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Neurology > Neurology disease > Flashcards

Neurology disease Flashcards

1
Q

Symptoms of muscle disease?

A

weakness of skeletal muscle, SOB, poor swallow, cardiomyopathy, cramp, pain, stiffness, myoglobinuria

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2
Q

Signs of muscle disease?

A

wasting/ hypertrophy, normal or reduced tone and reflexes, motor weakness (nOT sensory)

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3
Q

What are the congenital genetic classes of muscle disease?

A

structural- muscular dystrophies
Contractile- congenital myopathies
Coupling- channelopathies
Energy- enzymes/ mitochondria

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4
Q

What are the acquired classes of muscle disease?

A

metabolic, endocrine (thyroid, adrenal, vit D), inflammatory muscle disease, iatrogenic: medication (steroids/statins)

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5
Q

Examples of muscular dystrophies?

A

Duchenne’s MD, Becker’s MD, facioscapulohumeral MD, myotonic dystrophy, limb-girdle MD

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6
Q

What are channelopathies and give examples?

A

Disorders of Ca, Na, K and Cl channels,
examples include: familial hypokalemicperiodic paralysis (all Ca, Na, K), hyperkalemic periodic paralysis (Na), paramyotonia congenita (Na), myotonia congenita (Cl)

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7
Q

Examples of metabolic muscle diseases?

A

disorders of carbohydrate metabolism (glycogenoses), disorders of lipid metabolism, mitochondrial myopathies/ cytopathies

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8
Q

Examples of inflammatory muscle disease?

A

polymyositis, dermatomyositis

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9
Q

Investigations used for inflammatory muscle disease?

A

high CK, EMG (inflammation and myopathic), biopsy (polymyositis: CD8 cells, dermatomyositis: humeral-mediated, B cells and CD4 cells)

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10
Q

How do you treat inflammatory muscle diseases?

A

immunosuppresion

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11
Q

What is myasthenia gravis a disease of anf how does it present?

A

Myasthenia Gravis is a disease of the NMJ, and symptoms include: fatiguable weakness of limbs, muscles of mastication, ptosis, SOB and diplopia

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12
Q

What investigations would you use for Myasthenia gravis?

A

AChR ab, anti MuSK ab, neurophysiology (repetitive stimulation, jitter), CT chest

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13
Q

How would you treat myasthenia gravis?

A

symptomatic: acetylcholinesterase inhibitor (pyridostigmine), immunosuppresion (prednisolone, steroid saving agent (eg. azathioprine), immunoglobin/ plasma exchange, thymectomy

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14
Q

What does the peripheral nerve consist of?

A

sensory axons (small fibres for pain and temp and large fibres for joint position sense and vibration), motor axons, autonomic axons and nerve sheath (myelin)

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15
Q

Causes of generalised peripheral neuropathy?

A

Hereditary
Infectious (lyme, HIV, leprosy)
Metabolic (alcohol, diabetes, renal, B12)

Toxic (drugs
Inflammatory demyelinating (acute= Guillain Barre syndrome, chronic= chronic inflammatory demyelinating polyneuropathy)
Malignacy (paraneoplastic)

HIM TIM

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16
Q

Symptoms of disease of nerve root?

A

myoromal wasting and weakness, reflex change, dermatomal sensory change

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17
Q

Symptoms of disease of individual nerve?

A

wasting and weakness of innervated muscle, specific sensory change

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18
Q

Symptoms of disease of generalised peripheral neuropathy?

A

sensory and motor symptoms, usually starting distally and moving proximally

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19
Q

Investigations for disorders of the peripheral nerve?

A

blood tests, genetic analysis, nerve conduction studies, lumbar puncture (CSF analysis), nerve biopsy (nb sensory nerve)

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20
Q

What disease is caused from disorder of the anterior horn cell?

A

Motor neuron disease (amyotrophic lateral sclerosis)

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21
Q

Symptoms of motor neuron disease?

A

Combination of UMN and LMN signs: muscle fasciculations, wasting, weakness, increased tone, brisk reflexes (no sensory involvement)

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22
Q

Treatment of Motor Neuron disease?

A

supportive- PEG feed, non-invasive ventilation, physio, OT
Riluzole
Anticipatory/ palliative care

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23
Q

What are the expected signs of cord pathology on upper motor neuron?

A

no wasting, increased tone, increased reflexes (extensor plantar), pyramidal pattern of weakness

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24
Q

What are the expected signs of root pathology on lower motor neuron?

A

decreased tone, decreased reflexes (flexor plantar), weakness

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25
Q

If the dorsal column is affected what symptoms can you expect?

A

decreased vibration snese and joint position sense

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26
Q

If the spinothalamice tract is affected what symptoms can you expect?

A

decreased pain and temperature

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27
Q

What sensory signs can you expect from cord damage?

A

myelopathy- sensory level loss and hemicord Lesion (Brown-Sequard syndrome)

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28
Q

What sensory signs can you expect from root damage?

A

radiculopathy- dermatomal sensory loss

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29
Q

Surgical causes of myelopathy or radiculopathy

A

tumour, vascular abnormalities (haemorrhage, ABM, dural fistula), degenerative, trauma

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30
Q

Types of tumours of spinal cord?

A

extradural, intradural/ extramedullary, intramedullary

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31
Q

Medical congenital/ genetic causes of myelopathy?

A

Friedrich’s ataxia, spinocerebellar ataxias, hereditary paraparesis

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32
Q

Medical acquired causes of myelopathy?

A

Inflammation, infection, vascular, metabolic, malignant, idiopathic

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33
Q

Inflammatory causes of myelopathy?

A

demylination (multiple sclerosis), autoimmune (antibody mediated eg aquaporin 4, lupus)

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34
Q

Infective causes of myelopathy?

A

viral-herpes simplex/zoster, EBV, CMV, measles, HIV
Bacterial- TB, borrelia (Lyme), syphilis, brucella
Other- schistosomiasis

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35
Q

Metabolic causes of myelopathy?

A

B12 deficiency

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36
Q

Causes of spinal cord ischaemia

A

atheromatous disease, thromboembolic disease, arterial dissection, systemic hypotension, thrombotic haematological disease, vasculitis, venous occlusion, decompression sickness, meningovascular syphilis

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37
Q

How does a spinal cord stroke present?

A

pain- back pain/radicular, visceral referred pain, weakness (paraparesis), numbness and paraesthesia, urinary retention followed by bladder and bowel incontinence

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38
Q

How is demyelinating myelitis characterised?

A

by pathological lesions of inflammation and demyelination leading to temporary neuronal dysfunction, white matter is affected

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39
Q

What is pernicious anaemia?

A

autoimmune condition in which antibodies to intrinsic factor prevent B12 absorption

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40
Q

How does B12 deficient myelopathy present?

A

paraesthesia hands and feet, areflexia, degeneration of: corticospinal tracts (paraplegia), dorsal columns (sensory ataxia), painless retention of urine

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41
Q

Types of primary headacche?

A

tension type headache, migraine, cluster headache

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42
Q

Types of secondary headache?

A

tumour, meningitis, vascular disorders, systemic infection, head injury, drug-induced

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43
Q

What are the 5 steps of a migraine?

A

Premonitor, aura, early headache, advanced headache, postdrome

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44
Q

Describe the symptoms in the premonitor stage of a migraine

A

mood changes, fatigue, cognitive changes, muscle pain, food craving

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45
Q

Describe the symptoms in the aura stage of a migraine

A

fully reversible, neuroligal changes: visual somatosensory

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46
Q

Describe the symptoms in the early headache stage of a migraine

A

dull headache, nasal congestion, muscle pain

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47
Q

Describe the symptoms in the advanced headache stage of a migraine

A

unilateral throbbing, nausea, photophobia, phonophobia, osmophobia

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48
Q

Describe the symptoms in the postdrome stage of a migraine

A

fatigue, cognitive change, muscle pain

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49
Q

How long does the aura stage of a migraine last and why?

A

15-60 minutes

and you get transient neurological symptoms resulting from cortical or brainstem dysfunction

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50
Q

Define a chronic migraine

A

Headache on >/=15 day/month, of which >= days are migraines, for more than 3 months`

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51
Q

What medication should you avoid if pregnant

A

anti-epileptics

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52
Q

Types of trigeminal autonomic cephalagias?

A

cluster headache, paroxysmal hemicrania, SUNCT and SUNA

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53
Q

What does SUNCT and SUNA stand for?

A

SUNCT-short-lasting unilateral neuralgiform headache with conjunctival injection and tearing

SUNA- Short-lasting unilateral neuralgiform headache with autonomic symptoms

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54
Q

Go over trigeminal autonomic cephalagias?

A

on spreadsheet

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55
Q

Go over migraines

A

on spreadsheet

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56
Q

Difference in type of pain between cluster headache/ paroxysmal hemicrania and SUNCT

A

cluster headache/ paroxysmal hemicrania= sharp, throbbinf

SUNCT= stabbing, burning

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57
Q

What presentations are more likely to have a sinister cause?

A

associated head trauma, thunderclap onset, new daily persistent headache, change in headache pattern or type, returning patient

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58
Q

Some redflag symptoms or signs of headaches?

A

new onset, new or change in headache and aged over 50 or immunosuppresion or cancer, change in ha frequency, characteristics , focal/non-focal neurological symptoms, abnormal neurological examination, neck stiffness/fever, high pressure (worse lying down, wakening patient up, precipitated by: physical exertion, valsalva manoeuvre), risk factors for cerebral venous sinus thrombosis, low pressure headache, Giant cell arteritis

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59
Q

Go over thunderclap headache, subarachnoid haemorrhage and intracranial hypotension, giant cell arteritis

A

on spreadsheet

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60
Q

causes for raised intracranial pressure?

A

glioblastoma multiforme, cerebral abscess, meningioma, hydrocephalus, venous infarct with focal area of haemorrhage, pappilloedema

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61
Q

Severity of head injury as represented by GCS

A 
13-15 = mild injury
9-12 = moderate injury
3-8= severe injury
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62
Q

Describe a linear skull fracture

A

commonly temporo-parietal from blow or fall onto side or top of the head (eg fall on pavement) and may continue on to the skull base, “hinge” fracture

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63
Q

Describe a depressed skull fracture

A

focal impact which may push fragments inwards to damage the meninges, blood vessels and brain, increases the risk of meningitis and post-traumatic epilepsy

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64
Q

Describe a comminuted skull fracture

A

fragmented skull

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65
Q

Describe a ring skull fracture

A

fracture line encircling the foramen magnum caused by a fall from height, leading to the skull base and cervical spine being forced together

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66
Q

Describe a contre-coup skull fracture

A

fracturing of the orbital plates caused by a fall onto the back of the head

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67
Q

Go over haemorrhages

A

on spreadsheet

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68
Q

Go over cerebral oedema and contusions and diffuse traumatic axonal injury

A

on spreadsheet

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69
Q

The 3 categories of syncope

A

Reflex, orthostatic and cardiogenic

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70
Q

Causes of reflex syncope

A

taking blood/ medical situations, cough, micturation

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71
Q

Causes of orthostatic syncope

A

dehydration, medication related (anti-hypertensive), endocrine, ANS

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72
Q

Causes of cardiogenic syncope

A

arrhythmia, aortic stenosis

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73
Q

How to assess syncope

A

examinaton- heart sounds, pulse, postural BPs, ECG

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74
Q

symptoms of cardiogenic syncope

A

chest pain, palpitations, SOB, clammy/sweaty, came around quickly, seemed to stop breathing when passes out, unable to feel pulse while passed out

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75
Q

Causes of provoked seizures

A

alcohol or drug withdrawl, few days after head injury, within 24hrs of stroke, neurosurgery, severe electrolyte disturbance, eclampsia

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76
Q

Types of generalised seizures

A

absence sei.., generalised tonic-clonic s, myoclonic epilepsy, atonic sei

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77
Q

Types of focal seizures

A

simple partial seizures, complex partial seizures, secondary generalised, or by localisation of onset

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78
Q

Describe primary generalised?

A

no warning, <25 years, history of absences and myoclonic jerks, generalised abnormality on EEG, family history

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79
Q

Describe focal/ partial epilepsies

A

may get an “aura”, any age, simple partial and complex partial seizures can become secondarily generalised, focal abnormality on EEG, MRI may show causes

80
Q

Go over seizures

A

spreadsheet

81
Q

Ischaemia definition

A

;lack of blood flow

82
Q

Hypoxia definition

A

lack of O2

83
Q

Interruption of supply of O2 is caused by cjanges in what?

A

vessels wall, blood flow and pressure and blood consituents

84
Q

3 main causes of localised interrupted blood flow?

A

atheroma + thrombosis, thromboembolism, ruptured aneurysm

85
Q

Which bracnh of the internal carotid artery tends to get ischaemia as a result of atheroma and thrombosis?

A

middle cerebral artery

86
Q

What kind of stroke do you get due to a ruptured vessel?

A

haemorrhage and distal ischaemia due to spasm of artery

87
Q

What are the 2 common sites of ruptured vessels causing haemorrhagic stroke?

A

basal ganglia- microaneursyms

Circle of Willis- berry aneursym

88
Q

Causes of generalised interrupted blood supply or hypoxia?

A

Low O2 in bloof, inadequate supply of blood and inability to use O2

89
Q

Causes of low O2 in blood?

A

CO2 poisoning, near drowning, respiratory infarct

90
Q

Causes of inadequate supply of blood?

A

cardiac arrest, hypotension, brain swelling

91
Q

causes of inability to use O2?

A

cyanide poisoning

92
Q

What kind of injury is causes by generalised interrupted blood supply due to hypotension?

A

watershed infarction

93
Q

What kind of injury is causes by generalised interrupted blood supply due to cardiac arrest?

A

cortical infarction

94
Q

Name the common types of primary brain tumour

A

Neuroepithelial tissue (glioma- glioblastoma multiforme), meninges (menigioma), pituitary (adenoma)

95
Q

What are the commonest tumours that spread to the brain?

A

renal cell, lung and breast carcinoma, malignant melanoma and GI tract

96
Q

Describe glioma carcinomas?

A

Gliomas are derived from astrocytes, they are graded by WHO I-IV, IV is the most common and most aggressive known as Gliobastoma multiforme and is spread by white matter and CSF pathway

97
Q

Describe meningiomas

A

arise from arachnoid, they are slow growing normally benign tumours, they frequently occur along the falx, convexity or sphenoid bone and are completly cured if removed

98
Q

Describe pituitary tumours

A

adenoma, only 1% are malignant, present with visual distubance and hormone imbalance

99
Q

How do brain tumours present?

A

raised intracranial pressure, focal neurological deficit, epileptic fits, CSF obstruction

100
Q

Symptoms of raised ICP

A

morning headache, n/v, visual disturbance, somnolence, cognitive impairment, altered consciousness

101
Q

Signs of raised ICP

A

papilloedema, 6th nerve palsy, cognitive impairments, altered consciousness, 3rd nerve palsy

102
Q

How much CSF is produced in a day?

A

400-450 cc/day

103
Q

Where is a tumour likely to be if hydrocephalous is a symptom?

A

posterior fossa tumours

104
Q

Focal neurological deficit symptoms

A

hemiparesis, dysphasia, heminaopia, cognitive impairment, cranial nerve palsy, endocrine disorders

105
Q

What tumour is likely to be found in the cerebellum?

A

Menigioma

106
Q

In what type of lesions do you get epilepsy as a symptom?

A

in lesions above tentorium

107
Q

Management options for glioblastoma multiforme

A

complete surgical excision, steroids, anticonvulsants, radiotherapy, chemotherapy (temazolamide)

108
Q

Management options for metastasis brain tumour

A

steroids, anticonvulsants, radiotherapy, surgery

109
Q

When should you not perform a lumbar puncture and why?

A

when there are signs and symptoms that suggest an intracranial mass lesion and because it could cause a herniation syndrome and death of patient

110
Q

what are the functions of the frontal lobe

A

Voluntary control of movement (precentral gyrsu), speech (pars opercularis, pars triangularis), saccadic eye movements (frontal eye field), bladder control (paracentral lobule), gait (periventricular), higher order (restraint, initative, order (RIO))

111
Q

What job does the orbitofrontal cortex have?

A

restraint- mediates empathic, civil and socially appropriate behaviour

112
Q

How would you test the function of the orbitofrontal cortex?

A

Is speech and behaviour appropriate, go/no-go tests, stroop tests

113
Q

How would you exam the function of the frontal lobe?

A

inspection- decorticate posture, magnetic gait, urinary catheter, abulia, UMN signs, pronator drift, saccadid eye movements, primitive reflexes, speech

114
Q

What is the job of the supplementary motor cortex/ anterior cingulate

A

Initiative

115
Q

How would you test the supplementary motor cortex function?

A

lack of motivation, apathy, abulia, depression

116
Q

What is the function of the dorsolateral prefrontal cortex?

A

Order- integration of sensory infor, generation of responses to environmental challenges, selection of most appropriate reponse, maintenance of task seet, sequential ordering of data, self-evaluation of performance

117
Q

How would you test the dorso-lateral cortex

A

Ability to make and appointment and keep to time, ability to give coherent account of history, spell WORLD, say as many words as possible with a particular letter

118
Q

How would you exam someone’s language ability?

A

1st ensure their hearing is intact and speak english, check fluency (Broca’s), normal aphasia, repetition (arcuate fasciculus), 3 step command (Wernicke’s), “Baby hippopotamus” (cerebellar), orofacial movement (ppp, ttt, mmm), reading, writing

119
Q

What are the functions of the parietal lobe?

A

Primary somatosensory area, multimodality assimilation, visuospatial coordination, language, numeracy

120
Q

How would you examine the parietal lobe when looking at cortical sensory symptoms?

A

sensory inattention, astereoagnosia, dysgraphasthesia, 2 point discrimiation

121
Q

What symptoms could you expect when the parietal lobe is affect on the dominant side? (Gerstman’s syndrome)

A

Dyscalculia, finger anomia, left/ right disorientation, agraphia

122
Q

What symptoms could you expect when the parietal lobe is affected on the non-dominant side?

A

ideomotor apraxia-“How to do”- light a match, ideational apraxia- “what to do”- What’s a comb for,constructional apraxia- draw this 3d box,dressing apraxia, hemineglect, loss of spatial awareness

123
Q

What are the functions of the temporal lobe?

A

process auditory input (Heschl gyrus), language, encoding declarative long0term memory (hippocampus), emotions (amygdala), visual fields (Meyer’s loop)

124
Q

Symptoms when the cerebellum is affected?

A 
DANISH P
Dysdiadochokinesia
Ataxia
Nystagmus
Intention tremors
Slurred speech
Hypotonia
Past pointing
125
Q

Patient who presents with magnetic gait, a urinary catheter and decorticate posture is likely to have which lobe of the brain affected?

A

Frontal lobe

126
Q

Patient who presents with failed stroop test and is speaking to you inappropriately is likely to have which lobe of the brain affected?

A

In the frontal lobe- the orbitofrontal cortex

127
Q

Patient who presents with failure to give coherent account of history, can’t spell words backwards and can’t provide any words when asked to name as many words possible starting with “P” is likely to have which lobe of the brain affected?

A

Frontal lobe- dorsolateral prefrontal cortex

128
Q

Patient who presents with lack of motivation, depression and abulia is likely to have which lobe of the brain affected?

A

Supplementary motor cortex of the frontal lobe

129
Q

Patient who presents with sensory inattention, inability to identify an object by touch, inability to determine what’s been written on them by touch alone and 2 point discrimination is likely to have which lobe of the brain affected?

A

Parietal lobe

130
Q

Patient who presents with maths difficulty, inability to distinguish fingers, loss in ability to communicate through writing and left/right disorientation is likely to have which lobe of the brain affected?

A

Dominant side of parietal

131
Q

Patient who presents with inability to wave, get dressed, has hemineglect and loss of spatial awareness is likely to have which lobe of the brain affected?

A

Non-dominant side of parietal lobe

132
Q

Patient who presents with loss of long-term memory is likely to have which lobe of the brain affected?

A

Temporal lobe

133
Q

Patient who presents with slurred speech, hypotonia and a broad, course and low frequecny tremor is likely to have which lobe of the brain affected?

A

Cerebellum

134
Q

Define abulia

A

Inability to act instinctively

135
Q

Define Astereoagnosia?

A

Inability to identify an object by touch

136
Q

What is the clinical definition for inability to determine what is being written on you rhand by touch alone?

A

Dysgraphasthesia

137
Q

Define finger anomia?

A

Inbility to distinguish fingers

138
Q

Define dyscalculia?

A

Maths difficulty

139
Q

Define agraphia?

A

Loss in ability to communicate through writing

140
Q

Define Ideomotor apraxia?

A

Inability to perfom tools and waving, eg ask patient to show how you would light a match

141
Q

Define ideational apraxia?

A

Inability to conceptualise, plan and execute complex sequences of motor actions eg ask them what is the pur[ose of a comb

142
Q

Define constructional apraxia?

A

Inability of patients to copy accurately a drawing of a 3D oblect

143
Q

Describe an intention tremor

A

broad, course and low frequency tremor

144
Q

How do you know it’s radiculopathy?

A

unilateral, single myotome, single dermatome, LMN

145
Q

How do you know it’s a peripheral nerve affected?

A

unilateral, motor and sensroy deficit fits with pn, LMN

146
Q

How do you know it’s myelopathy

A

bilateral motor and sensory level, UMN

147
Q

What common symptoms do you get with peripheral neuropathy?

A

feels like wearing glove and stockings.

148
Q

Myelopathy symptoms

A

clonus, upgoing plantars, hypertonicity, Hoffman’s sign, brisk reflexes, proprioception impairment (Romberg’s test, tandem walking)

149
Q

What supplies the anterior circulation of the brain?

A

2 internal carotid arteris, 2 anterior cerebral artery, 2 middle cerebral artery

150
Q

What supplies the posterior circulation of the brain?

A

2 vertebral arteries, 3 pairs of cerebellar arteries, 2 posterior cerebral arteries

151
Q

What are the symptoms of anterior cerebral artery occlusion?

A

Contra-lateral: paralysis of foot and leg, sensory loss over foot and leg, impairment of gait and stance

152
Q

What are the symptoms of middle cerebral artery occlusion?

A

Contra-lateral- paralysos/ sensory loss of face/arm/leg, homonymous heminaopia, gaze paralysis to opposite side,
aphasia if stroke is of dominant side
Unilateral neglect and agnosia if non-dominant side

153
Q

What are the symptoms of middle cerebral artery occlusion of the left hemisphere (dominant)

A

Hemiplegia, homonymous hemianopia, dysphasia

154
Q

What are the symptoms of middle cerebral artery occlusion of the right hemisphere (non-dominant)

A

Left hemiplegia, homonymous hemianopia, agnosias- visual, sensory, anosagnosia, prosopagnosia

155
Q

Define anosagnosia

A

denial of hemiplegia

156
Q

Define prosopagnosia

A

Failure to recognise faces

157
Q

Lacunar stroke syndromes

A

No dysphasia, neglect or hemianopia

Can be pure motor stroke, pure sensory stroke, dysarthria (clumsy hand syndrome), ataxic hemiparesis

158
Q

Posterior circulation occlusion symptoms?

A

coma, vertigo, n/v, cranial nerve palsies, ataxia, hemiparesis, hemisensory loss, crossed sensori-motor deficits, visual field deficits

159
Q

What anatomy is involved when there is posterior circulation occlusion

A

brain stem, cerebellum, thalamus, occipital and medial temporal lobes

160
Q

When a patient presents with impairment of gait, has a paralysed right foot and sensory loss in leg and foot where is there a vessel occluded?

A

left anterior cerebral artery occlusion

161
Q

When a patient presents with right paralysis of leg and sensory loss in leg, homonymous hemianopia and gaze paralysis to right side where is there a vessel occluded?

A

Left middle cerebral artery occlusion

162
Q

When a patient presents with incoordinated movements along with weakness in one side of the body (ataxic hemiparesis) and complains of dropping things ore often what type of stroke would you expect?

A

Lacunar stroke syndrome

163
Q

When a patient presents with paralysis on one side of the body (hemiplegia), dysphasia and homonymous hemianopia where is there a vessel occluded?

A

Dominant side, middle cerebral artery occlusion

164
Q

When a patient presents with left paralysis of body (hemiplegia) but denies this paralysis (anosagnosia), inability to process sensory information (sensory agnosia) and failure to recognise their family (prosopagnosia)where is there a vessel occluded?

A

non-dominant hemisphere, middle cerebral artery

165
Q

When a patient presents with vertigo, n/v, 1 dilated pupil, ptosis, visual field deficitis, incoordinated movements (ataxia), hemipareis where is there a vessel occluded?

A

in posterior circulation

166
Q

How would you treat a stroke?

A

thrombectomy, aspirin (ischaemic), stroke units, tissue plasminogen activator

167
Q

Name 4 members of the stroek unit

A

clinical staff, stroke nurses, physiotherapists, speech and language therapists, occupational therapists, dietician, psychologist, orthotpist

168
Q

What are the 4 OCSP stroke classifications?

A

Total Anterior Circulation Stroke, Partial anterior circulation stroke, lacunar stroke, posterior circulation stroke

169
Q

OCSP table

A

on sheet

170
Q

When would you use tissue plasminogen activator

A

<4.5hrs from symptom onset, disabling neurological deficit, symptoms present >60 mins, consent obtained

171
Q

Exclusion criteria for IV tissue plasminogen activator?

A

Anything increasing chance of haemorrhage- blood on CT scan, recent surgery, recent episodes of bleeding, coagulation problems,
BP>185 sytolic or >110 diastolic
Glucose <2.8 or >22mmol/L

172
Q

What investigations would you complete for stroke?

A

routine blood tests (FBC, glucose, lipids, ESR), CT or MRI, ECG, echocardiogram, carotid doppler ultrasound, cerebral angiogram/ venogram, hyper-coagulable blood screen`

173
Q

What is used for secondary prevention of strokes?

A

Anti-hypertesnives, anti-platlets, lipid lowering agents, warfarin (AF), carotid endarectomy

174
Q

Define dementia

A

A syndrome consisiting of progressive impairment of multiple domains of cognitive function in alert patients leading to loss of acquired skills and interference in occupational and social role

175
Q

Causes of late onset dementia (65+ yrs)

A

Alzheimer’s, vascular, Lewy body, others (ALVO)

176
Q

Causes of young onset (<65yrs) dementia?

A

Alzheimer’s, vascular, frontotemporal, other (toxic (alcohol), genetic (Huntington’s), infection (HIV, CJD), inflammatory (MS)

177
Q

What are some treatable causes of dementia?

A

Vitamin deficiency eg B12, endocrine (thyroid disease), infection (HI, syphillis)

178
Q

What conditions can mimic dementia?

A

Hydrocephalus, tumour, depression- pseudodementia

179
Q

How would you diagnose dementia?

A

History, examination (cognitive function, neurological, vascular), investigations- blood, CT, MRI, CSF, EEG, functional imaging, genetics

180
Q

If the dementia had a rapid progression and the patient had the sign myoclonus, what would be the cause?

A

CJD

181
Q

If the dementia had a stepwise progression what would be the liekly cause?

A

vascular

182
Q

If the patient who’d been diagnosed with dementia also had abnormal movements what would you believe the cause was?

A

Huntington’s

183
Q

If the patient who’d been diagnosed with dementia also had parkinsonism what would you believe the cause was?

A

Lewy body

184
Q

What type of dementia is Alzheimer’s disease?

A

Temporo-parietal dementia

185
Q

What are the symptoms of Alzheimer’s disease (temporo-parietal dementia)?

A

early memory disturbance, language and visuospatial problems, personality preserved until later

TAM- temporo-parietal demntia= Alzheimer’s= memory loss

186
Q

What are the symptoms of frontotemporal dementia?

A

early change in personality/ behaviour, often changes in eating habits, early dysphasia, memory/ visuospatial relatively preserved

187
Q

What are the symptoms of vascular dementia?

A

Mixed picture, stepwise decline

188
Q

Symptomatic treatment of dementia?

A

Info and support, dementia services, OT, social work/ support, insomnia, behaviour, depression

189
Q

Specific treatment for Alzheimer’s disease

A

Cholinesterase inhibitors (donepezil, rivastigmine, galantamine), NMDA antagonist (memantine)

190
Q

Define Parkinsonism

A

A clinical syndrome caused by loss of dopamine in the basal ganglia, with >/=2 of: bradykinesia (slow movement), rigidity, tremor, postural instability

191
Q

Causes of parkinsonism?

A

Idiopathic-dementia with Lewy bodies

Drug induced (dopamine antagonists)

Vascular parkinsonism

Parkinson’s plus syndromes (multiple system atrophy, progressive supranuclear palsy/ corticobasal degeneration)

192
Q

What is the early medical treatment of Parkinson’s

A

Levodopa,

MAO-B inhibitors- selegiline, rasagiline, safinamide

COMT inhibitors- entacapone

Dopamine agonists- ropinirole, pramipexole, rotigotine

193
Q

What is the late treatment of Parkinson’s

A

MAO-B inhbitors, COMT inhibitors, slow release levodopa (to prolong levodopa half life), add oral dopamine agonist, continuous infusion of apomorphine and duodopa

functional neurosurgery

194
Q

What are later drug-induced complications in Parkinson’s

A

motor fluctuation- as levodopa wears off, dyskinesias- involuntary movements (levodopa), hallucinations, impulse control

195
Q

What are later non-drug induced complications in Parkinson’s

A

depression, dementia, autonomic- BP, bladder, bowel, speech, swallow, balance

Neurology (7 decks)

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