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Phase 2 mine > Neurology > Flashcards

Neurology Flashcards

1
Q

Which diseases are stroke mimics?

A

Hypoglycaemia, labyrinth disorders, Migranious aura Typical and atypical, Mass lesios, postictal weakness simple partial sizures funcional hemiparesis

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2
Q

How is TIA managed In primary care?

A

Assess risk of stroke or TIA in next 7 days in guidance and refere to specialist if needed

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3
Q

What contributes to high risk of recurrent stroke or TIA?

A

ABCDsquared above 60 High BP clincial features duration diabetes AF more than one week or on anticoagulant

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4
Q

What to do in low risk TIA patient?

A

Refer from assessment, statin antiplatelet, treat BP no driving till seen specialist

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5
Q

What layer are the somites made of?

A

Mesoderm

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6
Q

What are derived from somites?

A

dermatomes and myotomes (skeletal only)

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7
Q

What are branchial arches?

A

Bumps belwo the head around the neck they are a feature of vertibrates

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8
Q

Which area are sympathetic nerves derived from?

A

T1-L2

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9
Q

Which cranial nerves are carying autonomic nerves/

A

3,7,9,10 1973

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10
Q

What makes up peripheral nervous system?

A

spinal cord C8 T12 L5 S5 some (1)coygeal ones, then the ones from the brain cranial nerves somatic branchial autonomic and special

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11
Q

Where are the Thoracic dermotomes?

A

They are from the sinal level at the back to slightly lower at the front they run from above the ribs down to the suprapubic area T1 gos down the inside of the outer arm

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12
Q

Where is the foregut pain felt/

A

In T5 to T9 dermatomes in epigastrium

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13
Q

Where does hindgut pain feld?

A

In T12 region suprapubically

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14
Q

Where does the spinal cord end?

A

At around L1

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15
Q

What is important about spinal cord deficites level?

A

Spinal cord level is where the bodies of the cells are in the cord where as the vertebral level is where they ender the spinal column

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16
Q

Where does the splanchnic nerves come from?

A

They come from the sympathetic chain

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17
Q

What is the corticospinal tract?

A

Motor tract from the cortex through internal capsule in thalamus, to thepons and medulla where 85% cross to the contralateral side to the lateral corticospinal tract 5% are on ipsilateral spinal tract the other 1-0 are in the ipsilateral anteria corticospinal tract

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18
Q

What is significance of decusation of the corticospinal tract?

A

if you hafe brain or stem injury it will affect contralateral side otherwise it affectsthe same side if below the medulla

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19
Q

What does anterior corticospinal tract do?

A

Muscles of the trunk

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20
Q

What happens with anterior decussation?

A

Happens in the thoracic cord not the pyramids

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21
Q

What is in the ventral horn of the spinal cord?

A

the motor nerves

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22
Q

What are in the dorsal horm of spinal cord?

A

The sensory nerves

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23
Q

What happens with thoracic spinal hemisection in corticospinal?

A

Loss of motor to the same side for the limb but opposite for the trunk

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24
Q

What doe the dorsal columns carry?

A

They carry touch vibration concious muscle/joint sense

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25
Q

What is in the fasciculus gracilis?

A

The leg sensation

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26
Q

What is in the fasiculus cuneatus?

A

the arm sensation

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27
Q

Where is the gracilis ?

A

In the middle

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28
Q

Where do the dorsal columns cross?

A

up the spinal cord on same side and then synapse in medull and cross then up to thalamus then to the cortex

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29
Q

How many neurones are in the dorasal columns pathway?

A

3 limb to medulla, decussation then new one tothalamus then corte

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30
Q

What are in the spinocerebellar pathways?

A

joint and muscle non concious sense anterior and posterior divisions

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31
Q

What is the pathway of the spinocerebellar/

A

Posterior decussates later anterior as soon as joins

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32
Q

What is carried in the spinothalamic tract?

A

Pain and extreme temperature and it decussates a few segments above where enters

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33
Q

What is Brown-Sequard syndrome?

A

A lesion at right level T10 vertebral elvel T6 ish will lose all normal sensations on the same side of body as dorsal columns cross in medulla lose pain and temperature on thecontralateral side a few segments down and also total loss of all sensation in ipsilateral side, paralysis on same side from injury down

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34
Q

What might happen in high spinal cord injury?

A

The tunk musscles on other side will get damaged.

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35
Q

Where is a lumbar puncture done and why?

A

In the lumber spine because the spinal cord takes up less space so its easier to not dammage the cord

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36
Q

What is difference between lumbar puncture and epiduuural?

A

The epidural is done with a blund needle outsided the dura whereas lumbar puncture should go into the dura

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37
Q

What is in the olfactory nerve?

A

85% on same side of brain and it is special sense not through the thalamus

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38
Q

What is the optic nerve?

A

Special sense 50% cross over when testing look at light then neuronal

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39
Q

What is the oculomotor

A

somatic and autonimic motor, lense and pupil control and the eye movements recti but nod lateral

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40
Q

What does the trochlea nerve do?

A

somatic motor tor superior oblique down and out if have occularmotor palsy

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41
Q

What does abducents nerve do?

A

Lateral recuts somatic motor

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42
Q

What does trigeminal do?

A

Branchial motor and sensory somatic bilateral motor to face and contralateral sensory to face also muscles of mastication nasal cavity and sinuses

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43
Q

What is in the facial nerve?

A

Motors autonomic branchial ans special sensory. does motor to bilateral forehead motor to contralateral rest of cace and sensory to the tongue the anterior

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44
Q

What are the common ways blood supply to the brain is interrupted?

A

85% embolic, 10% haemorrhagic and 5% have rarer causes

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45
Q

How can emboli in the brain form?

A

Infarction of endocardium and diseased valves, or in atherosclerotic events in great vessels common carotid internal carotid or vertebral arteries

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46
Q

Which blood vessels supply the basal ganglia?

A

The middle cerebral arteries, lenticular nucleus

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47
Q

What can happen if internal capsule ishaemmoraged?

A

the cotex function is blocked as well

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48
Q

What does the secondary auditory area?

A

the library of sounds that we know so if dammaged can hear things but not make sense of them

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49
Q

What parts of the body ares are affected in anterior infarction?

A

lower limb sensory and motor deficit

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50
Q

What areas of the body are affected in the posterior artery infarction/

A

Non as doesnt supple the motor homunculus

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51
Q

What is an extradural haemmorage?

A

On outside the dura

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52
Q

What is subdural haemorrage?

A

one between the dura and the arachnoid mater

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53
Q

What doe meningeal blood vessels do?

A

They run between the skull and dura and supply skull and dura with blood

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54
Q

Where are the veins of the brain?

A

Between the durathe periosteum and meningeal

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55
Q

What are bridging veins?

A

Veins that cross the subdural space between the

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56
Q

Which vessels are deep to the pia?

A

None

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57
Q

What can cause extradural haemorrhage?

A

Damage to the meningeal artery from trauma fractured skull, rise in intercranial pressure can cause coning and death

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58
Q

What stops the bleed of an extradural haemorrage?

A

When pressure in skull is the same as inside the vessels

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59
Q

What happens in the extradural haemorrage?

A

The blood builds up and squashes the brain causing a haematoma under the bone contained by a sutre

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60
Q

What causes a subdural haemorrhage?

A

smaller brains, alcoholicas dementia and babies with acceleration change, bridging vessels broken days or weeks later cause haematoma to lyse causing rise in ICP over time

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61
Q

What is a subarachnoid haemmorage?

A

Rupture of arteries from circle of willis berry aneurism, sudden sever onset photophobia thunderlap headache, rapidly fatal and commonest souce of organs for transplant

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62
Q

What happens in subarachnoid haemorrage to cause death?

A

blood causes vasospazm and ischaemia all over the brain

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63
Q

What is meningitis?

A

Inflammation of the meninges,

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64
Q

What are the causes of meningitis?

A

Bacterial viral funcal parasitic, paraneoplastic drug side effects and autoimmune

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65
Q

How can CNS be infected?

A

Direct contiguous spread from sinutes area, or from neurosurgery or trauma and via the blood stream

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66
Q

What is the pathophysiology of meningitis?

A

Blood vessels dilate when pathogen are in CSF, the macrophages and fluids into the CSF and brain and cause inflammationsometimes it isnt in the brain but othertimes it can get into the brain

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67
Q

What are symptoms of meningitis?

A

Fever headache and neck stiffness also nausea vomiting photophobia (irritiabilty confuson delirum and coma indicating severe disease)

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68
Q

How serious is meningits?

A

5% mortality, 20% complications

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69
Q

What to do if suspect meningits?

A

give antibiotics send straight to hospital

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70
Q

What are initial steps of management of menigitis?

A

GCS blood cultures broad spectrum antibiotics, Ceftiaone or ceftaxime steroids to reduce damage

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71
Q

What can be tested from lumbar pumcture?

A

4 samples one to miccrobiology, biochcemistry, microbiology againgram stain cultrue protein Virral PCR microbiology

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72
Q

What are the contrindications for Lumbar puncture?

A

Raised incracranial pressure abnormal clotting profile suspected abcess

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73
Q

Why would you do CT in meningitis patient??

A

When you suspect riased Intracranital pressure

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74
Q

When to do CT head before LP?

A

over 60 immunocompromoised histry of CNS disease, siezures<1 week GCS low focal neurological signs papiloedema, atypical hystory

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75
Q

What can cause chronic meningitis?

A

TB syphilis or cryptococcal fungus or others like parasitic lymes disease parasisc

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76
Q

What are causitice organisms of acute meningitis?

A

Neisseria meningitisi negatice diploccci, sterp pneymonia positieve diplococcia, listeria group strep haemophilisB and ecoli viral herpese smpes varicella zoster enterovirus

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77
Q

What guides empirical treatment?

A

age as different orgamisms are more common. eg neonates usually listeria Group B strep and E coli

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78
Q

What is indicative of Bacterial meningitis in CSF fluid?

A

cloudy high white cell cound pedominance of neutrophils high protein low glucose

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79
Q

What is normal CSF like?

A

clear, acellular WBCC 0-5 cells mm3

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80
Q

What is indicative of Viralmeningitis?

A

high WCCC lymphocytes high high protein normal glucose clear

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81
Q

What would be seen in chronic menigitisfrom TB or cryptocccal infectio/

A

fibrin web lymphocytes high protein low glucose high opening pressure of opening

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82
Q

What are DD for meiningitis?

A

Subarachnoig haemorrage (thunderclap headache), mignaine, flu and other ciral ilnesses, sinusitis, barain abscess and malaria

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83
Q

What to do with meningitis that isnt treating the patient?

A

Contact tracing prophylaxis and nottify PHE

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84
Q

What is encephalitis?

A

Cerebral cortex inflammation

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85
Q

What usually causes encephalitis?

A

Herpes simplex and varicella zoster, tropical travel viruses rabise west nile virus japanese encephalitis paraneoplastc or autoimmune

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86
Q

What is clinicalpictues for encepalitis?

A

consciouness changes GCS low siezures are common focal neuologicalism can sometiems have overlap with meningitis as well

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87
Q

How is encephalitis managed?

A

MRI or CT scan, LP viral PCR, supportive therapy someitiems antiviral,

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88
Q

What is tetanus?

A

caused cy clostridium tetani spore forming from direct innoculation of skin usually in failure to get vaccinated. produce tetanus plasmin that interferes with neurotransmitter relase increased neuron firing causeing muscle spazms

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89
Q

What is trismis?

A

lock jaw

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90
Q

What is Risus sardoinicus?

A

Smile in tetanus

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91
Q

What is key in management of tetanus?

A

supportive antimicrobials muscle relaxants and sedatives tetaus microglobulins to remove toxins

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92
Q

What is rabies?

A

viral infection from animals dogs bats usually spreads via peripheral nerves to CNS long incubation periot 2-weeks 1-3 months is average can get numbness and pain causes very acute syndrome

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93
Q

What are the types of rabies presentation?

A

Furious with spasms and seizures or paralytic weakness and

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94
Q

What is treatment for rabies?

A

There isnt one. 99.9% die. pre-exposure prophylaxias is key and post exposure prophylaxis vaccination and immunoglobulins
Managed with sedatives

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95
Q

How does neuromuscular junction work?

A

Calcium influx in terminal bulb from action potential by voltage gated channels then AcH is released to bind to the motor end plate to cause a muscle action potential

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96
Q

How does ACth cause mscle contraction?

A

IT causes depolarisation of the muscle then the is causes the sarcoplasmic reticulum to release calcium that was stored in it

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97
Q

What is myasthenia gravis?

A

Autoimmune condition agiand AChreceptor and MUsk part of the complex 80-85% are generalised and 50% include occular are positive or ACHR antibodies

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98
Q

How much or AChReceptors neeed ot be blocked for symptoms?

A

60%

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99
Q

What are the clinical features of MG?

A

Extra occular weaknes droopy eyes double visision. limb and bulbar weakness nasal speech dysarthria swallowing difficulties weak chewinf, worsening weakeness after prolongued and sustaind contraction fatiguability is hallmark, tendon reflexes and sensations are normal

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100
Q

What can cause complex opthamoplegia?

A

motorneyronitis multiplex diabetes plyarteritis nodosum amyloidosis, graves disease the muscles botulism kearns-sayre sydrome miller fish syndrome MF

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101
Q

What is ice pack test?

A

get an ice pack pu over the eye leave for a minute if the is improvement that is positive

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102
Q

What is Cogan’s lid twitch?

A

move pen up and down wont stop at midline and twitches

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103
Q

What are the subgroups of myesthenia gravis?

A

ocular myasthemia gravis, early onset AChR-myesthenia gravis, late onset AChR mysasthenia gravis, MuSK-myasthenia gravis seronegative myasthenia gravis

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104
Q

what is relevance of the thymus gland in myasthenia gravis?

A

Hyperplasia in early onset generalised myesthenia gravis

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105
Q

How is MG diagnosed?

A

History and examination EMG single fibre EMG repetitive muscle stimulation results in decremental potential highly sensitive single fiber EMG increased jitter and block specific antibody tests

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106
Q

Why do Myasthenia gravis need CT chest?

A

Tocheck thymus

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107
Q

Why is thymus important in Myasthenia gravis?

A

usually atrophys in adult life but can remain large in adult hood, can cause immune cell lymphoid hyperplasia some have thymoma

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108
Q

What is a myasthenic crisis?

A

Leads to respiratory failure impared swallow severe limb weakness one or all of these. 10-15% within 2- years of diagnosis MuSK are more comon quiet breathing reduced chest expansion tachycardia hyertension sugesting hypoxia ABG and sats can be normal. FVC needed or single breath count. Slow vital capacity if less then 1lite

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109
Q

What can precipitate myasthenia gravis crisis?

A

infections stress trauma withdrawal from drugs, rapid introduction of steroids electrolyte imbalace antibiotics antrheumatic drugce antihypertensives botulinum toxin

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110
Q

What is the pharmacological management of mysasthenia gravis?

A

Acetyle esterase inhibitors pyridostgmine. steroids for a bit then asathioprine ciclosporin methotrexate Retuximab if resistant to stop autoantibodies

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111
Q

What can help patient in myasthenia gravis crisis?

A

Plasma exchange immunoglobulin thymectomy

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112
Q

What is Eaton lambert syndrome?

A

Calcium channel antibodies to stop the movement of ions

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113
Q

What are brain tumours?

A

there are 150 types there are neuroepithelial cells can be in neurones or glial cell tumours, there are aastrocytes, oligodendrocytes and there are gliomas like astrocytoma oligodendrocytomas there are meninciomas craniophayngiomas germ cell tumours shwann cellomas lymphatic also secondary ones

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114
Q

What is the classification for brain cancer?

A

Not tnm as done metastisise. based on histology and molecular markes and genetic factors gradine 1 to 4 benign to malignant

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115
Q

What are grade 2 tumours of the brain?

A

slow growwing but will transform at some point in life

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116
Q

What affects brain tumour prognosis?

A

Size tumour kinetics, histology and molecular markers

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117
Q

What are the high grade gliomas?

A

Can be transfromed from 2 but can be new make upmost of brain cancers 85% survival can be from 2-5 years

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118
Q

What is the cause of brain cancer?

A

usually iatrogenic. Radiation therappy 5% family history neurofibromatosis tuberose sclerosis von hippel lindau, Immunosuppressions CNS lymphoma

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119
Q

How to brain tumours present?

A

Deends on what is grade and where generally headache sizures foca neurological symptoms and non focal

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120
Q

What is the type of headache in tumour?

A

Not really raised intractanial raised in morning and worse wih lying down associated n&V coughing and sneesing 24% first symptome 46% have at presentation only 2% only have headache

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121
Q

What is highest positive predict for brain tumour?

A

New onset siezure

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122
Q

What should red flag with headache?

A

headache with old age new or changed or previous history of cancer

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123
Q

What are focal brain symptoms?

A

symptoms that are associated with a specific brain area

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124
Q

What are focal symptoms?

A

Weakness sensory loss ataxia progressive

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125
Q

What are non-focal symptoms?

A

personality change or behaviour memory disturbance or confusion

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126
Q

how many people with tumours have siezures?

A

> 80%

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127
Q

What are signs of bran tumpur?

A

Papilloedema, hemiparesis visual field defect dysphasia

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128
Q

What are typical signs of low grade?

A

Siezures often incidental

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129
Q

What are the presentation of high grade tumours?

A

rapidly progresive neurological deficeite symptoms of raised intracriala pressure

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130
Q

What are red flags for brain tumour?

A

headache with focal nwurology, visual field defects, 6th nerve palsy papiloeema nwe onset focal siezure rapidly progressive focal neurology past history of cancer

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131
Q

What are Brain tumour investigation?

A

CT with contrast (but not good at ruling out) MRI much better especially pituatary FMRI for planning surgery
Biopsy/ surgery to work out which one it is

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132
Q

What to do when spot a brain tumour?

A

Histology molecular markers and genetics from a brain biopsy

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133
Q

What is treatment for brain tumours?

A

depends on grade and site and size it is non-curative unless grade 1

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134
Q

What are the high grade treatmetns?

A

Steroids to reduuce oedema, surgery, radiotherapy chemotherapy, temozolamide PCV

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135
Q

How are low grade tumours treated?

A

Surgery early resection radiotherapy and early chemotherapy can get survival from 7.8 to 13.3

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136
Q

What is an awake craniotomy?

A

assessing function during the operation to allow for preservation of function better removal and decreased risk of harming a patient

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137
Q

What can be red herrings of non sinister origins?

A

long histories other functional symtoms

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138
Q

What are backgrounds of lambert eaten myasthenic syndrme?

A

Its rare affecting NMJ and autonomic ganglia, Ab agains PQ type channels and 50-60% have underlying malignancy non cancer is associated with Type 1 DM and thyroid diseases present

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139
Q

When do LEMS present?

A

Non cancer are any age, otherwise over 50

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140
Q

What is presentation of Lambert eaton myasthenic sydrome?

A

Typically proxiamal muscle weekends and dry eyes dry mouth sexual dysfunction autonomic involvement also strength may increase with repeated effort rapid porgressione arly distle muscel involvment and ED

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141
Q

What are investigations of LEMS?

A

90% have antibodies to calcium channel and lots have small cel lung cancer RMG shows reduction on CMAP and subsequent increase of more than 100% with repeated stimulation

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142
Q

What is management of lambert eaton myasthenia?

A

Diamino pyridine helps bloc K and steroids help also treat cancer will help ACh esterase inhibitor

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143
Q

What is congenital myasthenic syndrome?

A

Not autoimmune due to mutation in NMJ proteins

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144
Q

What is neuromyotonia?Isacc;s syndrome

A

Peripheral hyperexcitibility, hyperhydrosis fasiculations crams, myokymia exercise intollerance from antibodies to potassium channels,

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145
Q

What is multiple sclerosis?

A

Inflammatory demyelinating disease specific to CNS usually begins between 20-40 years relapse and remitting but progressive

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146
Q

What does relapse and remitting mean?

A

Random attacks fmroe frequent in first 3 or 4 years recovery can cary disabilities accumulate

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147
Q

What are the factors influencine MS?

A

Genetic environment and chanch clear evidence for environmental factors (twin studies)

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148
Q

What is epidemiology of MS?

A

It varies a lot from country to country but affects wome more than men and white more than black

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149
Q

What is the pathophysiology of MS?

A

genetic succeptibility leading to activated aurto T lymphocytes and B lymphocytes becoming activated and compliment and macrophages causing demyelination

150
Q

What is thecharacteristic damage in MS?

A

the myelin sheath is damaged and then it is remyelinated with short interndes and thin layer

151
Q

What are the features of active MS lesions?

A

Demyelination, variable oligodendrocyte loss, hyercellular plaque edge due to infiltation of tisssue with inflammatory cells, perivenous inflammatory infiltrate blood brain barrier distruption central gliosis

152
Q

what are the features of inactive MS lesions?

A

Demyelination, variable oligodendrocyte loss, hypocellular plaque less inflammation minor blood brain barrier losss

153
Q

Where can MS lesions affect?

A

Many places but cerebral hemispheres giving silent and variable symptoms, spinal cord leading to tingling numbness snd paraplegia also bladder and sexual dysfunction, optic nerves with vision problems medull a and pons nystagmus vertigo cerebellar white matter dysarthria nystagmus intention tremmor

154
Q

What are typical symptoms of MS?

A

Optic neuritis impaired vision and eye pain, spacticity and pyramidal sings, sensory symptoms and signes Lhermitte’s sign nystagmys double vision and vertigo Bladder and sexual dysfunction

155
Q

What are some atypical presentatins of MS?

A

Aphasia, hemianopia, extrapyramidal movement disturbance, severe muscle wasting muscle fasiculation

156
Q

What are the usualy first symptoms in MS?

A

Weakness and parasthesia visual loss and incordination

157
Q

What ar the classifications of MS?

A

Relapse remitting, primary progressive, secondary progressive or progressive relapsing

158
Q

What is needed to diagnose MS?

A

Two or more CNS lesions dissminated in time and space exclusion of conditions giving a similar clinical picture

159
Q

How is CSF of MS patients analysed?

A

Electrophoresis to loog fo IgG banding

160
Q

What are common disease mistaken for MS?

A

SLE Primary sjogren’s syndrome bechets disease polyarteritis nodosa acute disseminated encephalomyelitis, Lye disease syphilis AIDS andrenomeloneurpathy mitochondrial encephalopathy, arnold-Chiari malformation olivopontocerebellar atrophy stroke

161
Q

What are treatmeent for MS?

A

Cant cure just slow progressions. might be able to modify interferon beta glatiramer dimethyl fumarate and terifunommide are first line methylprednisolone in acute relapse

162
Q

What are other treatmetns for MS?

A

treating the effects of the lesions themselves such as spacticity

163
Q

What are the lesions to be treated in MS?

A

Spacticity, tremor (orthotics drugs) sexual dysfunction, depressuon anxiety autonomic dysfunction fatigue

164
Q

What are charateristics of fatigue in MS?

A

different to normal exacerbated by heat, improves by cold makes other symptoms appear worse

165
Q

What can cause pain in MS?

A

Trigeminal neuralgia tonic siezures tic like or burning dysaesthetic pain optic neuritis, vertebral compression fracturs ulnar and eroeal palsise chronic joind and back pain painful spazms

166
Q

What are paroxysmal symptoms of MS/

A

breif duration occur frequently often similar timing to exacerbations, positive sumptoms triggered bu factors can be treated with anticonfulsant

167
Q

What can cause blackouts?

A

heart relates problems or low blood pressure, (stress-related non-epileptic seizures) hypoglycaemia storke or TIA systonia migrain benign paroxysmal positional vertigo, cataplexy, hyperventialtion, nonepileptic siezure

168
Q

What is an epileptic siezure?

A

Paroxysmal event which changes in behavour sensation of processes are caused by excessive hypercynchronous neuronal discharges in the brain

169
Q

What are the charicteristic symptoms of an epileptic attack?

A

30-120 seconds positive additional sensations ictal sumptoms postictal symptoms, can be in sleep , rhythmic jerking often lose control of bowel. tounge bting muscle pain cynaosis can be specific but not sensitive

170
Q

What indicates nonepileptic attack?

A

situational, longer usually 1-20 mins waxing waning course rapid or very slow posticta recovory may have history of somatofomr disorders, dramatic motor phenomina eyes closed ictal crying or speaking

171
Q

What is syncope?

A

Paroxysmal even in which changes in bahaviour sensatin and cognitive processes are cause by insuffficeint blood or oxygen supply to the brain

172
Q

What to consider when treating patients with epilepsy?

A

Is it actually epilepsy, is treatment indicated, what type of epilepsy is it what is the most appropriate drug?

173
Q

What ar the types of epilepsy?

A

Generalised and focal provoked or unclassified

174
Q

What dictate they type of siezure?

A

The location of the sizer beginning

175
Q

What is treatment for focal epilepsy?

A

Carbamazepine or imotragine

176
Q

What is idiopathic generalsied epilepsy?

A

no associated brain abnormality, manifestation usually under 30.

177
Q

What are types of seizures in idiopathic primary generalise epilepsy?

A

Absence siezures primary generalised tonic clonic.

178
Q

How do anti epileptic drugs act?

A

on the synapse on voltage gates sodium channels n presynaptic, noeurotransmitter release, potasssium channels or calcium channels some gaba receptors some gaba transaminase or gaba transporter to increase inhibitions

179
Q

How are anti epileptic drugs intrduced?

A

Monotherappy to increase to lowest possible effective dose, then increase to fully effective maximum tolerated dose can use combination

180
Q

How effective are anti epileptic drugs?

A

63% are siezure free but may take a while to find it

181
Q

What are common side effects of anti epileptics?

A

Significant cognitive side-effects, long term side effects, teratogenic, hepatic enzyme induction non-linear pharacokinetics drug interaction

182
Q

What to do if epilepsy is uncontrolled by drugs?

A

Vagal nerve implant stimulation (paliative), removal of siezzure prne area very effective if done right

183
Q

What are the types of inflammation on MS?

A

Macrophage, antibodies distal oligodendropathy apoptotsis and rimary oligdendroglia degeneration

184
Q

What are investigations of MS?

A

MRI scans Lumbar puncture for CSF immunoglobulins

185
Q

What are phases of MS?

A

Preclincial radiologically isolated. relapsing remitting and the progressive there isnt much to do inprogressive phase

186
Q

What affects prognosis of MS?

A

men worse than men late presentation early motor symptoms, shrot inter attack interval high resuidual disabilty

187
Q

How are relapses treated/

A

type 1 methyl prednisilone type 2 will response to plasma exchenge.

188
Q

When are relapses treated to prebvet?

A

if have 2 or more in 2 years, interferon Beta prevetion of immunoactivation, modicfying lymphocyte traffcking anti adhesion, Lymphocytes depletions immune reconsitiution with stem cell transplantation

189
Q

What are the characteristics of syncope?

A

Typically from sittion or standing rarely from sleep presyncopal symptoms, duration 5-30 seconds recovery within 30 seconds cardiogenic has less warning history of heart disease

190
Q

What is the most common brain cancer?

A

astrocytoma diffuse ones

191
Q

Where are childhood children often?

A

Posterior fossa

192
Q

What is larges group of CNS tumours?

A

Neuroepithelial, ependymal oligodroglial astrocytic embryonal pineal choroid plexus also meningeal tumours lymphomas(EBV) germ cell tumours
metastatic tumours

193
Q

What is most of clinical manifestation of brain tumours?

A

Depends of location of tumour, siezures Raised intracrainial pressure

194
Q

What is diffuse astrocytoma?

A

infiltrates diffusly and has propensity to undergo progresive anaplasia can’t cure cant resect all of it

195
Q

Which grades of brain cancer cannot be cured?

A

grade 2-4

196
Q

What marks progression of astrocytome?

A

hypercellularity pleomorphisms, mitoses and necrosis and vascular proliferation

197
Q

What is ISH1?

A

Isocitrate dehydrogenase mutations

198
Q

What is improtance of IDH1 in brain tumours?

A

IDH mutation is associated with a better prognosis in gliomas because it is not de novo

199
Q

What is the importance f IDH and oher genetics?

A

The add to histological view of prognosis for patients

200
Q

What are medulloblastoma?

A

Primitive small blue cell tumour of the cerebellym childhood, high malignant but can be cured by removal

201
Q

What happens as tumour size increases?

A

compensation hphase of reduction in ventrical volume and less CSF volume, then after this get somewhat expnential changes in pressure (intracranial pressure) Displacement of tissue happens

202
Q

How does the tracts get affected in brain tumours?

A

Get displacement of structures by tumours, can cause hydrochepalus if it blocks the ventricle flow

203
Q

Where can herniation happen in the brian?

A

through the tentorium cerebeli, and the framen magnum

204
Q

What defines headache disorder?

A

Cephalalgia

205
Q

What are the tyes of headache?

A

Priamy mignain cluster tension type, secondary, meningitis haemorage
Nerve pain, trigeminal neuraligia

206
Q

What is secondary headach and when to worry about it.

A

Over 50s history of HIV cancer trauma change in personality congniticve function vomiting with no other cause

207
Q

What is nemonic for secondary headache?

A

SNOOP 10
Systemic, neurological, onset sdden onset age 50 over, phenotype, pattern change, pregnancy, pregnancy, papillodema, painful eue, pathology, prepcipitants posture post trauma painkillers

208
Q

When is immediate refferal for headache?

A

Tunderclap, siezure and new headache, suspected meningitis, suspected encephalitis, red eye

209
Q

What are red flags for brain tumours?

A

cancer history, cluster headache, siezure, significantly altered consciousness behavioural change

210
Q

What is needed in history of headache?

A

SOCRATES history for each one onset duration how long why asking of help, photophobia phenophobia runny nose blocked nose, triggers what do they do, normal/persisting symptoms

211
Q

What can be examined for headache?

A

Fever, altered conciousness focal neurology fundoscopy, neck stifness/Kernigs sign BP

212
Q

What are migraines?

A

With and without aura chronicmigraine medication overuse headache

213
Q

What are most common headaches?

A

Migran med oversue tension type

214
Q

What is migrain without aura?

A

5 attacks last 4-72 hours tat fill the others, two of unilateral pulsing moderate severe agravatied by hysical activity, during headache nausea and or vomiting and photophobia or phonophobia?

215
Q

What is aura?

A

a visual or other disturbance missing part of ision zigzag can be followed after 60mins

216
Q

What are tension type headaches?

A

Mild to moderate, more than 10 over more thean 1 day or onth that are 30 minutes to 7 days, headache is bilateral,jfsdof odsafh dsofhsdoafhasfisdfhiosdhf

217
Q

What are cluster headache?

A

5 headaches that are severe or very severe unilateral orbital supraorbital and or temporal pain ipsilateral cranial autonomic features attachs from 1 per day to 8 per day, need to rule out other causes

218
Q

What is trigeminal neuralgia?

A

unilateral facial pain, in distribution of trigeminal nerve not beyond it, recurring in atacks to very short or a couple of mins sever intensity, electric shock like shooting stabbbing sharp perciptated by innoculus stimulit to the face

219
Q

How are headaches managed?

A

Accurate diagnosis and manage expectations, lifestyle modifications and trigger management, pharmacological treatments, psychological and behavioural treatments surgical treatments

220
Q

What is abortive treatment?

A

used to take when the headache is coming on to stop it from developing and can take NSAID asprin or paracetamol and can take anti emetics

221
Q

What is preventative treatment?

A

topiramate or proranolol as preventive also monoclonal antibodies

222
Q

What to do in resistant headache?

A

wrong diagnosis not effective for the patient compliance with treatment

223
Q

How investigate sub arachnoid haemorrage?

A

CT scan and lumbar puncure looking for Xanthechromia angiogram

224
Q

What is management of SAH?

A

A and E and neurosurgery

225
Q

How can idiopathic intracranial hypertension be treated?

A

CSF shunt, toparamide diuretics, high opening pressure

226
Q

What is giant cell arteritis?

A

Cause of secondary headache, jaw claudication

227
Q

What is chronic daily headache?

A

description of lots of headache can be many causes but can be chronic migraine or medication overuse headache

228
Q

What areas might have problems in neurology?

A

Cerebral hemispheres often unilateral, spinal cord(dermatome myotome) cerebellum discoordination, brian stemm cranial nerve palsies crossed modalities, peripheral nerves glove and stocking

229
Q

How is investigation questions in neurology?

A

where is the lesion what is the pathology

230
Q

What’s a surgical 3rd nerve palsy?

A

Pressing on fibres lose parassympathetic

231
Q

What a medical 3rd nerve palsy

A

might not lose parasympathetic

232
Q

What is internuclear opthalmoplegia?

A

Looking to one side asymetrical nystagmus as it moves to object lesion of medial longditudinal fasiculus from loss of

233
Q

What is lateral medullary syndrome?

A

infarct to brainstem Ipsilateral horners limb at

234
Q

What is weakness?

A

impared ability to move a body part in the will to move it

235
Q

What is paralyiss?

A

Inability to move a body part in response to will

236
Q

What is ataxia or incoordination?

A

Willed movements are clumsy ill-directined or uncontrolled

237
Q

What are involuntary movementes, spontaneous movement of a body pary independently of will

A

What is apraxia diorder of consiously organised patterns of movement or impared ability to recall acquird motor skills

238
Q

Where are lower motor neurons?

A

Located in the anterior horns of the spinal cord and cranile nerve nuclei in the brainstem

239
Q

What innervates stretch receptors?

A

Gamma motor neurones

240
Q

What happens in LMN lesions?

A

Reduced tone flaccid muscle wasting reduced reflexes and fasciculations

241
Q

What diseases affect LMN?

A

MND SMA poliomyelitis syringomeyelis syringobulbia spinal cord brainstem compression vascular disease

242
Q

What can affect peripheral nerves?

A

Distal weaknes glove and mononeuroitis mutiplex axonel degeneration

243
Q

Where do myopathies present?

A

Closer muscles

244
Q

What is pyramidal tract weakness?

A

general weakness, Decreased control of active movement slowness, spacticity velocity dependant cnage in muscle toneimb preservation of flexion in lower limbs

245
Q

What happens in upper motor neuron lesions?

A

increased tone or spacticity, tendon reflexes are brisk, planter responses like babinski sign get muscle weakness but with upper limbs extensorts weaker than flexors but lower limbs flexors weaker than extensors, finer more skillful movements severely impared and may ger emotional lability bay be present

246
Q

What can be affected in upper motor neurons?

A

Cortical lesions Internal capsule Brainstem Spinal cord

247
Q

What can be affected in upper motor neurons?

A

Cortical lesions Internal capsule Brainstem Spinal cord

248
Q

What does muscle wasting show?

A

Lower motor lesion, not MS

249
Q

What affects muscle tone?

A

The feedback from stretch receptors and golgi tenton organs.

250
Q

What are the sites of lower motor neuron damage?

A

motor nuclei of cranial nerves, motor neurones in the spinal cord, spinal ventral roots, peripheral nerves Neuromuscular junction

251
Q

What are signs and symptoms of MND?

A

Muscle atrophy in limbs fasiculations, split hand FDI wasting tongue wasting respiratory

252
Q

What can cause damage to motor neurons of the spina; roots?

A

Prolapses intervertebral disc, cervical or lumbar spondylosis, tumours(neurofiibroma and ependymoma) Malignant infiltration,

253
Q

What can cause problems with peripheral nerves ?

A

symmetrical polyneuropathy from diabetes or B12

254
Q

How can you locate the site of the lesion in motor neurons?

A

Knowletege of reflexes anatomy o f innervation of muscles, sensory and motor signs?, history of diurnal variability/fatigueability, fasciculations patterna of weakenss

255
Q

How should LMN be investigated?

A

Neuro-imaging MRI scan head spine neurophysiology, Blood testes muscle enzymes peripheral neuopathy screeen auto-antibodies lumbar puncture

256
Q

Where in the brain might there be upper motor neuron lesions?

A

Cortical lesions, internal capsule, brainstem and spinal cord

257
Q

What do cortical lesions lead to?

A

contralateral circumscribed weakness,

258
Q

internal capsule injury leads to/?

A

complete contralateral hemiparesis, descending fibres grouped closesly together in a very small area

259
Q

What happens in brainstem lesions?

A

Often bilateral weakness due to involvement of both descending corticospinal tracts may have cranial nerve involvment or bulbar envolvement

260
Q

Spinal cord lesions lead to ?

A

bilateral corticospinal tract lesions cervical will involve upper and ower limbs below cervical will be legs sensory level may help localising the site of the lesion

261
Q

Which diseases affect upper and lower motor nerones?

A

MND hereditary spastic paraplegia

262
Q

What are investigations for upper motor neurone problems?

A

MRI, blood tests for metabolic disorders CSF examination

263
Q

What is TLOC?

A

Transient losss of concessioness Spontaneous loss of consciousness with complete recovery

264
Q

Why is it important to investigate TLOC?

A

To find if its cardiac or neurological as they have higher mortality

265
Q

What are the challenges of TLOC investigation?

A

Main witness unconsiious so hard to know what happened, unpredictable occasionally life threatening, driving restrictions health and safety

266
Q

What are caues of TLOC?

A

Syncope (vasovagal, situational, orthostatic hypotension, cardiac), seizure and Non-epileptic attack disorder

267
Q

What are the key questions of TLOC?

A

What do they mean by black out. was there a trigger prodrome the attack and recovery how often does it happen

268
Q

What can help about prodrome?

A

atypical aura, pre syncopal loss of vision, provoking features assocciated symptoms what are the circumstances can they be prevented

269
Q

What is important to know about the attack?

A

did they lose consciousneess, how long was it change in complexiona verbal responsiveness, feel pulse, movemet jerking injuries

270
Q

What is important about the recovery?

A

Rapid or prologued confused or sleepy muscle pain, how much does they remember

271
Q

What is vasovagal syncope?

A

from standing up due to drop in BP PPP upright provocation, becom pale sweaty vision blurred hearing mufled brief duration reduced muscle tone and rapid recovery. can be convulsive but not typical,

272
Q

What is a key differentiation for vasovagal?

A

No post ictal confuusion often happens when standing up from sitting or lying

273
Q

What is cardiac syncope?

A

Sudden temporary reduction of blood supply to the brain and hence oxygen to the brain, this can be from vasodilation hypotension and arrhythmia

274
Q

What is it important to do if you suspect cardiac syncope?

A

ECG ask about arrhythmogenic drugs family history of cardiac disease or sudden death

275
Q

What is typical of epilepsy?

A

An aura dejavu olfactory or gustatory maybe visual, lsts 30 seconds to 180 seconds, prolongued post ictal confusion, head turning or posturing of body, stiffening of body and myoclonic jerking, abnormal behaviour of which patients do not remember, severe tongue biting

276
Q

How are siezures described?

A

They are described as the seizure types, epilepsy types epilepsy syndromes and aetiology

277
Q

What is a focal siexure?

A

Originate within networks limited to one hemisphere, may be discretely localized or more widely distributed

278
Q

What is a generalised siezure?

A

Originate in a pointbut rapidly engages networks bilaterally, can incluse cortical and subcortical structures doesnt have t be entire cotex

279
Q

Is a TIA TLOC?

A

No as doesn’t actually usually cause a loss of consciousness

280
Q

What is TEA?

A

transient epileptic amnesia doesnt involve loss of consciousness

281
Q

What is likely to indicate Non epileptic attack disorde?

A

gradual onset undulating motor activity with pauses, sinusoidal and asynchronous arm and leg movements prolongues atonis rhythmic pelvic movemnents sitde to side headd mviements, ppost ictal crying prlongued with fast recovery waxing waning course

282
Q

What is helpful vs not helpful in history?

A

Scant description frequent or long siezures different types of siezures crying during recovery is helpful, injury tongue biting and incontincence and siezures in sleep are not very helpful

283
Q

How do you make a diagnosis of non epileptic attack disorder disease?

A

Description/ nature of siezure changes with time good documantaion, unsually frequent drug unresponsie provoked by stress, histoy of somatoform disorder unexplaind systomes history of personality disorder self harm alcohol abuse self harm childhood abuse ask for a video of it

284
Q

Why is it important to diagnose Non-epileptic attack disorder?

A

Inappropriate to start AED as will have no effect, there is treatment for non epileptic attack disorder, reinforcement of abnormal illness behaviour evolution of functional symptoms, incapacity financial and social dependency

285
Q

What to do with TLOC in A and E or GP?

A

TLOC clinic with cardiology, ECG, first seizure clinic, advice on driving safety

286
Q

When is EEG indicated?

A

not to investigate blackout, when wanting to determine epilepsy type or for non epileptic attacks, helpful to capture recording

287
Q

When is an MRI indicated in epilepsy?

A

To look for structural abnormalities

288
Q

How can head injuries be classified?

A

Type of injury penetrating or blunt injuries, distribution of the lesions focal or diffuse or time course of damage follwing the traumatic event primay from injur or secondary after the event

289
Q

what is a scalp laceration?

A

A tear to an area of skin not from a sharp object indicates something severe has gone on

290
Q

What is involved in skull fractures?

A

Imples considerable force increased risk of haemotoma, infection or aerocele flat surface njuries cause flat linear fractures and sharp form distinct flocalised depressed fractures

291
Q

What is an extradural haematoma?

A

From a skul fracture and develops over a few hours often from middle meningeal artery, 10% of head injuries causes death by raised ICP

292
Q

What cause subdural haemotomae?

A

bridging veins rupturing can be chronic

293
Q

What can cause rapid cognitive deline?

A

dementia but also subdural haematoma which can be treated

294
Q

What can cause subarachnoid haematoma in injuries?

A

contusions and lacerations of the meningeal layers or skull fracture, dissection or rupture of the vertebral artery

295
Q

How does head injury get infection?

A

Skull fracture provides a way to let bugs in

296
Q

What are the focal brain damage mechanism?

A

Contact damage or accelleration or deceleration damage

297
Q

What is contact damage?

A

At or just deep to the point of impact

298
Q

What is a coup contusion?

A

Brain damach at the site of lesions happens on the crests of the Giri

299
Q

What is a contrecoup contusion?

A

One on the opposite side to the site of the blow to the brain of the coup mainly jsut from the skull being very close to the underside of the brain

300
Q

What are diffuse lesions?

A

Diffuse axonal vascular swelling vvascualer

301
Q

What is traumatic axonal injury?

A

can be focal or widespread can be from ischaemia and damage from acceleration often in rotational injury in brainstem

302
Q

What does traumatic axonal injury look like?

A

Spheroids of swollen axons, causing build up of amyloid at the site of damage

303
Q

What does traumatic axonal injury look like?

A

Spheroids of swollen axons, causing build up of amyloid at the site of damage can be mild or severe

304
Q

What are the effects of traumatic axonal injury?

A

discolouration of brain and loss of white matter tracts, can also damage blood vessels and cause bleeds petechial bleeds

305
Q

What is brainswelling/

A

Occurs very often in the brain after injusry raises intracrannial pressure from congestive brain swelling vasodilation and cerebral blood volume, vasogenic oedema or cytotoxic oedema release of proteins in CNS casing swelling

306
Q

What can be squished in the tentorial incisure?

A

The uncus in the media temporal lobe

307
Q

What happens in the foramen magnum in raised ICP?

A

herniation of tonsl of cerebellum and pressure on the medulla

308
Q

When do you get hypoxic ischaemia of the brain?

A

Hypotension for a while raised intracranial pressure can be widespread or confined to vulnerable regions border zones between major cerebral territories

309
Q

what visible things can you see in the brain with ischaemic hypoxia?

A

de distinction of the white and grey matter

310
Q

What can happen after years of injury?

A

More likely to develop epilepsy

311
Q

What is chronic traumatic encephalopathy?

A

from trauma, boxers and rugby players. 12% of adults have had a traumatic brain injury with loss of conciousness it is a risk factor for dementia and chronic traumatic encephalopathy

312
Q

Chronic traumatic encephalopathy presentation?

A

Irritibility agression and memory loss then dementia and parkinson like symptoms and MND but have Tau deposition and TDP-43 but in strange patterns not like

313
Q

What are the two main types of stroke?

A

Haemorrhagic stroke and ischaemic stroke

314
Q

What are the two areas you can group cerebral events/

A

is it a posterior or anterior circulation stroke?

315
Q

What is the most damaging area to have a stroke in?

A

Middle cerebral is really bad as does a lot cause high deficiet

316
Q

What are the characteristics of anterior circulation teritory stroke?

A

leg weakness, sensory disturbance in the legs, Gait apraxia truncal ataxia, incontincence drowsiness, Akinetic mutism decrease in spontaneous speech stupurus state

317
Q

What does a stroke look like on a scan?

A

darker area as it is less dense from exocutotoxicity and the cells swell/retain water

318
Q

How long does it take for stroke to show on a CT scan?

A

4 or so hours

319
Q

What do you get with a middle cerebral artery stroke?

A

Contralateral arm and leg weakness, contralateral sensory loss, hemianopia, aphasia dysphasia, facial droop

320
Q

What happens in large middle cerebral artery strokes?

A

Displacement of ventricals, mallicangnant MCA syndrome causing coning

321
Q

What are symptoms of posterior cerebral artery stroke?

A

Contralateral homonymous hemianopia, Cortical blindness with bilateral involvement of the occipital lobe branches, visual agnosis prosopagnosia dyslexia anomic aphasia colour naming discrimination problems headaches unilateral

322
Q

Which are worse anterior circulation or posterior circuation?

A

Posterior as stops signals getting down

323
Q

What is common signs of posterior circulation strokes?

A

Motor deficits such as hemiparesis or tetraparesis and facial paresis, dysarthria and speech swallowing impairment vertigo nausea vomiting, visual disturbances, altered consciousness

324
Q

What kind of scan for posterior?

A

MRI as shows the water content of the brain so can show areas more clearly

325
Q

What is lacunar stookes?

A

They affect one modality often

326
Q

What are warning syndromes?

A

Symptoms that are warning of stokes happening fluctuating symptoms from reperfusion

327
Q

What are the treatments for stoke?

A

break up the thrombotic embolus, or thrombectomy to remove the thrombus

328
Q

What are conditions for thrombolysis?

A

IV treatment, up to 4.5 hours after onset, cant have if had recent surgery, recent arterial puncture, hisory of active malignancey evidence of brain aneurisms, patient on anticoagulation severe liver disease acute pancreatitis liver disease or has a clotting disorder

329
Q

What are the two types on neurological motor disorders?

A

Physical problems Parkinson’s Huntington’s, Also software problems, essential tremmor, dystonia and tourette’s

330
Q

What are the usual presentations of Parkinson disease

A

Initial gate problems and gradual worsening of symptoms on one side of the body, wehen walking drag leg walk slowly, stiffness reduce armswing, importance of time progressive but not always there, affects one side more than the other later might have both

331
Q

What are the three cardinal features of Parkinson’s?

A

Brady/Akinesia(typing buttons smaller writing walking deteriorated, tremor at rest may be unilateral, rigidity pain problems with turning in bed

332
Q

What are important examination findings of Parkinson’s?

A

small stepped gait with stooped posture reduced armswing one side more than the other, increased tone=regidity, tone increased over entire radius of joint movement, rest tremor with frequecy 3-6HZ, often asymmetrical also some postural tremor, decreasing amplitude/accuracy of repetitive movements much better at the beginning gradual worsening

333
Q

What causes pathology in parkinsons?

A

intracytoplasmic inclusion bodies Lewy bodies in the substantia ngra cells

334
Q

What is DaTSCAN?

A

Radiolabelled ligand for the substantia nigra end of neurones and find signal is reduced in Parkinson’s not necessarily specific

335
Q

What are causes of Parkinson’s?

A

Risk factors, Toxin induced, Parkinson’s genes, susceptibility factors, mitochondrial dysfonction, oxidative stress causing cell loss in the substantia nigra

336
Q

What to do to speak to patients about prognosis of parkinsons?

A

It is slowly progressive, it does not change its nature over night you are the expert
No cure no disease modifying treatment but plenty of symptomatic treatment options compensate for loss of dopamine

337
Q

What drugs for Parkinson’s?

A

L-dopa a precursor to dopamine, Dopamine agonist to act on the recptors also monoamino-oxidase inhibitors and catechol-o-methyl-transferase to stop break down

338
Q

What are the use of anticholinergics for Parkinsons?

A

Block the parasympathetic to allow mroe effect of dopamine, they affect cognition, and others

339
Q

What are the motor complications of late-stage PD?

A

Wearing off medication doesnt work for as long, on-dyskinesia hyperkinetic choreiform movements when work, off dysckinesia painful dyskinesia and losss of function

340
Q

When should you treat parkinson’s?

A

depend on symptoms, not sure it makes an effect on disease

341
Q

How to chose which drug?

A

inhibitors are not very powerful, agonist first line in younder good for soft sideeffects like tirednes gambiln hypersexuality and L dopa is most powerful and go to, greater risk of SE

342
Q

What are types of L-Dopa?

A

dispersible kick start in morning standard release for day time slow release for night time

343
Q

What is cognitive disease in PD?

A

Depression very common, other psyciatric problems phobias, aniety hallucialtion autonomic problems constipation increased urinary frequency urinary incontinence not typical denentia

344
Q

Which signs are not usually present in Parkinson’s?

A

Dementia, symmetry, early falls, incontinence

345
Q

What is in the sensory ganglion?

A

the cell bodies of the sensory neurones which lie out of the spinal cord

346
Q

What fibres carry pain?

A

C fibres and A delta fibres

347
Q

What fibres cary light touch and pressre?

A

ABeta

348
Q

Which nerves carry propriaceptopn?

A

Aalpha

349
Q

What can cause nerve damage?

A

Demyelination or axonal damage

350
Q

What is mononeuopathy?

A

Problem with one nerve

351
Q

What is polyneuopathy?

A

Problem with multiple nerves

352
Q

What are common mononeuropatheis?

A

Carpal tunnel syndrome ulnar neuropathy cubital tunnel, peroneal neuopathy entrapment at fibular hedcranial nerve palsys

353
Q

What are the two main types of polyneuropothies?

A

Large fibre neuropathies or small fibres

354
Q

What are the types of large fibre neuropathties?

A

Chronic or acute axonal or demyelinating

355
Q

Which fibres are most likely to be affected first?

A

temperature and pain from small C fibre loss

356
Q

What is ataxia?

A

Poor balance sensory loss of proprioception or cerebellar dysfunction when sensory it gets worse with eyes closed

357
Q

What are motor symptoms of peripheral europathy?

A

Muscle cramps, high arch foot weaknes fasiculations and atrophy

358
Q

What cause asymmetrical sensory?

A

patch distribution, dorsal root ganglia affected uncommone part of paraneoplastic, Sjogren’s Gluten sensiticity

359
Q

What causes asympetrical sensorimotor?

A

vasculitis, mononeuritis multiplex

360
Q

What causes symerical nerve los?

A

length-dependent initially sensory but sensorymotor often from diabetes B12

361
Q

How to make a diagnosis of peripheral neuropathy/

A

History, clinical exam sensory and motor deficites, reduced or absent tendon reflexes neurophysiolocgical examinations

362
Q

What differentiates demyelinating from axonal loss?

A

slow conduction axonal is reduced amplitudes of the potentials in NCS

363
Q

What can cause axonal PN?

A

systemic disease (b12 diabetes CD CKD alcohol hypothyroidism amyloidosis connective tissue disease HIV hepatitis immune mediated vasculitis diabetes metabolic disorders pharmaceuticals hereditary

364
Q

What are the chronic demyelinatice neuropathies

A

Charcot marie tooth disease umbrella term all genetic, Hereditary

365
Q

What are the acute polyneuropathies?

A

Guillain Barre syndreme

366
Q

What is guillian Barre syndrome?

A

Demyelinating Axonal motor axonal sensorymotors rapid ascending paralysis and sensory deficits, infection might proceed it needs immediate treatment ICIG plasma exchane ITU

367
Q

What can cause death in guillian Barre syndroem?

A

autonomic failure infection or non-creatment

368
Q

How are neuropathies treated/

A

pain amytriptiline cramps with quinine balance through physio usually symptomatic also aim to identify the cause and treat

369
Q

What is involved in risk management of stoke post stroke/

A

Aspirin and clopidogrel, statins AF treatment warfarin NOAC’srivaroxabam Blood pressure treatment

370
Q

What are other stroke treatments?

A

Clot retrieval thrombectomy, intraarterial thrombolysis decompressive craniectomy

371
Q

What to do with stroke straight away?

A

CT head

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