cord compression

A

MRI whole spine ASAP
-chest x-ray if malignancy suspected

177
Q

management of spinal cord compression

A

1st= dexamethasone until Tx plan confirmed
surgical decompression (laminectomy, microdiscetomy)
chemo if needed

178
Q

what is caudal equina syndrome and what do the nerve provide innervation for

A

surgical emergency
nerver roots of caudal equina @ end of spinal cord= compressed L2/3 downwards

nerve roots of caudal equina provide motor + sensory innervation to:
-lower limbs
-perineum
-bladder + urethral sphincters
-rectum

179
Q

what are 4 causes of caudal equina

A

lumbar herniation @ L4/5 or L5/S1 level
tumours
trauma
infection/abscess

180
Q

presentation of caudal equina syndrome

A

sudden onset
leg weakness w. LMN signs eg ipsilateral hypotonia, hyporeflexia, loss of ankle reflex
saddle anaesthesia > perianal numbness
bladder/bowel dysfunction + sphincter involvement (incontinence)

181
Q

investigations and management for cauda equina syndrome

A

urgent MRI spine (diagnostic) + testing nerve roots and reflexes > absent ankle reflex L5-S1

Tx= surgical decompression ASAP

182
Q

what is damaged in foot drop and what are some causes of this damage

A

foot drop= difficulty lifting front part of foot= dragging of the toes

caused by damage 2 common peroneal nerve L4-S2 via:
-injury
-lower back damage
-cauda equina syndrome
-tumour
-hip replacement
-multiple sclerosis

183
Q

how would you manage foot drop

A

brace/splint
physiotherapy
specialised shoes
nerve stimulation
surgery if needed

184
Q

what is brown sequard syndrome and what is the classic presentation

A

hemisection of the spinal cord (mc. cervical region)

  1. ipsilateral hemiplegia (corticospinal tract)
  2. ipsilateral loss of proprioception, fine touch and vibration (DCML tract)
  3. contralateral pain + temp sensation defects (spinothalamic)
185
Q

investigations + management for brown sequard syndrome

A

1st- bloods
plain radiographs for penetrating/blunt trauma

GOLD= MRI spine + neurological examination 2 see extent of injury eg checking reflexes

Tx=
surgery- spine immobilisation, decompression
steroids to reduce swelling (IV methylprednisolone)

physio/occupational therapy

186
Q

list 3 reflexes and where the nerve that innervate them originate from

A

L3/4= knee jerk
L5= big toe jerk
S1= ankle jerk

187
Q

what are peripheral neuropathies + name 5 causes

A

damage to peripheral nerves resulting in transmission blockages between CNS & PNS

causes=
DMT2
demyelination > Guillian- barre, B12 def
infection eg shingles
alcohol excess
surgery

188
Q

name 5 mechanisms that cause peripheral neuropathy

A

demyelination
axonal damage
nerve compression
vasa nervosum infarction
wallerian degeneration (nerve= cut + distally dies)

189
Q

describe mononeuropathy, mononeuritis complex and polyneuropathy

A

mononeuropathy= single nerve affected

mononeuritis complex= several individual nerves- causes = WARDS PLC

polyneuropathy= diffuse, often symmetrical pathology

190
Q

what is the pneumonic for causes of mononeuritis complex

A

WARDS PLC

Wegner’s vasculitis
AIDS/amyloidosis
RA
DMT2
Sarcoidosis
Polyarteritis nodosa
Leprosy
carcinomas

191
Q

describe carpal tunnel syndrome

A

mononeuropathy
-compression of median nerve (C6-T1) passing thru carpal tunnel

median nerve provides innervation 2 palmar side of hand:
thumb + index + middle finger + half of ring finger
motor innervation of thenar muscles

192
Q

what are some risk factors/causes of carpal tunnel syndrome

A

female
acromegaly
hypothyroidism
RA
pregnancy
obesity
repeat strains

193
Q

presentation of carpal tunnel syndrome

A

gradual onset-
weakness of grip + aching hand and forearm > worse @ night, relieved by hanging hand over side of bed (wake + shake)
parathesia of hand
wasting of thenar eminence

194
Q

investigations and management of carpal tunnel syndrome

A

Dx= clinical based on Sxs

Phalen test= make fist + flex wrist for 1 min
positive> pain + parathesia

Tinel test= tapping wrist > causes tingling

Electromyogram> diagnostic if above tests uncertain

Tx= wrist splint @ night + steroid injections
last resort > surgery 2 decompress

195
Q

describe wrist drop

A

radial nerve palsy > C5-T1, innervates forearm extensor muscles

Sxs= wrist drop + loss of sensation in dorsal hand & lateral 3.5 fingers

Tx= splint + simple analgesia

196
Q

describe claw hand

A

ulnar nerve palsy>C8-T1, motor innervation to part of forearm + most of hand

Sxs= claw hand, difficulty straightening fingers, numbness along forearm, wrist, ring + little finger

Tx = splint + simples analgesia

197
Q

what is sciatica and what are causes of it

A

lower back pain + Sxs associated w. irritation of the sciatic nerve: L4-S3

causes:
spinal= disc herniation/prolapse
non-spinal= piriformis syndrome, tumours, pregnancy

198
Q

presentation of sciatica

A

unilateral pain from buttock > down lateral leg > pinky toe
weak plantar flexion + absent ankle jerk reflex
leg weakness

199
Q

investigations and management of sciatica

A

Dx=
1st- SOCRATES + physical examination (no ankle reflex + can’t do straighten leg raise test w.out pain)

GOLD= MRI spinal cord

Tx= analgesia - NSAIDS/amitriptyline
+ physio

surgery- decompression

200
Q

what are causes of motor and sensory polyneuropathies

A

polyneuropathies= glove + stocking presentation

MOTOR= mc Guillian Barre
SENSORY= mc. diabetic neuropathy

other causes= vasculitis, malignancy, B12 def, RA

201
Q

what are cranial nerve lesions and where do CN 3-12 stem from

A

damage to a nerve via trauma, compression, infection> results in interruption of axonal continuing

nerves 3-12 come from brainstem
therefore brainstem pathology = cause
eg trauma, tumour, multiple sclerosis

202
Q

describe lesions of cranial nerves 1-6

A
  1. olfactory= impared/loss of sense of smell
  2. optic= blindness, visual field defects

3.occulomotor= ptosis, down + out eye, fixed and dilated pupil

  1. trochlear= diplopia looking down
  2. trigeminal= jaw deviates to 1 side, loss of corneal reflex, causes= trigeminal neuralagia: sensory/motor jaw pain in v1/2/3
  3. abducens= adducted eye, inability 2 look laterally > sign of raised ICP
203
Q

describe lesions of cranial nerves 7-12

A
  1. facial= facial droop w. forehead sparing
    causes= Bell’s palsy + parotid inflammation
  2. vestibulocochlear= loss of hearing + balance
    causes= skull changes (eg Paget’s) compression, middle ear disease
  3. glossopharyngeal= impaired gag reflex
  4. vagus= impared gag reflex, swallowing, respiration, vocal issues
    causes= jugular foramen lesion
  5. accessory= can’t shrug shoulders or turn head against resistance
  6. hypoglossal= tongue deviation towards affected side
204
Q

describe myasthenia gravis

A

autoimmune condition causing disorders of neuromuscular transmission > due 2 binding of autoantibodies to components of the neuromuscular junction
-mc. acetylcholine receptor

(antibodies destroy the connections between nerves and muscles= weakness in skeletal muscles)

205
Q

describe the pathology of myasthenia gravis and what is condition related to in females/males

A
  1. autoantibodies bind to post-synaptic receptor> competitively inhibit Ach binding
  2. more receptors blocked during exertion - leads 2 more muscles weakness
  3. autoantibodies activate compliment system > damages cells at post-synaptic membrane

females- related 2 autoimmune disease
males- related to thyoma

206
Q

presentation of myasthenia gravis

A

Sxs get worse throughout the day:
musc weakness- worse w. exercise, better w. rest- starts @ head and neck > progresses to lower body

weak eye muscles- diplopia, ptosis
weakness more marked in proximal muscles
jaw fatiguability
swallowing difficulty
myasthenia snarl > difficulty smiling , looks creepy

(DDx= Lambert Eaton syndrome BUT Sxs improve w. exertion)

207
Q

investigations for myasthenia gravis

A

GOLD= clinical diagnosis + serology:
-detection of Acetylcholine receptor antibodies (ACh-R)
-detection of MuSK (Muscle-specific kinase antibodies)

208
Q

management of myasthenia gravis

A

1st= acetycholinesterase inhibitors eg pyridostigmine or neostigmine

2nd= immunosuppression (steroids> prednisolone)

209
Q

what is a myasthenic crisis + treatment

A

acute Sxs worsening + acute respiratory weakness

Tx= plasma exchange + IVIg + BiPAP ventilation 4 resp failure

210
Q

describe Guillain barre and who does it mc affect

A

acute polyneuropathy causing rapid damage to peripheral nerves = in demyelination + axonal degeneration

mc. males: peak ages
15-35
50-75

211
Q

what is mc common cause of Guillain barre and what is the underlying pathology

A

GB mc. presents post GI infection
-CAMPYLOBACTER JEJUNI

also can be caused by EBV, CMV, HIV

path=
B cells create antibodies against antigens on pathogen that caused infection
- these antibodies also match proteins on the nerve cells
>therefore they may target proteins on the myelin sheath of the motor nerve cell or axon

212
Q

presentation of Guillain Barre

A

post infection, presents w/:
ascending asymmetrical weakness + paralysis (from nose 2 toes)
parathesia
loss of deep tendon reflexes
peripheral loss of sensation or neuropathic pain
cranial nerve facial weakness
absent reflexes (LMN sign)

+in 50%- autonomic nervous system involvement >decreased sweating + heat intolerance, urinary hesitation

+ in 35% > resp failure

213
Q

investigations for Guillain Barre

A

1st=
Bloods- FBC (normal WCC), U&Es, LFT (raised AST + ALT)

lumbar puncture @L3/4= raised protein + normal WCC > inflammation + no infection

nerve conduction studies > decreased conduction velocities, downward conduction block

spirometry + resp func test

GOLD= Brighton criteria>
> clinical Sxs + lumbar puncture CSF analysis + nerve conduction studies

214
Q

management of Guillain Barre

A

IVIg for 5 days with plasma exchange (CI in IgA def patients- allergic reaction)
DVT prohylaxis- LMWH

215
Q

describe wernicke’s encephalopathy

A

reversible acute emergency due to severe B1 (thiamin) deficiency
cause= mainly alcohol

Sxs= ataxia, confusion, ophthalmoplegia (paralysis/weakness of extra-ocular muscles)

Dx= clinical Dx, supported w. microcytic anaemia + deranged LFTs

Tx= pabrinex 5 days
oral thiamine prohylaxis

216
Q

describe Duchenne Muscular dystrophy (including Sxs + who is normally affected)

A

x-linked recessive condition- characterised by progressive musc. wasting + weakness
muscle replaced with adipose

only affects boys

217
Q

presentation, diagnosis and management of Duchenne muscular dystrophy

A

difficulty getting up (gower’s sign)
skeletal deformities eg scoliosis

Dx=
raised serum creatinine kinase
musc. biopsy w. assay for dystrophin protein

GOLD= genetic analysis

Tx= purely supportive

218
Q

what is Charcot Marie tooth disorder

A

autodom mutation causing damage to myelin or axons causing PNS polyneuropathy

childhood> adulthood onset

219
Q

presentation, diagnosis and management of Charcot Marie tooth disorder

A

Sx=
foot drop, stork legs (v. thin calves), hammer toes (toes always curled up), feet- pes cars (high foot arch), reduction in deep tendon reflexes

Dx= nerve conduction studies, genetic testing

Tx=orthotics + physio

220
Q

define depression and name 4 risk factors

A

persistent low mood, loss of interest and enjoyment + reduced energy causing social and occupational dysfunction

RFs= postnatal status, FHx, dementia, stress

221
Q

investigations for depression

A

need 5/9 Sxs most of the day, nearly everyday:

1.persistent low mood
2.lack of interest/pleasure
3.wt. loss/gain
4.inability to sleep/oversleeping
5.physcomotor agitation
6.fatigue
7.feelings of guilt/worthlessness
8.lack of concentration
9.thoughts of death/suicide

b. Sx cause sig stress in daily life
c. not due to sub. or other med conditions
d. Sx cannot be explained by another mental disorder
e. no mania episodes

222
Q

management of depression

A

non-pharm= physical activity, healthy diet, physcotherapy, CBT

antidepressants=
SSRIs eg citalopram
manomine oxidase inhibitors eg isocarboxazid
tricyclic antidepressants eg amitriptyline

Phase 2a (12 decks)

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