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FINALS > Neurology FC > Flashcards

Neurology FC Flashcards

1
Q

what are the two types of stroke?

A

ischaemic or haemorrhagic

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2
Q

describe a stroke

A

A clinical syndrome consisting of rapidly deteriorating clinical signs

focal or global disturbance lasting over 24 hours or leading to death

no other apparent cause other than that vascular origin

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3
Q

what two things can lead to an ischaemic stroke

A

vascular occlusion or stenosis causing a decrease in blood flow

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4
Q

what are the causes of vascular occlusion which leads to ischaemic stroke

A

large artery atherosclerosis causing thrombus formation

small vessel (lacunar) thrombosis

cardio embolism venous thrombosis vasculitis

sickle-cell anaemia

hyper- coagulated state

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5
Q

what are the risk factors of ischaemic stroke

A 
over 55 
past medical history of TIA or ischaemic stroke 
hypertension 
smoking diabetes 
mellitus 
atrial fibrillation 
carotid stenosis
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6
Q

what areas of the brain does the anterior cerebrum artery supply

A

part of the frontal lobe
- motor cortex sensory cortex

part of the parietal lobe

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7
Q

what areas of the brain does the middle cerebral artery supply

A

lateral aspect of the frontal lobe
- part of the motor cortex and sensory cortex

part of the parietal lobe

part of the temporal lobe

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8
Q

what part of the brain does the posterior cerebral artery supply

A

the occipital lobe

some of the temporal lobe

some of the parietal lobe

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9
Q

what is a function of the frontal lobe

A

executive functions thinking planning organising problem-solving emotions and behavioural control/personality

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10
Q

what is a function of the parietal lobe

A

perception
making sense of the world
arithmetic
spelling

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11
Q

what is the function of the temporal lobe

A

memory understanding, language

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12
Q

what are two quick toolkits that can assess the risk of symptoms being caused by stroke

A

FAST + ROSIER

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13
Q

describe the presentation of stroke

A

anonymous Hemienopia/transient visual defects aphasia ataxia dysarthria

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14
Q

what visual defect is classic for a stroke involving the posterior cerebral artery

A

diplopia

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15
Q

what visual defect is a classic sign for a stroke involving the anterior cerebral artery

A

gaze paresis

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16
Q

if hemiparesis is present what type of stroke causes indicate

A

lacunar

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17
Q

what must you exclude in the diagnosis of a stroke

A

hypoglycaemia

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18
Q

what is the key window of time between onset of symptoms and management in a stroke

A

four and 1/2 hours so urgent admission in less than four hours is required

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19
Q

what investigation should you order promptly when arriving to hospital with a patient with suspected stroke

A

non-contrast CT (due within one hour of admission)

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20
Q

what are the criteria for ordering a non-contrast to CT in a ?stroke

A 
patient on anticoagulation 
indications for thrombolysis 
bleeding tendency GCS <13  
unexplained progressive or fluctuating symptoms severe headache at onset of stroke symptoms papilloedema 
neck stiffness or fever
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21
Q

why does a normal CT scan not rule out stroke

A

particularly in the first few hours CT scan can be normal or show very subtle changes of ischaemia

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22
Q

in a patient with ?stroke what should be done if GCS is rapidly decreasing or is <8

A

endotracheal intubation

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23
Q

what should the target oxygen be in a patient with ?stroke

A

~96% give oxygen only asserts less than 95%

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24
Q

what is the first-line treatment of an ischaemic stroke if caught within 4/2 hours

A

I V altepase

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25
Q

why is it tight glycaemic control important in the management of stroke

A

hyperglycaemia is associated with intracranial bleeding and poor outcomes

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26
Q

would you give antihypertensive medication to individuals with ?stroke

A

only if they are in a hypertensive crisis such as hypertensive encephalopathy hypertensive neuropathy hypertensive cardiac failure/myocardial infarction aortic to section pre-eclampsia/eclampsia

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27
Q

what continuous checking should you perform in a patient with an ischaemic stroke

A

BMs, 12hr ECG for AF and monitoring ICP

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28
Q

if a ?stroke patients ICP is increasing what should you do

A

repeat CT

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29
Q

what are the indications for urgent referral to neurosurgery

A

large MCA or cerebellar impactsor PCA or if thrombolysis is contraindicated

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30
Q

what is the ongoing management of stroke

A

aspirin or an antiplatelet

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31
Q

what is the most common reason for haemorrhagic stroke

A

cerebrovascular changes induced by hypertension

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32
Q

what are the causes of haemorrhagic stroke

A

uncontrolled hypertension cerebral amyloid angiopathy (this is one of the few primary non-hypertensive causes) anticoagulant associated haemorrhage cerebrally infarct also rebuild tumour brain AVM cocaine and amphetamine drug abuse

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33
Q

what are the symptoms of a haemorrhagic stroke

A

headache (either insidious or thunderclap) sudden onset which progressively worsens neurological symptoms depend on the location of the bleed but are very similar to that of an ischaemic stroke

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34
Q

what features in a patient’s history would indicate a subarachnoid haemorrhage/haemorrhagic stroke

A

thunderclap headache and symptoms of meningism

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35
Q

what as a first-line diagnostic test for haemorrhagic stroke

A

CT with or without angiogram - angiogram will be performed later anyway but sometimes not the first step

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36
Q

what blood should you perform in a haemorrhagic stroke

A

full blood count renal function tests clotting factors

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37
Q

apart from blood tests and imaging what else would you perform in a patient with ? Haemorrhagic stroke

A

ECG looking for ischaemic changes or arrhythmias

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38
Q

what is the target range of blood pressure in a haemorrhagic stroke and why is this important

A

160-140 // blood pressure which is too high will worsen the symptoms especially in subarachnoid haemorrhage so you wouldn’t want to lower the blood pressure but still maintains cerebral perfusion

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39
Q

a patient presents with a haemorrhagic stroke when you monitor their ICP rapidly increases what does this indicate

A

acute hydrocephalus

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40
Q

what is the management of an acute hydrocephalus

A

external ventriculostomy

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41
Q

what is management of raised ICP

A

analgesia and sedation external drainage mannitol or hypertonic saline neuromuscular blockade and deep sedation high-dose barbiturates nb. In causes of increased ICP that aren’t of inflammatory nature such as a tumour or infection corticosteroids are not useful

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42
Q

what are the indications for neurosurgery in the management of a haemorrhagic stroke

A

de-compensating or becoming clinically unstable or has a large bleed greater than 3 cm

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43
Q

patients are not surgical candidates what is the management of a haemorrhagic stroke

A

hydration and nutrition

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44
Q

what is a TIA

A

transient episode of neurological dysfunction caused by focal brain spinal or retinal ischaemia without acute infarction lasting from the minutes to 24 hours but never more than 24 hours

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45
Q

what scoring system can help establish if thrombosis is necessary

A

NIHSS – National Institutes of Health Stroke Scale

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46
Q

what is the main indication that the TIA has occurred not/

A

most TIAs already have a score which is decreasing within an hour of onset of symptoms (ROSIER score)

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47
Q

what is the initial management of a TIA

A

loading dose of aspirin

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48
Q

is CT required in TIA

A

no because the changes on TIA are so small CT cannot pick up

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49
Q

what investigations should be performed in a TIA

A

FBC PTT+INR fasting lipid electrolytes glucose ECG (trying to find any causes)

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50
Q

what is the management of a TIA

A

after initial loading dose of aspirin referred to a TIA clinic within 24 hours and then start statin as soon as TIA has been confirmed

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51
Q

why is referral to a TIA clinic within the next 24 hours important

A

risk of stroke is very high within the 10 days following TIA

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52
Q

what is amourisis fougax

A

a temporary painless loss of vision in one or both eyes

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53
Q

what are the causes of amourisis fougax

A

embolus (carotid atherosclerosis GCA vasculitis) anything which blocks the retinal ophthalmic or ciliary artery ocular causes (blepharitis iritis conjunctivitis) neurological conditions (optic new writers papilloedema MS migraine tumour) TIA and stroke

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54
Q

how would you investigate amourisis fougax

A

usually investigation depends on what other symptoms are accompanying amourisis fougax

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55
Q

what would be the management of anything atherosclerotic in amourisis fougax

A

aspirin

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56
Q

what is a subdural haematoma

A

a collection of blood between the juror and the arachnoid matter

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57
Q

describe the layers of the brain

A

insert image here

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58
Q

what is the pathophysiology of a subdural haematoma

A

usually caused by trauma anything which impacts the bridging cortical veins which empty dural venous sinuses

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59
Q

what is the presentation of a subdural haematoma

A

recent trauma with loss of consciousness or decreased GCS seizures ( can have loss of bladder and bowel function) headaches nausea and vomiting confusion diminished by response motor or vertebral response decreased in GCS score

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60
Q

what do unequal pupils indicate

A

herniation

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61
Q

what are the signs of a basilar skull fracture

A

ortorrhoea / rhinorrhoea / racoon eyes

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62
Q

what three things should you check quickly when dealing with a sub dural haematoma

A

check hypoglycaemia temperature and venous blood gases (this is the deadly triad

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63
Q

what should you try and establish in the history of a patient with a subdural haematoma

A

use of aspirin or anticoagulant/antithrombotic and any history of liver or renal disease to assess platelet and coagulation factors

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64
Q

what is the criteria for performing a CT head scan in the patient with ? Subdural haematoma

A

GCS lesson 13 on initial assessment or lesson 15 at two hours after initial assessment suspected open or depressed skull fracture any sign of basal skull fracture any focal neurological deficit episode of vomiting or post-traumatic seizure

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65
Q

for subdural haematoma in CT

A

banana shaped bleed

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66
Q

what is the management of subdural haematoma

A

any haematoma greater than 10 millimetre requires surgery + medical management. Othwerwise just medical management. - prophylactic antiepileptic’s coagulopathy correction and managing ICP

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67
Q

what the usual causes of an extradural haematoma

A

trauma

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68
Q

why do extradural haematoma is usually occur

A

temporo-parietal lobe

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69
Q

which vessel is usually affected in an extradural haematoma

A

middle meningeal artery

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70
Q

describe the pathophysiology of extradural haematomas

A

an increased volume of blood strips the juror and the meninges away from the skull and have large enough compresses the brain structures and increases ICP death can occur from midline shift or tentorial herniation

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71
Q

what is presentation of an extradural haematoma

A

history of trauma with loss of consciousness or fluctuating consciousness with then a period of lucidity occurring followed by rapid deterioration loss of consciousness reduced GCS may have blown pupil and contralateral hemiparesis

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72
Q

what does a blown pupil indicate in an extradural haematoma

A

there is a cranial nerve three palsy

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73
Q

what the station is diagnostic of an extradural haematoma and what is the result

A

non-contrast CT showing lemon -shaped bleed

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74
Q

what is the management of an extradural haematoma

A

surgery is almost always required medical management is based on reducing ICP but is often used alongside surgery

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75
Q

what are the complications associated with extradural haematoma’s

A

infections if there is skull fracture ischaemia post-traumatic epilepsy cognitive impairment hemiparesis hydrocephalus brainstem injury and death

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76
Q

what are the two most common causes of subarachnoid haemorrhage

A

traumatic or from spontaneous burst of aneurysm

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77
Q

what is the function of the arachnoid and pia mater

A

the arachnoid and pia mater cover the brain service and key in protecting from intracerebral infections the arachnoid also holds arachnoid villi which absorb CSF

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78
Q

what is the presentation of a subarachnoid haemorrhage

A

thunderclap headache peaking at one – five minute lasting around one hour with associated symptoms of vomiting nausea photophobia with a reduced and falling GCS and meningism

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79
Q

what is the initial management of subarachnoid haemorrhage

A

intubate them subarachnoid haemorrhages will always require intubation eventually so into early give isotonic fluids and check pupils every 20 minutes

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80
Q

what investigations should be performed in a subarachnoid haemorrhage

A

FBC U+E LFT non-contrasted CT +/- angiogram

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81
Q

when is a lumbar puncture indicated in the investigation of the subarachnoid haemorrhage

A

from onset of symptoms

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82
Q

as soon as you diagnose a subarachnoid haemorrhage what is the first line management

A

nifedipine preventing cerebrally ischaemia

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83
Q

how does nifedipine prevents cerebral ischaemia

A

stops arterial vasospasm

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84
Q

if the subarachnoid haemorrhage was caused by an aneurysm what is the long-term management

A

aneurysm should be secured within 48 hours so-called neurosurgeon

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85
Q

what are some potential consequences of subarachnoid haemorrhage

A

re bleed or acute hydrocephalus

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86
Q

Describe the typical symptoms of parkinsonism

A

bradycardia rigidity tremor and postural instability

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87
Q

described the pathophysiology of Parkinson’s disease

A

an unknown process causes loss of dopaminergic neurons in the substantia nigra of the basal ganglia/cells in the substantia nigra degenerate and deposit proteins which formally bodies these correlates with dementia and cognitive impairment/decrease in the dopamine production causing a decreased activation of direct basal ganglia pathway thus decreasing the movement initiation/decrease of inhibition of the indirect basal ganglia pathway increases movement inhibition there is also impaired regulation of muscle tone causing hypotonia and impaired postural reflexes causing postural instability/these altered feedback loops also cause psychiatric manifestations causing anxiety and depression

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88
Q

describe their direct basal ganglia pathway and how it’s affected in Parkinson’s

A

the motor cortex releases glutamate which activates the striata (dopamine is released by the substantia nigra which also stimulates a straight him)the striatum produces a gabapentin which has inhibit treatment that affects on the globus pallida’s and the substantia nigra these produce some gabapentin which inhibits the thalamus thus allowing for increased excite a treat signals to be produced increasing muscle movement in Parkinson’s decrease in dopamine will mean that the thalamus isn’t inhibited so the thalamus in itself can inhibit excitatory signals to the motor cortex thus decreasing movement initiation

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89
Q

what are syndromes which mimic Parkinson’s disease

A

progressive super nuclear palsy multiple system atrophy Lewy body dementia corticobasal syndroma

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90
Q

what is the presentation of Parkinson’s disease

A

bradycardia resting tremor rigidity micrograph ear decreased facial expressions and hypo phony due to relax muscles and larynx cognitive decline anxiety and depression

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91
Q

if cognitive decline is present what does this mean about the Parkinson’s disease

A

it is advanced

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92
Q

describe the tremor associated with Parkinson’s

A

resting tremor usually asymmetrical at 4 – 6 Hz

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93
Q

describe what is meant by rigidity in Parkinson’s

A

Increase resistance on passive movements and cog wheeling shuffling and astute gate

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94
Q

if there are symptoms of Parkinson’s in anyone under the age of 40 what disease process is actually going on

A

Wilson’s

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95
Q

describe the features of Wilson’s disease and how they differ to Parkinson’s disease

A

Wilsons has an acute not progressive onset Wilsons has a rapid progression of the slow progression Wilsons has early cognitive involvement not late disease stage Wilsons has a symmetrical neurological deficit whereas Parkinson’s is usually asymmetrical Wilsons has upper motor neuron signs

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96
Q

what investigation should you perform in an individual with ?Parkinson’s disease

A

a trial with dopaminergic drugs if there are objective improvements then it is diagnostic any atypical presentations then you should do a MRI ( MRI also indicated if there is cognitive involvement)

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97
Q

describe the management of very mild Parkinson’s disease

A

MOAI - rasagillina dna selegine ( inhibit dopamine catabolism)

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98
Q

describe the management of mild Parkinson’s disease

A

dopamine agonist rapinirole carbidopa levodopa or anti-cholinergics

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99
Q

when word dopamine agonists be first line in the treatment of Parkinson’s

A

in over 70s

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100
Q

why would dopamine agonists not be first line management in individuals younger than 70

A

have a higher side-effect profile of dyskinesia orthostasis and hallucinations

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101
Q

in who wouldnt you give anti-cholinergic drugs for the treatment of Parkinson’s

A

in the elderly (over 65/70) as they have an increased side-effect risk

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102
Q

what is the management of moderate Parkinson’s disease

A

ad anti-cholinergic beta-blocker or DBS to dopamine agonists if symptoms are uncontrolled or if there are motor fluctuations you can try extended action dopamine agonists

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103
Q

nausea and vomiting is a common side effect of anti-Parkinson’s drugs what would you used to treat this

A

domperidone

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104
Q

what is meant by parkinsonian-ism plus

A

Parkinson’s which isn’t idiopathic and has an extra layer to it

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105
Q

what are the types of parkinsonian is plus

A

super nuclear policy called co-basal degeneration multiple system atrophy Lewy body dementia

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106
Q

described the presentation of super nuclear palsies in parkinsonian plus

A

postural instability with vertical gaze palsy symmetrical onset and truncal rigidity

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107
Q

what is the pathophysiology behind super nuclear palsy parkinsonian plus

A

TAU tangles

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108
Q

describe the presentation of cortical basal degeneration in parkinsonian plus

A

apraxia aphasia AsteroGenesis

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109
Q

what is the pathophysiology behind cortical basal degeneration

A

TAU tangles

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110
Q

describes the presentation of multiple system atrophy in parkinsonian-ism plus

A

autonomic dysfunction of postural hypotension bladder dysfunction and cerebellar signs

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111
Q

describe the pathophysiology behind parkinsonian plus multiple system atrophy

A

cell loss and gliosis

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112
Q

what is the most common type of parkinsonism plus

A

Lewy body dementia

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113
Q

what are the symptoms of parkinsonism plus Lewy body dementia

A

variation in cognition visual hallucinations rem sleep disturbances or orthostatic hypotension

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114
Q

what is the pathophysiology behind Louis body dementia

A

alpha synuclein + ubiquitin aka lewi bodies

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115
Q

what genetic defect causes Huntington’s disease

A

repetition of the CAG gene

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116
Q

the XXXX CAG repeats the XXXXX age of onset of symptoms

A

more / younger

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117
Q

Describe the pathophysiology of Huntington’s disease

A

increased to CAG repeat causes excess glutamine to be produced this causes abnormal protein cleavage and accumulations of intracellular toxic aggregates this causes both neural abnormalities from cell death and a global atrophy as well as basal ganglia atrophy and thalamic atrophy . there is also a relative access and dopamine caused by the overexpression of the CAG gene depleting the GABA neurones of the straighten causing an over activation of the indirect pathway so there is less movement inhibition

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118
Q

what other non-neuronal abnormalities of Huntington’s disease

A

death of cardiac myocytes causing cardiomyopathy and skeletal muscle atrophy

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119
Q

describe how chorea and athetosis occurs in Huntington’s disease

A

death of staiatum GABA cells means there is less GABA production thus less inhibition of the globus Pallas this means there is increased inhibition of the subsoil I make nuclei which decreases the activation of the substantia nigra and the globus pallida’s thus decreasing the inhibition on the calamitous and increasing the activation from with the laminators to the motor cortex so there is less inhibition of movements

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120
Q

what are the three modalities in which Huntington’s can present

A

movement cognition and other

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121
Q

describe the movement Sx of hunstingtons

A

Chorea twitching and restlessness Athestosis dysarthria dysphasia dystonia and weakness of muscles on prolonged contractions such as protruding the tounge

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122
Q

describe the cognitive manifestations of Huntington’s

A

changes in personal habits and hygiene disinhibition or unusually anxious behaviour depression obsessions and compulsions

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123
Q

what’s are the other features (apart from movement and cognitive) of Huntington’s

A

systolic heart failure and weight loss and muscle atrophy

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124
Q

what are the earliest manifestations of Huntington’s

A

decreased performance at school or at work

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125
Q

how do you manage chorea of huntingtons

A

tetrabenzine antipsychotics and benzodiazepines

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126
Q

when is tetrabenzine contraindicated

A

in patients with prominent behavioural problems use antipsychotics instead

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127
Q

drugs for chorea be lowered or stopped as disease progresses in Huntington’s

A

because as the disease progresses chorea decreases and rigidity increases the side effects of these drugs may actually make the chorea worse

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128
Q

how would you manage bradykinaesia in Huntington’s

A

dopamine antagonist

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129
Q

what nonphysical manifestation of Huntington’s should be addressed in its management

A

depression treat with SSRI counselling for patients and family

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130
Q

how do you diagnose Huntington’s disease

A

genetic testing looking at CAG repeat

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131
Q

what might you see on MRI or CT of huntingtons

A

caudate or striatal atrophy (only seen in late disease)

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132
Q

what are the differences between huntingtons and parkinsons

A

insert image page 16

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133
Q

What is the presentation of a migraine

A

headaches lasting four – 72 hours if untreated throbbing unilateral pain nausea and vomiting sensitivity to light aura and inability to function

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134
Q

what is acute management of migraine

A

simple analgesia plus a triptan if very nor she has add an antiemetic such as Metoclopramide

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135
Q

when would preventative management be given to migraine sufferers

A

if occurring more than once a week or when they occur they are very prolonged and severe if they are at risk of medication overuse headache such as taking analgesia something else if normal management is contraindicated or ineffective if they have uncommon migraines

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136
Q

what is classed as an uncommon migraine

A

migraine with hemiplegia or a prolonged aura

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137
Q

describes a stepwise treatment of preventative management of migraines

A

propranolol –> topyramate –> amitriptyline

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138
Q

if migraines are linked to the menstrual cycle what preventative management should be given

A

OCP to control cycle

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139
Q

what should the follow-up be of a migraine patient after they have started preventative therapy

A

follow-up after six – eight weeks and again after six – 12 months after a successful therapy has been found then consider withdrawing

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140
Q

What are alternative therapies that manage migraines

A

CBT acupuncture mindfullness riboflavin

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141
Q

when are riboflavins contraindicated

A

pregnancy

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142
Q

A patient presents with intense pain unilaterally around the eye/behind I and temporal area with pain lasting between 15min – 3h when these headaches occur they become restless and agitated and have watery eyes and runny nose sometimes they get nausea and vomiting with photophobia and phonophobia what is the diagnosis

A

Cluster headache

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143
Q

patient presenting with cluster headaches says that they get lacremation and rhinorrhoea What is the name given to these symptoms and what are other examples of this which can occur in cluster headaches

A

autonomic symptoms : partial Horner’s syndrome with ptosis and meiosis conjunctival injection facial swelling and redness

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144
Q

a patient presents with extremely severe pain unilaterally around the iron temporal area which has been lasting an hour and 1/2 new notice that on examination they have ptosis and meiosis what is this

A

partial Horner’s syndrome associated with cluster headaches

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145
Q

what can you tell me about the frequency of cluster headaches wonder they come on

A

attacks are usually psychical at the same time of day or the same time of year and occur in clusters which last seven days – one year with periods of remission in between clusters

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146
Q

what investigations should you perform in a patient who presents with extremely severe unilateral pain around the eye and temporal area

A

CT to exclude subarachnoid haemorrhage and also check for any causes secondary of cluster headaches ESR should be performed to exclude GCA

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147
Q

pituitary adenoma can sometimes cause cluster headaches apart from imaging what tests could you perform to exclude a pituitary adenoma

A

TFT LH FSH cortisol prolactin

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148
Q

describe the acute management of a cluster headache

A

sub cut injection of sumotriptan or intranasal O2 hundred percent for 15 – 20 minutes

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149
Q

how does the management of cluster headaches (acute) change if the patient has cardiovascular disease or uncontrolled hypertension

A

give intranasal Lidocaine instead of sub cut sumatriptan or oxygen therapy

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150
Q

what is the ongoing management of cluster headaches

A

high-dose corticosteroids for transitional therapy or a greater occipital nerve block

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151
Q

a patient presents to you saying that they have ongoing headaches which are dull occurring across all the head feel like a tight band around the head they have no associated autonomic features or aura but do experience some peri-cranial tenderness what is the most likely diagnosis

A

tension-type headache

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152
Q

what is the management of tension-type headaches

A

simple analgesia usually works but if they are chronic relaxation CBT and physiotherapy can help relieve symptoms

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153
Q

which medications can cause medicine overuse headaches

A

basically anything: triptan opioids NSAIDS paracetamol

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154
Q

what is the criteria for a medicine overuse headache

A

headaches occurring on 15 or more days per month if paracetamol or simple analgesia (if trip towns or opioids for combined analgesics 10 or more days) as a result of regular use of headache medication there is been the use of medication for three months or more in a person with a pre-existing headache disorder

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155
Q

what is the management of medicine overuse headache

A

explain what medicine overuse headache is that the only way to make it better is to withdraw analgesia simple analgesia and trip towns can be stopped abruptly and should be stopped for at least one month that they may experience withdrawal symptoms and symptoms may worsen initially to keep a diary of symptoms and maintain good hydration and follow-up should be given after one – two months of stopping analgesia

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156
Q

what other risk factors associated with medicine overuse headache

A

psychological comorbidities family history acquired central sensitisation neurotransmitter abnormalities (reduction 5-HT) people with an underlying headache condition women aged 40 to 45

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157
Q

what is a dermatome

A

an area of skin supplied by a single spinal nerve root and used in sensation

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158
Q

what is a miyotome

A

A group of muscles innovated by a single spinal nerve used for movement and power

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159
Q

shoulder shrugging describes what nerve root

A

C4

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160
Q

shoulder Abduction and external rotation as well as elbow flexion describes what nerve root

A

C5

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161
Q

wrist extension describes what nerve root

A

C6

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162
Q

elbow extension and wrist flexion describes what nerve root

A

C7

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163
Q

thumb extension and finger flexion describes what nerve root

A

C8

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164
Q

finger abduction described what nerve root

A

T1

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165
Q

hip flexion describes what nerve root

A

L2

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166
Q

knee extension describes what nerve root

A

L3

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167
Q

ankle dorsiflexion describes what nerve root

A

L4

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168
Q

big toe extension describes what nerve root

A

L5

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169
Q

ankle plantar flexion describes what nerve root

A

S1

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170
Q

bladder and rectum motor supply describes what nerve root

A

S4

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171
Q

what nerve roots are involved in the cervical plexus

A

C1 – C4

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172
Q

what does the cervical nerve plexus innervate

A

the diaphragm shoulders and neck

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173
Q

what nerve roots are involved in the brachial plexus

A

C5 – T1

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174
Q

what does the brachial plexus innovate

A

the upper limbs

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175
Q

what does the lumbosacral plexus innerate

A

the lower extremities

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176
Q

what nerve roots are involved in the lumbosacral plexus

A

L2 – S1

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177
Q

what is Multiple Sclerosis

A

a demyelinating inflammatory disease characterised by episodic neurological dysfunction in at least two areas of the central nervous system separated in space and time

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178
Q

the patient presents to you with greying or blurring of their vision and some pain when they move one of their eyes it has lasted two days and they have no other symptoms they noted that they have had similar episodes in the past but not as severe and it resolved quickly what would you be suspicious of

A

Multiple Sclerosis

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179
Q

how can Multiple Sclerosis present initially

A

with a history of transient motor cerebellar sensory gait or visual dysfunction periods lasting over 48 hours and are not accompanied by other intercurrent illnesses less commonly can present with onset of weakness after repetitive movements (such as walking long distances causing foot dragging) or in voluntary movements such as cramping or jerks urinary frequency or bowel dysfunction or spasticity and increased muscle tone

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180
Q

how can spinal-cord lesions present in Multiple Sclerosis

A

present with asymmetrical findings and episodes of odd sensations such as wetness or tingling they may also get band like sensations across the body

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181
Q

the patient presents to you with greying or blurring of their vision and some pain when they move one of their eyes it has lasted two days and they have no other symptoms they noted that they have had similar episodes in the past but not as severe and it resolved quickly what investigation should be performed in what may be found

A

optic neuritis showing a pale optic disc

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182
Q

would Multiple Sclerosis show upper motor neurone signs or lower motor neuron signs

A

upper motor neuron

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183
Q

if you suspect a patient has Multiple Sclerosis and when examining the eye movements note nystagmus what does this indicate

A

cerebellar dysfunction

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184
Q

if you suspect the patient has Multiple Sclerosis what is the diagnostic test for MS

A

MRI with contrast

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185
Q

what blood test would you want to perform to exclude differentials for Multiple Sclerosis

A

thyroid function tests vitamin B12 diabetes mellitus (HbA1c and blood glucose)

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186
Q

what are oligoclonal bands and when would they be found

A

in CSF analysis of a patient with MS

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187
Q

what are the four subtypes of Multiple Sclerosis

A

progressive relapsing Multiple Sclerosis secondary progressive Multiple Sclerosis primary progressive Multiple Sclerosis relapsing remitting Multiple Sclerosis

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188
Q

a steady decline since the onset with superimposed tax which then partially resolve what type of Multiple Sclerosis does this describe

A

progressive relapsing

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189
Q

initially has unpredictable attacks which may or may not leave permanent deficits but usually resolved to some degree followed by periods of remission then suddenly begins to have progressive decline without any periods of remission and any superimposed attacks what type of Multiple Sclerosis does this describe

A

secondary progressive

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190
Q

a steady increase in disability without attacks - what type of Multiple Sclerosis does this describe

A

primary progressive

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191
Q

unpredictable attacks which may or may not leave permanent deficits followed by periods of remission what type of Multiple Sclerosis does this describe

A

relapsing remitting

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192
Q

what is the management of an acute flare of Multiple Sclerosis

A

new thou prednisolone IV high-dose oral plasma exchange for patients with severe/rapidly progressing disability

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193
Q

what is the ongoing management of Multiple Sclerosis

A

symptom management and immunomodulators such as interferon beta 1 Alpha - in relapsing remitting corticosteroids in secondary progressive monoclonal antibodies in primary progressive

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194
Q

patient with Multiple Sclerosis has lots of sensory symptoms such as pain what would you give to manage this

A

low-dose anticonvulsants such as gabapentin

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195
Q

a patient with Multiple Sclerosis has an increase in muscle tone what would you give to manage this

A

anti-spasticity medication such as baclofen clonazepam gabapentin

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196
Q

patient with Multiple Sclerosis has a tremor what would you give to manage this

A

propranolol or clonazepam

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197
Q

what is the pathophysiology of Multiple Sclerosis

A

immune system attacks the myelination of neurons this causes demyelination and is disrupts axonal supports leading to its destabilisation causing degeneration

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198
Q

what are signs of upper motoneuron lesions

A

everything goes up brisk reflexes spastic hypertonia muscle weakness babinski sign and other primitive reflexes

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199
Q

where do lesions commonly occur in Multiple Sclerosis

A

the optic nerve the brainstem basal ganglia and spinal-cord

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200
Q

what are the signs that lesions have occurred on the optic nerve in Multiple Sclerosis

A

blurred vision over days optic atrophy can cause optic neuritis

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201
Q

what assigns the lesions occurred on the brainstem in Multiple Sclerosis

A

pyramidal weakness muscle weakness and spastic paraparesis

202
Q

what are signs that lesions have occurred on the basal ganglia/cerebellum in Multiple Sclerosis

A

nystagmus tremor slowed movement ataxia

203
Q

what are signs that lesions have occurred on the spinal-cord in Multiple Sclerosis

A

pins and needles muscle spasms muscle weakness odd sensations such as wetness/tingling band -like sensation

204
Q

what is myasthenia gravis

A

a chronic autoimmune disorder of the post-synoptic membrane at the neuromuscular junction in skeletal muscles

205
Q

what is the pathophysiology of myasthenia gravis

A

chronic autoimmune disorder of the postsynaptic membrane at the neuromuscular junction in skeletal muscles

206
Q

a patient presents with diplopia ptosis with pupils sparing which gets worse as the day goes on what could this be

A

myasthenia gravis with ocular presentation

207
Q

in which three modalities can myasthenia gravis present

A

ocular oropharyngeal generalised

208
Q

what are oropharyngeal symptoms of myasthenia Gravis

A

dysphagia with difficulties chewing dysarthria nasal or slurred speech

209
Q

a patient presents with diplopia and ptosis but pupils bearing some dysphasia you note that they have a flattened or transverse smile and on examination they have proximal with limb weakness with difficulty getting in and out of chairs they tell you that they have trouble also climbing the stairs in their home however there is no evident muscle wasting and reflexes and normal with sensation intact - what could be the diagnosis

A

myasthenia Gravis

210
Q

if a patient with myasthenia Gravis has wasting of muscles what does this mean

A

they have anti MuSK antibodies

211
Q

how does anti MuSK myasthenia Gravis differ from normal myasthenia Gravis

A

the presentation of M US K is more severe has severe facial weakness and atrophy of the face and tongue has a muscle wasting of muscles of the legs and back has a predominant neck and respiratory muscle weakness with frequent progression Myesthenia Gravis crisis also has a poor response to cholinesterase inhibitor therapy

212
Q

what investigations should be performed in a patient which is ? Myasthenia Gravis

A

anti-cholinesterase receptor antibody assay MuSK Ab assey CT of chest

213
Q

why would you want to perform a CT chest in a newly diagnosed patient of myesthenia Gravis

A

to exclude thymoma or thymac hyperplasia

214
Q

what should you do if serological testing is unremarkable in a patient with? myasthenir Gravis

A

repetitive nerve stimulation testing

215
Q

describe the stepwise management of myasthenia Gravis

A

pyridostigmine –> add in corticosteroids or immunosuppressants such as prednisolone or azathioprine do Simek to me if indicated –> add plasma exchange or IVIG –> rituximab –> . Estate mean with immunosuppressants and intermittent IVIG

216
Q

what is a myasthenic crisis

A

is a complication of myasthenia gravis and a medical emergency it’s an exacerbation causing no respiratory drive

217
Q

what is the management of myasthenia Gravis crisis

A

mechanical ventilation plasma exchange or IVIG with adjacent corticosteroids (second line rutiximab) you can also add in galantamine or pyridostigmine

218
Q

what is the management of myasthenic crisis post crisis

A

intermittent IVIG

219
Q

what is the basis for intubation in a myasthenic risis

A

low forced vital capacity and low negative in spiritual force you should not wait for an AVG as acidosis occurs late in the clinical decompensation should have a high level of suspicion

220
Q

what are the triggers of an MG crisis

A

infection aspiration high-dose corticosteroids surgery drug reactions in contraindicated medication failure to comply with medication some cancer therapy trauma

221
Q

what type of drug is galantamine

A

anti-cholinesterase

222
Q

what type of drug is pyridostigmine

A

cholinesterase inhibitor

223
Q

described the difference in pathophysiology between MG and LEMS

A

the function of the presynaptic voltage-gated calcium channels is impaired by autoantibodies resulting in the impaired ACH release rather than the destruction of ACH receptors

224
Q

describes the distribution of MG and LEMS

A

MG: crania bulbar LEMS: largely truncal

225
Q

describe the fluctuations in MG and LEMS

A

MG: worse after exertion LEMS: better after exertion

226
Q

describe whether MG + LEMS are somatic versus autonomic

A

MG: somatic LEMS: somatic + autonomic

227
Q

describe the presence of reflexes in MG and LEMS

A

MG: present even in fatigue LEMS: absent but restore

228
Q

describe the result of the 1Tensilon test in MG and LEMS

A

MG: positive LEMS: negative

229
Q

which antibodies are present in MG?

A

Anti nAChR + sometimes anti MSK

230
Q

which antibodies are present in LEMS?

A

Anti VGCC

231
Q

what diseases are associated with myasthenia gravis

A

thymic or autoimmune disease

232
Q

what diseases are associated withLEMS?

A

cancer mostly S CLC

233
Q

what is Duchenne muscular dystrophy

A

a progressive generalised muscular disease causing the breakdown of muscle with most patients losing the ability to walk by 12 years and requiring ventilatory support by 25

234
Q

describe the pathophysiology of Duchenne muscular dystrophy

A

there is absence of the glycoprotein dystrophin distribution provides skeletal structural stability to the skeletal cell membrane without dystrophin there is ongoing cell membrane depolarisation due to calcium entering the cell this in turn causes degeneration and regeneration of muscle fibres however degeneration occurring much faster so muscle fibres undergo necrosis muscle cell proteins are then replaced by adipose and connective tissue causing the muscle to progressively weaken

235
Q

which other areas apart from skeletal muscle does Duchenne muscular dystrophy affect and how

A

affects the brain and smooth muscle cells causing increased processing time reviewing lower intelligence and causing cardiomyopathy and prolonged intestinal transit

236
Q

parent comes to you with the child they are worried because they are having delayed motor milestones you notes that there is calf hypertrophy and proximal hip girdle muscle weakness causing a strange gait what could be the diagnosis

A

Duchenne muscular dystrophy

237
Q

how can Duchenne muscular dystrophy present at birth

A

are floppy hypotonic baby this is uncommon

238
Q

how does Duchenne muscular dystrophy manifest in children

A

there is an imbalance of strength with flexors being stronger than extensors at all lower extremity pivots causing growers sign and muscular tenderness contractures

239
Q

describe growers sign in Duchenne muscular dystrophy

A

the patient climbs up their body to come to a stand

240
Q

what do muscular tenderness contractures cause in children with Duchenne muscular dystrophy

A

lumbar lordosis and heel cord contracture causing patients to walk on their toes with a wide based modelling unstable gait

241
Q

a patient presents with their child who has lordosis and walks on their toes causing a wide base waddling unstable gate you note that there is some heel cord contracture and when the child wants to come to stand they have to climb up the body on examination reflexes are diminished muscle tone is diminished but sensation is preserved what is the diagnosis

A

Duchenne muscular dystrophy

242
Q

what behavioural changes do children with Duchenne muscular dystrophy show

A

hyperactive with attention deficit and learning disorders

243
Q

how would you diagnose Duchenne muscular dystrophy

A

creatinine kinase is a first-line investigation this is normally very elevated once this has been found DNA analysis is performed which is diagnostic

244
Q

what is the management of a child with Duchenne muscular dystrophy who is ambulatory

A

corticosteroid physiotherapy exercise and psychological support

245
Q

what is the management of a child with Duchenne muscular dystrophy who is a non-ambulatory

A

supportive therapy trying to maintain activities of daily living using aids such as wheelchairs and psychological support

246
Q

what is the management of a child with Duchenne muscular dystrophy who needs ventilation

A

ventilation of IP PV to support inspiration muscles

247
Q

what complications can occur in Duchenne muscular dystrophy and what is the management

A

muscle contractions – surgery heart failure - lisinopril malnutrition due to tachyopnea - intermittent positive pressure ventilation and nutritional supplements scoliosis over 40° - surgery

248
Q

What are the five types of motor neuron disease

A

ALS and Merlot trophic lateral sclerosis PBP progressive bulbar palsy PP pseudo-bulbar palsy PMA progressive muscular atrophy MMA monomelic amylotrphy

249
Q

describe what occurs in amylotrophic lateral sclerosis

A

death of voluntary muscle neurons - there is neurodegeneration characterised by the degeneration of motor neurons in the cortical brain stem in the ventral cord

250
Q

describe what occurs in progressive bulbar palsy

A

neuron death of bulbar muscles like head and neck

251
Q

describe what happens in pseudobulbar palsy

A

inability to control facial muscles without any neuron death

252
Q

what is the general presentation of ALS

A

combination of upper motor neuron and lower motor neuron symptoms commonly present with limb or bulbar onset less frequently can present with respiratory onset

253
Q

describe upper motor neuron signs of ALS

A

stiffness and poor balance spastic and unsteady gait painful muscle spasms of hyperreflexia

254
Q

Describe lower motor neuron signs of ALS

A

difficulty arising from chairs and climbing stairs foot drop difficulty maintaining correct posture muscle atrophy

255
Q

what is an early sign of ALS

A

thenar wasting

256
Q

individual present to you with muscle twitching and pianful cramps, there is some muscle waisting and they complain that they have recently had trouble swallowing and also trouble doing up their buttons what is one of your differential diagnoses

A

ALS

257
Q

as disease progresses what can manifest in symptoms in ALS

A

spastic tetra paresis dysphonia coughing and choking strained slurred speech poor respiratory drive

258
Q

how do you diagnose ALS

A

is a clinical diagnosis of exclusion there is neural imaging of the whole spine and brain (especially if there are any signs of bulbar onset) EMG and NCS for show abnormalities a CSF analysis and HIV screen should be performed to find other causes and creatinine kinase will be raised

259
Q

what is the management of ALS

A

rulizole + managing symptoms

260
Q

how would you manage spasticity in ALS

A

baclofen

261
Q

how to manage muscle weakness in ALS

A

physiotherapy

262
Q

how would you manage poor inspiratory drive in ALS

A

non-invasive positive pressure ventilation

263
Q

if a patient has significant bulbar upper motor neuron signs what compliaction can occur

A

abnormal affect this is called pseudobulbar affect and can be treated with amitriptyline

264
Q

what is encephalopathy

A

inflammation of the brain power and climate associated with neurological dysfunction – altered state of consciousness or focal neurological signs

265
Q

which type of pathogen usually causes encephalopathy

A

viruses

266
Q

which viruses most commonly cause encephalopathy

A

herpes most common and enteric viruses such as coxsackie poliovirus but really most viruses can

267
Q

which bacteria can cause encephalopathy

A

Neisseria meningitidis syphilis listeria some strains of strep and staph TB kleibisella

268
Q

what are non-infectious causes of encephalopathy

A

/and haemorrhage SLE vasculitis metabolic hypoglycaemic autoimmune drugs and alcohol

269
Q

what are the signs and symptoms of encephalopathy

A

altered mental status can have focal neurological abnormalities such as hemiparesis pyramidal signs cranial nerve deficits in voluntary movements seizures and any signs of the causative agent such as fever or rash

270
Q

describe the differences between meningitis and encephalitis

A

both usually have fever and leucocytosis encephalitis will only sometimes have meningeal irritation but will nearly always have mental status changes (meningitis slightly less often) seizures are very uncommon in meningitis but very common in encephalitis and focal neurological findings are hallmark feature of encephalitis whereas it is an advanced feature of meningitis (even then only occurs in 50%)

271
Q

what should you be aware of when performing a lumbar puncture and CSF analysis in ? Encephalopathy

A

causative agent is only identified in 50% of cases

272
Q

what investigations should you run in encephalopathy

A

lumbar puncture and CSF analysis plus cultures full blood count U+E blood cultures liver function test urine cultures MRI chest x-ray if signs of things like a stroke or a vasculitis look for autoantibodies and performer CT head

273
Q

what is the management of encephalopathy

A

it is a medical emergency requiring management in ICU if you suspect a viral cause start empirical antivirals if you suspect bacterial cause start empirical antibiotics suspect fungal cause start IV fluconazole he suspect autoimmune cause give high-dose corticosteroids or immunomodulators

274
Q

what is the management of viral encephalitis

A

IV acyclovir or ganciclovir if CMV

275
Q

what is the management of encephalitis if you do not find a causative agent/ have no idication as to cause

A

This may include endotracheal intubation and mechanical ventilation, circulatory and electrolyte support, prevention and management of secondary bacterial infections, deep venous thrombosis prophylaxis, and gastrointestinal (ulcer) prophylaxis ICP raises give high-dose corticosteroids

276
Q

define a generalised seizure

A

both hemispheres are involved

277
Q

define a focal seizure

A

one part of the brain/lobe is involved

278
Q

an episode of losing consciousness suddenly and then quickly regaining it occurs transiently and the individual doesn’t recognise that they have lost consciousness often looks like they are daydreaming may have poor performance in schools what type of epilepsy has this

A

absence seizure

279
Q

very brief episode usually lasting less than 30 seconds where there is repetitive jerking movements such as headbanging what type of epilepsy is this

A

myoclonic

280
Q

a sudden increase in muscle tone causing them to stiffen and fall what type of epilepsy is this

A

tonic

281
Q

there is a sudden increase in tone causing a fall followed by rhythmic jerking excess saliva production may have tongue biting and incontinence lasting a few minutes

A

tonic-clonic

282
Q

why are tonic-clonic seizures particularly dangerous

A

can cause irregular breathing which can lead to cyanosis

283
Q

an individual has a tonic-clonic seizure they then fall into a deep sleep for several hours this is normal

A

yes deep sleep is a normal feature of tonic-clonic seizures

284
Q

sudden reduction in tone causing an individual to become floppy and can be accompanied by jerky repetitive movements (myoclonic movements) what type of epilepsy is this

A

atonic

285
Q

an individual begins marching and waving arms in circular motions for a transient period of time (hyperkinetic movements) what type of seizure assess

A

frontal lobe

286
Q

when would a Jacksonian March be typical in epilepsy

A

in frontal lobe seizures

287
Q

and individual has auditory and sensory phenomena with feelings of déjà vu they can be lipsmacking and sucking clothing at the same time what type of seizures this

A

temporal lobe

288
Q

and individual gets periods of transient visual distortion what could this be (epilepsy)

A

occipital

289
Q

and individual get altered sensations on one side of the body and a distorted body image at the same time this is transient what type of epilepsy is

A

parietal

290
Q

how would you diagnose epilepsy

A

before EEG do a CT/MRI to exclude any causes of epilepsy as well as bloods blood glucose electrolytes toxicology to exclude other causes

291
Q

if you want to distinguish between a non-epileptic events and a generalised tonic-clonic seizure 10 – 20 minutes after the seizure has ended what test could you perform

A

serum prolactin it is raising generalised tonic-clonic seizures accurately in 10 to 20 minutes after seizure

292
Q

what are antiepileptic drugs which are used in the management of epilepsy

A

sodium valproate carbamazepine Lamotrigine topiramate

293
Q

when would you use gabapentin in the management of epilepsy

A

focal epilepsy

294
Q

describe what a febrile seizure

A

a self-limiting event occurring in afebrile child between the ages of six and five in children who do not have intracranial infections metabolic disorders or histories of febrile seizures

295
Q

what febrile seizures associated with

A

URTI tinnitus media gastroenteritis

296
Q

what are two features which are very indicative of febrile seizures

A

absence of managers am rapid recovery of consciousness after seizure - within 30 minutes preceding febrile illness usually at the start of the illness

297
Q

what are indications for a lumbar puncture in febrile seizures

A

neck stiffness a maculopapular rash focal prolonged or multiple seizures occurring within 24 hours impairment of consciousness history of persistent irritability or lethargy

298
Q

what is management or febrile seizure which lasts over five min

A

benzodiazepine

299
Q

what is status epilitius

A

a convulsive seizure that continues for longer than five minutes or multiple seizures occurring one after the other with recovery in between

300
Q

what is non-convulsive status epilepticus

A

changes in mental status or behaviour from baseline associated with continual seizure activity on EEG just without convulsions

301
Q

in the ABCD management what should you look for in A - status epilepticus

A

signs of obstruction respiratory distress can have compromise from excess secretions blood vomit tongue obstruction jaw lock

302
Q

which type of airway is commonly inserted in status epilepticus

A

nasopharyngeal

303
Q

in ABCD management of status epilepticus what should you look for in step C

A

blood pressure pulse and temperature of peripheries and body temperature capillary refill heart sounds - at this stage trying IV access

304
Q

in the ABCD management of status epilepticus what should be done in step D

A

blood gases blood glucose take bloods if possible check pupillary response do an AVPU

305
Q

what blood should get checked for in status epilepticus

A

cultures a urea and electrolytes liver function tests full blood tests

306
Q

in the ABCD management of status epilepticus what should be looked for in thE

A

assessor skin for rashes marks bruises and ? pregnancy

307
Q

describe the stepwise management of status epilepticus

A

buccal mid as alarm or IV Lorazepam administer second dose of benzodiazepine usually IV Lorazepam call anaesthesiologist and give it phenytoin IV at this point I see is largest should be arriving to give propofol Ivy and muscle relaxants to then intubate

308
Q

what are side effects of Lorazepam

A

bradycardia hypotension respiratory depression has less cardiorespiratory side-effects than diazepam

309
Q

describe the side-effects of phenytoin

A

continuous blood pressure and respiratory rate monitoring is required as well as ECG monitoring as has cardiac effects which can cause arrhythmia bradycardia and heart block

310
Q

what are causes of status epilepticus

A

nonadherence or withdrawal form and come alcohol withdrawal so you will haemorrhage drug overdose metabolic abnormalities of hyponatraemia infections hypoglycaemia hypoxaemia tumour hypothermia eclampsia

311
Q

what should you do one status epilepticus has stabilised

A

find cause and do CT head

312
Q

In which age group are primary brain tumours common

A

children less than 15 years old

313
Q

which cancers can metastasise to the brain commonly

A

lung - this is the most common breast thyroid testicular renal colorectal and skin (malignant melanoma)

314
Q

what is the presentation of the brain tumour

A

symptoms of raised intracranial pressure headaches worse in the morning decreased consciousness nausea and vomiting blurred vision and double vision focal neurological signs can be part of the presentation

315
Q

what focal neurological signs are commonly associated with brain tumours

A

parasthesi of limbs speech disorders and dysphasia seizures and by temporal hemienopia in pituitary cancers

316
Q

what other risk factors associated with brain tumours

A

familial syndromes such as neurofibromatosis ionising radiation and x-ray exposure immunosuppression EBV and HIV previous history of cancer

317
Q

what cancers are associated with HIV

A

primary CNS lymphoma

318
Q

what cerebellar signs can be present in brain tumours

A

disdidokineasi ataxia slurred speech hypoTonia intention tremor nystagmus gait abnormalities

319
Q

why does blurred vision occur if there is raised intracranial pressure

A

because of papilloedema

320
Q

why would a double vision occur in brain tumours

A

a paralytic squint from compression of cranial nerves

321
Q

which diagnostic test is used for brain tumours

A

MRI with contrast of brain chest and abdomen and pelvis (especially if adult to find primary tumour) and biopsy

322
Q

what should you always do before performing a lumbar puncture in cases of raised intracranial pressure

A

perform imaging to assess risk of coning

323
Q

what blood tests are useful in assessing brain tumours

A

FBC U+E calcium liver function tests CRP TFT PSA ( if suspecting prostate cancer)

324
Q

what is the management of brain tumours if there are seizures

A

give anticonvulsants and high dose dexamethasone if seizures are thought to be because of raised intracranial pressure (dexamethasone)

325
Q

if after performing postural changes and giving dexamethasone the ICP is still high in a brain tumour patient what should you do

A

give mannitol

326
Q

if hydrocephalus occurs as a side-effect of brain tumour what is the management

A

ventriculoperitoneal shunt

327
Q

what are side effects of dexamethasone

A

sleep disturbances increase appetite or weight gain and GI reflux

328
Q

what are side effects of radiation to the head for a brain tumour

A

cognitive impairment bone growth retardation hair loss nausea tissue healing problems and skin problems such as blistering and lesions

329
Q

what are consequences of neurosurgery which may occur after surgery for brain tumour

A

paralysis seizures altered personality hydrocephalus

330
Q

what are complications of chemotherapy

A

nausea vomiting anorexia alopecia pain nerve damage cognitive dysfunction increased susceptibility to infections headaches

331
Q

what is a meningioma

A

slow-growing tumour the forms from the arachnoid cells found in the meninges

332
Q

who typically gets meningiomas

A

females aged 45

333
Q

is a meningioma and aggressive cancer

A

now it is usually benign and surgically viable and rarely metastasises

334
Q

why would visual loss occur in a meningioma

A

from optic nerve compression

335
Q

how would you diagnose a meningioma

A

apart from usual blood tests and imaging and angiography is often needed for diagnosis

336
Q

what is a pituitary adenoma

A

a mostly benign brain tumour which can be functional and secrete hormones

337
Q

what are some side effects of having a pituitary adenoma

A

Cushing’s acromegaly diabetes insipidus by temporal Henry Napier hydrocephalus hypopituitarism

338
Q

a pituitary adenoma is diagnosed as a prolactinoma what medical management can be used

A

dopamine agonist

339
Q

what is pituitary apoplexy and wonders occur

A

but unitary apoplexy is a sudden haemorrhage in the pituitary gland which causes a rapid increase in size of the lesion causing tissue necrosis and resulting in sudden onset of visual loss headaches and hydrocephalus it is common in individuals with pituitary adenomas

340
Q

what is an acoustic neuroma

A

a benign tumour of the vestibulocochlear schwann cells

341
Q

what is a presentation of an acoustic neuroma

A

gradual onset of unilateral sensorineural deafness headaches vertigo dizziness unilateral face numbness absent corneal reflex nystagmus and gait abnormalities can occur in large tumours

342
Q

what causes hearing loss in acoustic neuroma

A

compression of the cranial nerve eight

343
Q

what is a craniopharyngioma

A

a fairly common childhood brain tumour derived from residual cells in Rathkes patch arising in the pituitary stalk which can affect both the hypothalamus and the pituitary

344
Q

what is the presentation of a cranipphyaryngioma

A

gross failure diabetes insipidus disorders of sexual dysfunction hydrocephalus by temporal Hemienopia pituitary insufficiency

345
Q

what is a primary CNS lymphoma

A

a type of diffuse large B cell lymphoma

346
Q

what should you test for in primary CNS lymphoma

A

HIV EBV check CD4 count and perform lumbar puncture and cytology

347
Q

what is management of primary CNS lymphoma

A

methotrexate and chemotherapy with radiation and dexamethasone however has poor prognosis

348
Q

what is a medulloblastoma

A

the most common malignant tumour in children which is highly metastatic

349
Q

what is a glioma

A

the most common primary brain tumour in adults and includes astrocytoma glioblastoma multiforme pilocytiticastrocytoma epindymona and oligodendroglioma

350
Q

what is Guilian barre syndrome

A

an acute inflammatory polyneuropathy which is classified according to symptoms by dividing it into axonal and demyelinating

351
Q

describe the pathophysiology of Guilian barre syndrome

A

immune-mediated attack on Schwann cells or the myelin sheath of sensory and motor nerves this is triggered by previous infection most commonly you RTI or gastroenteritis CMV or C. jejuni

352
Q 
a patient presents to you withnumbness
pins and needles
muscle weakness
pain
problems with balance and co-ordination
A

Guilian barre syndrome

353
Q

describe the progression of the muscle weakness which occurs in Guilian barre syndrome

A

symmetrical progressive muscle weakness affecting lower limbs first then upper extremities of distal muscles before moving to the proximal muscles

354
Q

what are the features of Guilian barre syndrome

A

progressive symmetrical muscle weakness ,paraesthesia in feet and hands can occur before the onset of weakness pain may also proceed weakness this can mimic cord compression sinus tachycardia hypertension and can have postural hypotension as well as autonomic symptoms

355
Q

which autonomic symptoms are associated with Guilian barre syndrome

A

urinary retention and ileus

356
Q

described later symptoms of guillian barre symptoms

A

flaccid paralysis with areflexia blurred or double vision poorest rotary drive and dysphasia persistent and severe pain

357
Q

how long does guillian barre symptoms last and how do symptoms change during this time

A

progressively worsens for about a month and then has a period of symptoms remaining the same before gradually recovering

358
Q

what is the diagnosis of guillian barre symptoms

A

imaging such as MRI or CT to differentiate from spinal-cord compression CSF nerve conduction studies and anti-ganglioside antibodies

359
Q

what will the CSF show in guillian barre symptoms

A

raised proteins

360
Q

what is the management of guillian barre symptoms

A

plasma exchange / IVIG plus supportive management of ventilation is respiratory involvement

361
Q

when our IVIG contraindicated in the management of guillian barre symptoms

A

renal failure or IgA deficiency

362
Q

what is cavernous sinus thrombosis

A

formation or thrombus within the cavernous sinus which can either be septic or aseptic

363
Q

where does the infectious origin usually arise in cavernous sinus thrombosis (septic type)

A

middle third of the face of the sinuses teeth or mouth most commonly acute sinusitis

364
Q

what usually causes aseptic cavernous sinus thrombosis

A

thrombotic process as a result of trauma iatrogenic injuries or prothrombic conditions

365
Q

a patient presents who is acutely unwell they say that they have had a unilateral headache around the eyes and back of nose they have a fever and unilateral periorbital oedema although the otherwise starting to look swollen they appear septic what is the most likely diagnosis

A

cavernous sinus thrombosis

366
Q

what is the difference between aseptic and septic presentation of cavernous sinus thrombosis

A

do not demonstrate signs of meningitis or infections and appear less acutely unwell however they still have focal neurological deficits and orbital signs

367
Q

describe the orbital signs associated with cavernous sinus thrombosis

A

unilateral periorbital oedema which spreads to the contralateral eye within 40 hours extra ocular muscle weakness causing proptosis painful ophthalmoplegia

368
Q

describing why the headache associated with cavernous sinus thrombosis is unilateral and in those specific areas

A

because caused by pain from cranial nerve five which innovates the ophthalmic and maxillary branches of the facial nerve

369
Q

why do patients with cavernous sinus thrombosis get ophthalmaplegia which is painful

A

due to pressure on the sixth cranial nerve

370
Q

what structures are found within the cavernous sinus

A

insert picture

371
Q

what investigations should anyone with focal neurological signs and orbital signs require immediately

A

contrast CT/MRI and angiography may be performed if ? Thrombotic cavernous sinus

372
Q

one investigations apart from imaging are required in cavernous sinus thrombosis

A

full septic screen

373
Q

if you suspect cavernous sinus thrombosis what is the immediate management

A

vancomycinwith ceftriaxone

374
Q

once type of cavernous sinus thrombosis has been confirmed what is the management of both aseptic and septic cavernous sinus thrombosis

A

IV antibiotics anticoagulation if there is no haemorrhagic complications and surgical drainage (aseptic requires thrombin lysis supported therapy and anticoagulation unless there is haemorrhage in which case supportive therapy only)

375
Q

what is the most common cause for peripheral neuropathy

A

diabetes

376
Q

what are the most common causes of peripheral neuropathy

A

diabetes thyroid dysfunction vitamin B12 and B6 deficiency renal disease hepatic disease inflammatory disorders such as GBS line amyloidosis vasculitis is sarcoidosis anaemia and multiple myeloma

377
Q

what test should you do to exclude multiple myeloma in the presentation of peripheral neuropathy

A

serum or urine immuno electrophoresis

378
Q

how would you manage peripheral neuropathy caused by diabetes

A

glycaemic control and neuropathic pain can be treated with amitriptyline pregabalin or gabapentin

379
Q

what are the treatment of neuropathic pain

A

amitriptyline pregabalin gabapentin

380
Q

what drugs can give peripheral neuropathy

A

metronidazole nitrofurantoin

381
Q

what signs would you see on the skin in a patient with peripheral neuropathy caused by diabetes

A

drive thin shiny skin which may be hyper pigmented hair loss calluses and ulcers

382
Q

what is polyneuropathy

A

generalised disease of the peripheral nerves which is a frequent manifestation of systemic illnesses

383
Q

what are the more common causes of polyneuropathy

A

diabetes at GBS monoclonal tomography cauda equina toxins and metabolic factors( these usually cause axonal neuropathys)

384
Q

describe the classic manifestation of polyneuropathy

A

symmetrical numbness and paraesthesia in the feet and distal lower extremities fit the stocking and glove distribution

385
Q

what are early motor symptoms associated with polyneuropathy

A

atrophy of the intrinsic muscles and ankle weakness

386
Q

what are the autonomic features which can be associated with polyneuropathy

A

the autonomic nervous system may be involved resulting in changes in bowel habit sweating disturbances and orthostatic light-headedness

387
Q

what is a radiculopathy

A

painting of the nerves at the root which can sometimes also produce pain weakness and numbness such as an sciatica

388
Q

what is myelopathy

A

compression of spinal-cord itself symptoms are usually more severe including poor coordination trouble walking or paralysis

389
Q

describe the nerve distribution of the hand

A

insert picture

390
Q

while most common mono neuropathies of upper extremities

A

compression neuropathies including carpal tunnel syndrome ulnar neuropathy and radial neuropathy

391
Q

what usually causes compression neuropathies

A

mechanical injury and trauma

392
Q

where does compression usually occur which causes carpal tunnel syndrome

A

median nerve at the wrist

393
Q

where does the compression usually occur which causes unar neuropathy

A

elbow

394
Q

where does the compression usually occur which causes radial neuropathy for the axilla

A

trauma or compression of the radial nerve over the spiral groove

395
Q

a patient presents with wrist drop what is the most likely diagnosis

A

radial palsy

396
Q

the patient presents with trouble doing fine movements such as doing up buttons or using coins and there is some pain in the pinkie finger what is most likely diagnosis

A

ulnar palsy - all the nerves supplying the small muscles of the hand

397
Q

patient presents with pain in the thumb index and middle finger which radiates down to the wrist and is worse in the morning the struggles open doors and thus found the pain is worse when texting what is most likely diagnosis

A

carpal tunnel

398
Q

what does the presence of multiple mono neuropathies outside of a compression site suggest

A

vasculitis or segmental demyelination although these are rare

399
Q

what are sensory manifestations of mono neuropathies

A

pins and needles numbness and less ability to feel pain or changes in temperature (particularly in feet burning or sharp pain usually in the feet feeling of pain from something that should not be painful such as a light touch loss of balance or coordination caused by the diminished ability to tell the position of the feet or hands

400
Q

what are the motor manifestations of mono neuropathies

A

twitching and muscle cramps muscle weakness or paralysis thinning or wasting of muscles difficulty lifting up the front part of your foot a.k.a. foot drop or wrist drop if in the hand

401
Q

what are autonomic symptoms of mono neuropathies

A

constipation or diarrhoea feeling sick bloated all belching low blood pressure rapid heartbeat excess sweating or lack of sweating erectile dysfunction difficulty emptying bladder loss of bowel control

402
Q

when can double vision occur in a mono neuropathy

A

cranial nerves are used for vision

403
Q

what type of neuropathy is Bell’s palsy

A

moral neuropathy of the facial nerve cranial nerve seven

404
Q

7/2 of the forehead is unresponsive to movement what type of mono neuropathy is this

A

cranial nerve seven a.k.a. Bell’s palsy

405
Q

the patient can’t abduct the eye (the lateral rectus muscle) what type of mono neuropathy is this

A

cranial nerve six

406
Q

the patient can’t depress rotate or adduct their right (superior oblique) what type of mono neuropathy is this

A

cranial nerve for

407
Q

the patient has a deviated jaw and tongue what type of mono neuropathy is this

A

trigeminal nerve deviated towards the lesion

408
Q

a patient has ptosis of one I and it is also depressed and abducted down and out the people however is reactive what type of mono neuropathy is this

A

cranial nerve III

409
Q

what are the most common types of cervical radiculopathy

A

C5 and 6, C7, C8 and T1

410
Q

what do C5 and C6 do and what would a radiculopathy effect

A

elbow flexion and sensation in the thumb also accounting for bicep reflexes

411
Q

what does C7 do and what would a radiculopathy effect

A

elbow extension and sensation of the middle finger also tricep reflexes

412
Q

what do C8 and T1 do and what would a radiculopathy effect

A

movement of the hand and sensation of the middle of the hand and the forearm

413
Q

what are the most common lumbar radiculopathy is

A

sciatica involving nerves L42S3

414
Q

what does L5 innovate and what would a radiculopathy effect

A

dorsiflexion (standing on heels) sensation of the big toe and dorsum of foot

415
Q

what does S1 innovate and what would have radiculopathy effect

A

plantar flexion (standing on toes) allows the sensation of the little toe and the sole and heel of the foot as well as the ankle jerk reflects

416
Q

what does a radiculopathy mean

A

nerve root compression at the root

417
Q

patient presents with sharp pain in the back and legs which may worsen with certain activities weakness or loss of reflexes of the ankle numbness of the skin and pins and needles in the legs back and bum area what is this

A

sciatica also known as lumbar radiculopathy

418
Q

what other features of radiculopathy is

A

sharp pain in the Dermot home weakness or loss of reflexes in the mire tome numbness of skin pins and needles or feeling abnormal sensations such as paraesthesia in the Dermot home

419
Q

what are the causes of radiculopathy

A

herniated discs bony spurs ossification’s spinal ligaments a.k.a. anything which causes spinal stenosis

420
Q

and individual gets chest pain when walking downhill and they look down at their feet what does this indicate

A

cervical radiculopathy is looking down narrows the spinal canal further

421
Q

what are the investigations of radiculopathy

A

physical exam and examinations to elicit symptoms x-ray or MRI/CT (MRI is best)

422
Q

what is the management of a radiculopathy

A

NSAIDs and other pain medication muscle relaxant (diazepam) physiotherapy and weight loss steroid injections and surgery in severe cases

423
Q

what can be used to manage chronic pain in radiculopathy is

A

amitriptyline

424
Q

what nerve root is affected if a patient has an inability to rise upon tiptoes and inability to plantar flex

A

S1

425
Q

what nerve roots are affected if a patient has foot drop and they are unable to Dorsey Flex

A

common peroneal nerve/L5

426
Q

what nerve roots are affected if a patient has pins and needles and weakness of the farm and index finger as well as loss of bicep weakness/reflex

A

C6

427
Q

one our roots are affected if a patient has middle finger weakness and pins and needles and weakness of triceps/tricep reflex loss

A

c7

428
Q

What is hydrocephalus

A

buildup of fluid in the ventricles within the brain which increases the size of the ventricles and put extra pressure on the brain

429
Q

who is hydrocephalus common in

A

infants and the elderly (over 60)

430
Q

which are three ways in which hydrocephalus can occur

A

obstructive poor absorption overproduction

431
Q

describe the pathophysiology of obstructive hydrocephalus

A

partial obstruction of the normal flow of CSF from one ventricle to another or from the ventricles to other spaces of the brain

432
Q

describe the pathophysiology of poor absorption hydrocephalus

A

poor absorption from the blood vessels often related to inflammation or injury to the brain

433
Q

described a pathophysiology of overproduction hydrocephalus

A

this is the most rare type of hydrocephalus where CSF is produced too quickly then it is absorbed

434
Q

what other risk factors for hydrocephalus in newborns

A

abnormal development of CNS causing obstruction bleeding within the ventricles which is a complication associated with premature birth infection in the uterus such as rubella or syphilis that causes inflammation of brain tissue

435
Q

while the risk factors for hydrocephalus in adults/children

A

lesions or tumours of the brain or spinal-cord CNS infections such as bacterial meningitis or mumps bleeding from the brain from a stroke or head injury traumatic injury to the brain

436
Q

what other types of hydrocephalus

A

communicating non-communicating normal pressure

437
Q

describe a communicating hydrocephalus

A

CSF can flow between ventricles but is blocked at the exit of the ventricles

438
Q

describe a non-communicating hydrocephalus

A

also known as obstructive hydrocephalus the flow of CSF is blocked between ventricles most commonly at the aqueduct of Sylvius

439
Q

where is the aqueduct of Sylvia found

A

between the third and fourth ventricle in the middle of the brain

440
Q

describe a normal pressure hydrocephalus

A

a form of communicating hydrocephalus most commonly in the elderly population arising from the subarachnoid haemorrhages trauma or tumours however can also be idiopathic

441
Q

what is the presentation of hydrocephalus in an infant

A

unusually large head rapidly increasing size of herd a bulging or tense fontanelle poor feeding poor responsiveness to touch poor growth eyes fixed downwards (some setting of the eyes)

442
Q

describe the presentation of hydrocephalus in adults

A

headaches lethargy vomiting loss of coordination/balance loss of bladder control or frequent urge to urinate impaired vision decline in memory/concentration and other skills

443
Q

what other first-line investigations in a? Hydrocephalus

A

ultrasound scan followed by MRI or CT no contrast

444
Q

a patient presents with the loss of coordination and balance and a decline in memory concentration and other skills wonder if it is Parkinson’s disease and perform a leave a dopa challenge however there is no response to therapy what is the alternative diagnosis

A

hydrocephalus

445
Q

what would you see if you perform a lumbar puncture in an individual with hydrocephalus

A

increased opening pressure and symptoms which improve after lumbar puncture

446
Q

what is the treatment of hydrocephalus

A

shunt for endoscopic third ventriculostomy

447
Q

describe the pathway of CSF

A

CSF flows from the lateral ventricles to the interventricular foramina to the third ventricle through three cerebral aqueduct to the fourth ventricle through the lateral and median apertures to the subarachnoid space to the arachnoid villi of the dural venous sinuses to turning to venous blood to the heart and lungs were turns to arterial blood and goes back to their respective ventricles which then secrete it

448
Q

describe cerebral palsy

A

because of neurodevelopmental delay causing abnormalities of movement and posture and limited activity. It is non-progressive disturbance caused by injuries which occur any utero or when younger than two years old

449
Q

what are the types of cerebral palsy

A

spastic: hemiplegia quadriplegic diplegic dyskinetic ataxic

450
Q

what are the possible manifestations of cerebral palsy

A

reduced cognition disturb communication perceptual and sensory disturbances behavioural disturbances seizures secondary MSK problems

451
Q

there is increased muscle tone and brisk reflexes with an abnormal gait which type of cerebral palsy does this describe

A

spastic

452
Q

patient has a spastic cerebral palsy mainly affecting the arms with facial sparing what type of cerebral palsy has this

A

hemiplegic

453
Q

patient has a spastic cerebral palsy affecting the trunk with extensor posturing and poor central tone all four limbs are equally affected what type of cerebral palsy is this

A

quadriplegic

454
Q

what is the most common cause for or drip cerebral palsy

A

hypoxic ischaemic injury

455
Q

patient has spastic cerebrum palsy which affects the legs and arms but legs are affected much more than the arms and hand function is relatively preserved what type of cerebral palsy with this

A

diplegic

456
Q

what is the most common cause for diplegic cerebral palsy

A

periventricular brain damage

457
Q

patient has chorea athetosis and dystonia - what type of cerebral palsy is this

A

dyskinetic

458
Q

what is chorea

A

irregular sudden brief non-repetitive movements

459
Q

what is athetosis

A

slow writhing movements occurring distally such as at the fingertips

460
Q

what is dystonia

A

simultaneous contractions of extensors and flexors of the trunk causing twisting of the body

461
Q

what are the main features of a tactic cerebral palsy

A

delayed motor developments in coordinate movements intention tremor a tactic gate

462
Q

what are the most common problems which children with atonic cerebral palsy can get

A

feeding difficulties

speech impairment

intellectual deficit

urinary incontinence

and variable sensory or proprioception of loss

463
Q

what are causes of cerebral palsy

A

T OR CH infections premature birth vascular incidents including thrombi from the placenta mothers with factor five Leyden causing focal lesions birth asphyxia hyperbilirubinaemia neonatal sepsis RDS intraventricular haemorrhage head injuries neonatal’s seizures early onset meningitis

464
Q

what can cause birth asphyxia

A

instrumental delivery prolonged labour trauma placental abruption

465
Q

what are the investigations for cerebral palsy

A

every child with an equivocal diagnosis of cerebral palsy should have an MRI of the brain

466
Q

what interventions can be done early (nonpharmacological) in soluble palsy

A

early intervention services physiotherapy occupational therapy speech therapy family education directed at helping the child achieved developmental milestones

467
Q

what is the pharmacological management of spasticity in cerebral palsy

A

benzodiazepines Botox phenols severe spasticity using neurosurgical procedures such as intrathecal baclofen

468
Q

what is the medical management of dystonia in cerebral palsy

A

Carbon day or leave a doper as well as —> benzodiazepines and Botox

469
Q

what is the medical management of athetosis in cerebral palsy

A

haloperidol pimozine

470
Q

was the medical management of ataxia in cerebral palsy

A

clonazepam or propranolol - tremour amantadine - balance and coordination

471
Q

what is Alzheimer’s disease

A

a chronic progressive neurodegenerative disorder characterised by global non-reversible impairment in cerebral functioning

472
Q

described the pathophysiology of Alzheimer’s disease

A

characterised by senile amyloid plaques neuro fibrillar eat how tangles and neuronal loss leading to brain atrophy was defects in Ach synthesis at a cellular level

473
Q

what are risk factors for Alzheimer’s disease

A

increasing age female genetic inheritance or family history Down’s syndrome hyperlipidaemia diabetes cerebrovascular disease cardiovascular disease high blood pressure obesity

474
Q

if Alzheimer’s develops before the age of 65 what does this mean

A

it is considered a young onset dementia/early onset Alzheimer’s

475
Q

describe the features associated with Alzheimer’s disease

A

memory loss disorientation nominal dysphasia ape of the declining activities of daily living and instrumental activities of daily living personality changes visuospatial function decline

476
Q

which type of memory loss occurs early in the disease process of Alzheimer’s disease

A

recent memory first

477
Q

how does disorientation usually present in Alzheimer’s disease

A

misplacing items progressing to getting lost

478
Q

when does a pithy manifest in Alzheimer’s disease

A

is a more progressive symptom becoming passive sleeping more not wanting to perform usual activities

479
Q

how do visuospatial decline manifesting Alzheimer’s disease

A

problems with driving or messy handwriting

480
Q

what are features of advanced Alzheimer’s disease

A

severe gait disturbance: slow shuffling gait with stooped posture
poorly dressed
confused disorientated
low mood

terminal disease marked by rigidity and inability to walk or speak

481
Q

what would an MRI show in Alzheimer’s disease

A

general eight trophy with the hippocampus being particularly shrunken

482
Q

what are specific treatments for Alzheimer’s disease

A

cholinesterase inhibitors such as donezepil or rivastigmine in severe disease switch to or add in memantine ethyl aspartate inhibitor

483
Q

however psychiatric manifestations of Alzheimer’s disease treated

A

using SSRI or atypical antipsychotics such as haloperidol

484
Q

what specialist investigations can be employed for Alzheimer’s disease

A

FDG or PET scan CSF fluid analysis for tau or amyloid concentrations which are raised

485
Q

what is Lewy body dementia

A

and neurodegenerative disorder with parkinsonism and progressive cognitive decline prominent executive dysfunction and visuospatial impairment

486
Q

what is the difference between Parkinson’s disease and Lewy body dementia

A

in Parkinson’s disease more motor symptoms occur first in Lewy body dementia cognitive symptoms appear first it all depends on where Lewy bodies first deposit in the brain - base of the brain equals motor symptoms outer layers of the brain equals cognitive symptoms

487
Q

a patient presents with recurrent visual hallucinations of animals cognitive fluctuations REM sleep behaviour disorders and features of parkinsonism such as resting tremor and rigidity what is the most likely diagnosis

A

Lewy body dementia

488
Q

describe how symptoms change as Lewy body dementia progresses

A

gets more motor symptoms (inc. risk of aspiration)and cognitive symptoms become similar to that of Alzheimer’s disease with short-term memory loss behavioural changes and agitation and restlessness

489
Q

what word an MRI show in Louis body dementia

A

generalised cortical atrophy with relatively preserved hippocampus

490
Q

what is a specialist test for Lewy body dementia

A

single photo and emission CT

491
Q

how can you give a definitive diagnosis of Lewy body dementia

A

you can’t can only be made post-mortem with pathological investigation to find Lewy bodies

492
Q

what a Lewy bodies made out of

A

alpha synuclein

493
Q

what is the pharmacological management for Lewy body dementia

A

carbidopa/levodopar for motor symptoms cholinesterase inhibitors - rivastigminw plus psychiatric management of atypical antipsychotics like risperidone and SSRI

494
Q

described vascular dementia

A

are chronic progressive disease of the brain causing cognitive impairment

495
Q

describe the pathophysiology of vascular dementia

A

reduction in blood supply to the brain due to vascular events such as stroke or haemorrhage causing loss of brain parenchyma

496
Q

describes the progression of vascular dementia

A

in theory has a stepwise degeneration with rapid cognitive decline after each vascular event however in practice is not noticeable

497
Q

a patient presents with problems planning organising and decision-making difficulties following series of steps and slowed processing of information (they have functional impairment of higher processing systems) ape with the disinhibition and poor attention with less fluent speech and reduced visuospatial skills what is this type of dementia

A

vascular - has very little memory loss and is not an early symptom of the dementia

498
Q

what our frontal release reflexes and when would they be found

A

things such as grasping or georgette which are signs of frontal cognitive syndrome is usually associated with retrieval memory deficit - associated with vascular dementia

499
Q

what would CT or MRI show in vascular dementia

A

cerebrovascular lesions

500
Q

what is the management of vascular dementia

A

antiplatelet therapy and lifestyle modification with restricted blood pressure control and statin therapy

FINALS (24 decks)

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