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Med Student Finals > Neurology > Flashcards

Neurology Flashcards

1
Q 
Patterns of Motor Loss
Cortical Lesions (3)
A

Unexpected pattern of weakness of all movements of a hand or foot
Normal/reduced tone
Increased reflexes more proximally in the arm or leg will suggest an UMN rather than LMN

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2
Q

Patterns of Motor Loss

Internal Capsule and Corticospinal Tract Lesions (3)

A

Cause contralateral hemiparesis
If occurs with epilepsy, reduced cognition or hoonymour hemianopia then lesion is in cerebral hemisphere
A cranial nerve palsy (III-XII) contralateral to a hemiplegia implicates the brainstem on the side of the cranial nerve palsy

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3
Q

Patterns of Motor Loss Cor lesions (2)

A

Paraparesis (both legs) or quadriparesis/tetraplegia (all limbs)
Find lesion by finding a motor and reflex level- power is unaffected above the lesion, with LMN signs at the level of the lesion and UMN signs below the lesion

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4
Q 
Patterns of Motor Loss 
Peipheral neuropathies (4)
A

Most cause distal weakness eg. foot drop
In Guillain-Barre weakness if often proximal due to root involvement
Involvement of a single nerve (mononeuropathy) occurs with trauma or entrapment eg. carpal tunnel
Involvement of several nerves (mononeuritis multiplex) eg. DM/vasculitis

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5
Q

Patterns of Sensory Loss

Tracts (2)

A

Pain and temp. travel along small fibres in peripheral nerves and the spinothalamic (anterolateral) tracts in the cord and brainstem
Joint-position and vibration sense travel in large fibres in peripheral nerves and the large dorsal columns of the cord

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6
Q

Patterns of Sensory Loss

Distal Sensory Loss (3)

A

Suggests a neuropathy
May involve all sensory modalities or be selective, depending on size of involved fibre
Individual nerve lesions are identified by their anatomical territories, which are usually more sharply defined than dermatomes (root lesions)

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7
Q 
Patterns of Sensory Loss
Sensory level (2)
A

Hallmark of a cord lesion- ie. decreased sensation below lesion, normal sensation above
Hemicord lesions cause a Brown-Sequard picture with dorsal column loss on the side of the lesion and contralateral spinothalamic loss

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8
Q

Patterns of Sensory Loss

Dissociated sensory loss (3)

A

Occur in cervical cord lesions- loss of fine touch and proprioception without loss of pain and temp.
Lateral brainstem lesions show both dissociated and crossed sensory loss with pain and temp. loss on the side of the face ipsilateral to the lesion, and contralateral arm and leg sensory loss
Lesions above th ebrainstem give a contralateral pattern of generalised sensory loss

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9
Q

Patterns of Sensory Loss

Dissociated sensory loss (3)

A

Occur in cervical cord lesions- loss of fine touch and proprioception without loss of pain and temp.
Lateral brainstem lesions show both dissociated and crossed sensory loss with pain and temp. loss on the side of the face ipsilateral to the lesion, and contralateral arm and leg sensory loss
Lesions above the brainstem give a contralateral pattern of generalised sensory loss

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10
Q 
Patterns of Sensory Loss
Cortical lesions (1)
A

Sensory loss is confined to more subtle and discriminative sensory functions

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11
Q 
Cerebral Artery Occlusion 
Carotid artery (2)
A

At worst, internal carotid artery occlusion causes total fatal infarction of the anterior 2/3rd of its hemisphere and basal ganglia
More often, the picture is like middle cerebral artery occlusion

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12
Q

Cerebral Artery Occlusion

Anterior cerebral artery (4)

A

Supplies the frontal and medial part of cerebrum
Occlusion may cause a weak, numb contralateral leg +/- similar (usually milder) arm symptoms
Face is spared
Bilateral infarction can cause akinetic mutism from damage to the cingulate gyri (also a rare cause of paraplegia)

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13
Q

Cerebral Artery Occlusion

Middle cerebral artery (2)

A

Supplies lateral part of each hemisphere
Occlusion may cause contralateral hemiparesis, hemisensory loss (especially face and arm), contralateral homonymous hemianopia due to involvement of optic radiation, cognitive change including dysphasia with dominant hemisphere lesions + visuospatial disturbance with non-dominant lesions

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14
Q

Cerebral Artery Occlusion

Posterior cerebral artery (2)

A

Supplies the occipital lobe

Occlusion gives contralateral homonymous hemianopia

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15
Q 
Cerebral Artery Occlusion 
Vertebrobasilar Circulation (4)
A

Supplies the cerebellum, brainstem + occipital lobes
Occlusion causes signs relating to any or all 3: hemianopia, cortical blindness, diplopia, vertigo, nystagmus, ataxia, dysarthria, dysphasia, hemi/quadri-plegia, unilateral or bilateral sensory symptoms, coma
Infarctions of the brainstem can cause vertigo, vomiting, dysphagia, nystagmus
Locked in syndrome is due to pontine artery occlusion (can’t move but aware)

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16
Q

Causes of Acute Single Episodes of Headache

9

A

Meningitis (fever, photophobia, stiff neck, purpuric rash, coma)
Encephalitis (fever, odd behaviour, fits, reduced consciousness)
Subarachnoid haemorrhage (sudden onset)
Head injury (usually lasts 2 weeks but rule out subdural/extradural)
Venous sinus thrombosis (subacute/sudden, papilloedema)
Sinusitis (dull, constant ache over sinuses with tenderness, worse on bending)
Tropical illness (malaria)
Low pressure headache (CSF leak)
Acute glaucoma (elderly, constant ache around eye, reduced vision, cloudy cornea)

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17
Q

Causes of Acute Single Episodes of Headache

9

A

Meningitis (fever, photophobia, stiff neck, purpuric rash, coma)
Encephalitis (fever, odd behaviour, fits, reduced consciousness)
Subarachnoid haemorrhage (sudden onset)
Head injury (usually lasts 2 weeks but rule out subdural/extradural)
Venous sinus thrombosis (subacute/sudden, papilloedema)
Sinusitis (dull, constant ache over sinuses with tenderness, worse on bending)
Tropical illness (malaria)
Low pressure headache (CSF leak)
Acute glaucoma (elderly, constant ache around eye, reduced vision, cloudy cornea)

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18
Q

Migraine

Symptoms (6)

A 
Visual or other aura lasting 15-30 mins followed by unilateral, throbbing headache 
Nausea 
Vomiting 
Photophobia
Phonophoia 
Allodynia- all stimuli produce pain
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19
Q

Migraine

Associations (2)

A

Obesity

Patent foramen ovale

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20
Q

Migraine

Stages (4)

A

Prodrome: precedes headache by hours/days, yawning, cravings, mood/sleep change
Aura: precedes headache by mins
Headache
Postdrome: fatigue, cognitive changes, muscle pain

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21
Q

Migraine

Triggers (9)

A 
Chocolate 
Hangovers 
Orgasms 
Cheese 
Oral contraceptives
Lie-ins 
Alcohol 
Tumult 
Exercise
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22
Q 
Migraine
Differential diagnosis (4)
A

Cluster headache
Tension headache
Intracranial pathology
Sinusitis/otitis media

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23
Q 
Migraine
Acute therapy (5)
A

Restrict to 2 days a week
Aspirin 900mg
Ibuprofen 400-600mg
Triptans: sumatriptan 1st choice (contraindicated if IHD, uncontrolled high BP; side effect arrhythmias)
Add antiemetic if vomiting: metoclopramide

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24
Q 
Migraine
Preventative therapy (6)
A

Consider if migraine is disabling and reduced quality of life or prolonged severe attacks
Propranolol 1st
Topiramate (side effect reduced memory) 2nd
Amitriptyline/other TCA
Candesartan
Others: sodium valproate (not for young women), pizotifen

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25
Q

Cluster Headache

Symptoms of attack (6)

A

Rapid onset of excrutiating pain
Around on eye, may become watery and bloodshot
Strictly unilateral (almost always affects same side)
Lasts 15-60 min
Occurs once/twice daily
Often nocturnal

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26
Q

Cluster Headache

Symptoms of bout (2)

A

Clusters last 4-12 weeks

Followed by pain free periods of months or even 1-2 years

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27
Q

Cluster Headache

Treatment of acute attack (3)

A

100% O2
Sumatriptan SC
Zolmitriptan nasal spray

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28
Q 
Cluster Headache 
Preventative treatment (4)
A

Suboccipital steroid injections
Verapamil
Lithium
Melatonin

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29
Q

Trigeminal Neuralgia

Symptoms (4)

A

Intense, stabbing pai
Lasts seconds
In trigeminal nerve distribution unilaterally (typically maxillary/mandibular)
Face screws up with pain

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30
Q

Trigeminal Neuralgia

Triggers (4)

A

Washing affected area
Shaving
Eating
Talking

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31
Q 
Trigeminal Neuralgia 
Secondary causes (4)
A

Compression of trigeminal nerve root by aneurysmal intracranial vessels or a tumour
Chronic meningeal inflammation
MS
Skull base malformation

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32
Q

Trigeminal Neuralgia

Investigations (1)

A

MRI to exclude secondary causes (approx. 14%)

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33
Q

Trigeminal Neuralgia

Treatment (5)

A 
Carbamazepine 
Lamotrigine 
Phenytoin 
Gabapentin 
Surgery if drugs fail
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34
Q

Giant Cell Arteritis

Aetiology (3)

A

Elderly
Takayasu’s if <55
Polymyalgia rheumatica

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35
Q

Giant Cell Arteritis

Symptoms (5)

A 
Headache 
Temporal artery and scalp tenderness 
Jaw claudication 
Sudden blindness, typically in on eye 
Extracranial symptoms: dyspnoea, moring stiffness, unequal/weak pulses
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36
Q

Giant Cell Arteritis

Investigations (6)

A 
ESR ++
CRP ++ 
Platelets + 
Alk Phos + 
Hb - 
Temporal artery biopsy
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37
Q

Giant Cell Arteritis

Treatment (2)

A

Prednisolone

Typically a 2 year course then complete remission

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38
Q

Tension Headache

Signs + Symptoms (3)

A

Bilateral
Non-pulsatile headache
+/- scalp tenderness

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39
Q

Tension Headache

Treatment (2)

A

Massage

Antidepressants

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40
Q

Raised Intracranial Pressure

Aetiology (7)

A 
Head trauma 
Infections 
Tumours 
Stroke 
Epilepsy/seizures 
Hydrocephalus 
Meningitis
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41
Q

Raised Intracranial Pressure

Signs + Symptoms (6)

A 
Headache worse on waking, lying, bending forward or coughing 
Vomiting 
Papilloedema 
Seizures 
False localising signs 
Odd behaviour
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42
Q

Raised Intracranial Pressure

Investigations (2)

A

Imaging to exclude a space-occupying lesion

LP contraindicated until after imaging (measure pressure )

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43
Q

Raised Intracranial Pressure

Treatment (4)

A

Head elevation to facilitate venous return
Reduce pressure by draining fluid through a shunt
Mannitol or hypertonic saline (remove fluid from body)
Sedation as anxiety raises BP which raises ICP

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44
Q

Medication Overuse Headache

Aetiology (3)

A

Mixed analgesics (paracetamol + codeine/opiates)
Ergotamine
Triptans

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45
Q

Medication Overuse Headache

Treatment (3)

A

Withdraw the analgesia- aspirin or naproxen may help rebound headache
Preventive may help once off other drugs (eg. tricyclics, valproate, gabapentin)
Limit use of over the counter analgesia (no more than 6 days/month)

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46
Q

Medication Overuse Headache

Treatment (3)

A

Withdraw the analgesia- aspirin or naproxen may help rebound headache
Preventive may help once off other drugs (eg. tricyclics, valproate, gabapentin)
Limit use of over the counter analgesia (no more than 6 days/month)

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47
Q

Vasovagal Syncope

Aetiology (1)

A

Due to reflex bradycardia +/- peripheral vasodilatation provoked by emotion, pain, fear or standing too long

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48
Q

Vasovagal Syncope

Signs + Symptoms (8)

A 
Onset over seconds 
Often preceded by nausea, pallor, sweating and closing in of visual fields (pre-syncope) 
It cannot occur if lying down 
Unconscious approx. 2 mins 
Brief clonic jerking of the limbs may occur (due to cerebral hypoperfusion leading to reflex anoxic convulsion) 
Urinary incontinence rare 
No tongue biting 
Recovery rapid
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49
Q 
Carotid Sinus Syncope 
Carotid sinus (3)
A

A collection of baroreceptors
Dilated area at the base of the internal carotid artery just superior to the bifurcation
Baroreceptors sense pressure changes by responding to change in the tension of the arterial wall

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50
Q

Carotid Sinus Syncope

Definition (1)

A

Hypersensitive baroreceptors cause excessive reflex bradycardia +/- vasodilatation on minimal stimulation eg. head turning, shaving

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51
Q 
Epilepsy
Seizure elements (3)
A

Prodrome lasting hours/days may rarely precede the seizure
Aura is part of seizure of which the patient is aware, may be strange feeling in the gut, sense of deja vu or smells/flashing lights (implying a focal seizure, often from the temporal lobe)

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52
Q 
Epilepsy
Seizure Classification (5)
A

Partial (focal) seizures: features referable to a part of one hemisphere, often structural disease
Primary generalised seizures: simultaneous onset of electrical discharge throughout cortex with no localising features referable to only one hemisphere, absence seizures, tonic-clonic seizures, myoclonic seizures
Absence seizures: brief (<10s) pauses, presents in childhood eg. suddenly stops talking mid-sentence then carries on where left off
Tonic-clonic: loss of consciousness, stiff limbs (tonic), then jerk (clonic), post-ictal drowsy
Myoclonic: sudden jerk of limb/face/trunk, may be thrown suddenly to the ground

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53
Q

Epilepsy

Aetiology (5)

A

2/3 idiopathic (often familial)
Structural: cortical scarring (eg. head injuries), developmental, space occupying lesion, stroke
Non-epileptic: trauma, stroke, haemorrhage, increased ICP, alcohol, drugs (cocaine), infection (meningitis)
Metabolic disturbance: hypoxia, high/low Na, low Ca, high/low glucose
Trigges: alcohol, stress, fevers, flickering lights

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54
Q

Epilepsy

Investigations (4)

A

EEG
MRI (structural lesions)
Drug levels
Bloods: Na, Ca, glucose

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55
Q

Epilepsy

Treatment of generalised tonic-clonic seizures (2)

A

1st sodium valproate/lamotrigine

2nd carbamazepine/topiramate

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56
Q

Epilepsy

Treatment of absence seizures (3)

A

Sodium valproate
Lamotrigine
Ethosuximide

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57
Q

Epilepsy

Treatment of myoclonic seizures (2)

A

1st sodium valproate/lamotrigine

Must avoid carbamazepine, which may worsen seizures

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58
Q

Epilepsy

Treatment of focal seizures (2)

A

1st carbamazepine

2nd sodium valproate/lamotrigine/topirimate

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59
Q

Epilepsy

Side effects of treatments (3)

A

Carbamazepine: blurred vision, impaired balance, drowsiness
Lamotrigine: maculopapular rash, Stevens-Johnson syndrome or TEN, blurred vision, photosensitivity
Sodium valproate: teratogenic, nausea v common, pancreatitis, weight gain

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60
Q

Acoustic Neuroma

Definition (1)

A

Schwannoma arising from the vestibular nerve

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61
Q

Acoustic Neuroma

Signs + Symptoms (3)

A

Often presents with unilateral hearing loss, vertigo occurs later
With progression- ipsilateral Vth, VIth, IXth and Xth nerves may be affected and ipsilateral cerebellar signs
Signs of increased ICP occur late and suggest large tumour

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62
Q

Gait Disorders

Spastic (1)

A

Stiff, circumduction of legs +/- scuffing of the toes of the shoes

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63
Q

Gait Disorders

Extrapyramidal (4)

A

Flexed posture, shuffling feet, slow to start, postural instability, apraxic
‘Gluing to the floor’ on attempting walk
Wide-based unsteady gait with a tendency to fall
Causes: normal pressure hydrocephalus, multi-infarct states

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64
Q

Gait Disorders

Ataxic (4)

A

Wide-based
Falls
Cannot walk heel-to-toe
Causes: cerebellar lesions (eg. MS, posterior fossa tumours, alcohol), proprioceptive sensory loss (eg. reduced B12)

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65
Q

Gait Disorders

Myopathic (2)

A

Waddle (hip girdle weakness)

Can’t climb steps or stand from sitting

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66
Q

Gait Disorders

Psychogenic (2)

A

Often a bizarre gait not conforming to any pattern of organic gait disturbance
Suspect if profound gait disturbance but without any signs on couch examination

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67
Q

Dyskinesia

Definition (2)

A

Abnormal involuntary movements

Impaired planning, control and execution of movement

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68
Q

Dyskinesia

Tremor (4)

A

Rest tremor: abolished on voluntary movement, caused by Parkinsonism
Intention tremor: irregular, large-amplitude, worse at end of purposeful acts eg. finger pointing, caused by cerebellar damage (eg. MS, stroke)
Postural tremor: absent at rest, present on maintained posture (arms outstretched) and may persist (but isn’t worse) on movement, caused by benign essential tremor (autosomal dominant), hyperthryoidism, anxiety
Re-emergent tremor: postural tremor developing after delay of approx 10 seconds (eg. Parkinson’s)

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69
Q

Dyskinesia

Chorea (2)

A

Non-rhythmic, jerky, purposeless movements flitting from one place to another, eg. facial grimacing, raising shoulders, flexing/extending fingers
Causes: Huntington’s disease

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70
Q

Dyskinesia

Hemiballismus (2)

A

Large amplitude, flinging hemichorea (affects proximal muscles) contralateral to a vascular lesion of the subthalamic nucleus (often elderly diabetics)
Recovers spontaneously over months

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71
Q

Dyskinesia

Athetosis (3)

A

Slow, confluent, purposeless movements (especially digits, hand, face, tongue)
Hard to distinguish from chorea
Causes: cerebral palsy

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72
Q

Dyskinesia

Tics (3)

A

Brief, repeated, stereotyped movements which patients may suppress for a while
Common in children and usually resolve
Common in Tourette’s (motor and vocal)

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73
Q

Dyskinesia

Myoclonus (2)

A

Sudden involuntary focal/general jerks arising from cord, brainstem or cerebral cortex
Seen in metabolic problems (low Na, high CO2) neurodegenerative disease and myoclonic epilepsies (infantile spasms)

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74
Q 
Dyskinesia
Tardive Syndromes (4)
A 
Tardive means 'delayed onset'
Common after chronic exposure to dopamine antagonists (eg. antiemetics, antipsychotics) 
Tardive dyskinesia (movements) 
Tardive dystonia (muscle spasms, twisting/turning character)
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75
Q

Dystonia

Definition (1)

A

Prolonged muscle contractions causing abnormal posture or repetitive movements

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76
Q

Dystonia

Idiopathic generalised dystonia (2)

A

Onset in childhood

Often starts with dystonia in one leg, spreading to that side of the body

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77
Q 
Dystonia 
Focal dystonias (3)
A

Confined to one part of the body eg. writer’s cramp
Rarely generalise
Worsened by stress

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78
Q 
Dystonia 
Acute dystonia (3)
A

May occur on starting neuroleptics and some antiemetics
May mistake for tetanus or meningitis
Rapidly disappear after a dose of anticholinergic

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79
Q

Stroke

Definition (1)

A

Rapidly developing clinical signs of focal (or global) disturbance of cerebral function, with symptoms lasting >24 hours

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80
Q

Stroke

Pathophysiology (2)

A

Ischaemic 85%

Haemorrhagic 15% (70% primary intracerebral haemorrhage, 30% secondary haemorrhage eg. SAH)

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81
Q

Stroke

Causes (5)

A

Small vessel occlusion
Cardiac emboli: AF, MI
Atherothromboembolism eg. from carotids
CNS bleeds: high BP, trauma, aneurysm rupture, anticoagulation, thrombolysis
Carotid dissection (spontaneous or from neck trauma)

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82
Q

Stroke

Blood supply to the brain (2)

A

Carotid system supplies most of the hemispheres and cortical deep white matter
Vertebro-basilar system supplies the brainstem, cerebellum and occipital lobes

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83
Q

Stroke

Non-modifiable risk factors (4)

A

Previous stroke
Age
Male
Family history

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84
Q

Stroke

Modifiable risk factors (8)

A 
High BP (exacerbates atheroma and increases involvement of smaller distal arteries) 
Smoking 
Diabetes 
The pill 
Sedentary lifestyle 
Lipids 
Heavy drinking 
AF
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85
Q

Stroke

Total anterior circulation syndrome (TACS) (5)

A 
Complete hemiparesis/numbness 
Loss of vision on one side (hemianopia) 
Loss of awareness on one side (inattention)- non dominant
Main artery to one hemisphere 
Dysphasia on its own
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86
Q

Stroke

Partial anterior circulation syndrome (PACS) (4)

A

Branch of main artery
2 of the 3 TACS criteria
Or one higher cortical deficit: inattention or dysphasia
Or monoparesis

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87
Q 
Stroke
Lacunar syndrome (LACS) (5)
A

Small perforating artery (basal ganglia, internal capsule, thalamus, pons)
Weakness/numbness of: face + arm + leg OR face + arm OR arm + leg
May have dysarthria
Ataxic hemiparesis
No affect on higher function (no dysphasia, inattention or hemianopia)

88
Q

Stroke

Posterior circulation syndrome (POCS)

A 
Any posterior artery 
Loss of balance/coordination 
Vertigo 
Double vision 
Dysarthria 
Visual loss (hemianopia)
89
Q

Stroke

Outcomes at 12 months (4)

A

TACS: 60% mortality at 1 year, 6% recurrence rate at 1 year
PACS: 16% mortality at 1 year, 17% recurrence rate at 1 year (common early)
LACS: 11% mortality at 1 year, 9% recurrence rate at 1 year
POCS: 19% mortality at 1 year, 20% recurrence rate at 1 year

90
Q 
Stroke
Differential diagnoses (6)
A 
Seizures 
Syncope 
Sugar (hypo or hyper) 
Sepsis (+ previous stroke) 
Severe migraine 
Space occupying lesions
91
Q

Stroke

Investigations (8)

A 
CT head: haemorrhagic- hyperdense lesion, ischaemic- normal/parenchymal darkness, loss of grey-white matter difference, hyperattenuation of artery (clot inside) 
FBC: exclude anaemia + thrombocytopenia 
U+E + creatinine: exclude electrolyte disturbance 
Glucose: exclude hypo/hyper 
Troponin: exclude MI
Clotting screen 
ECG: exclude MI + AF 
Carotid doppler ultrasound
92
Q

Stroke

Treatment of ischaemic stroke (4)

A

Thrombolysis (eg. tissue plasminogen activator- alteplase) if within 4.5 hours
Anti-platelet: aspirin
Secondary prevention: statin, anticoagulation if in AF (warfarin/DOAC), antiplatelet (clopidogrel)
Carotid endarterectomy

93
Q

Stroke

Contraindications to thrombolysis (8)

A 
Previous inrtacranial haemorrhage 
Seizure at stroke onset 
Intracranial neoplasm 
Lumbar puncture within 7 days 
Pregnancy 
Active bleeding 
Oesophageal varices 
Require CT 24 hours after to assess for haemorrhage
94
Q

Stroke

Treatment of haemorrhagic stroke (3)

A

Rapid BP control if within 6h and systolic 150-220, aiming 130-140 within 1h
Neurosurgical opinion
Stop anticoagulants and antiplatelets

95
Q

Stroke

Locating the infarct (4)

A

Ant. cerebral artery: supplies frontal + medial cerebrum, causes contralateral motor/sensory loss in legs > arms with face sparing
Middle cerebral artery: supplies lateral hemisphere, causes motor/sensory loss in face + arms > legs, contralateral homonymous hemianopia due to optic radiation involvement and cortical changes (dysphasia if dominant hemisphere; hemisensory neglect/apraxia if non-dominant)
Posterior cerebral artery: supplies occipital lobe causing contralateral homonymous hemianopia with macular sparing
Vertebrobasilar circulation: supplies brainstem, cerebellum + occipital lobe, causes hemianopia/cortical blindness, CN lesions, quadriplegia + sensory symptoms

96
Q

Transient Ischaemic Attack

Definition (3)

A

Sudden onset of focal CNS phenomena due to temporary occlusion of part of the cerebral circulation
Usually embolic
Symptoms <24 h

97
Q

Transient Ischaemic Attack

Aetiology (2)

A

Atherosclerotic thromboembolism (usually from carotids)
Cardioembolism (post mI, AF, valve disease)
Hyperviscosity (polycythaemia, sickle cell disease, myeloma)

98
Q

Transient Ischaemic Attack

Signs + symptoms (3)

A 
Mimic stroke in same arterial territory 
Global events (eg. syncope, dizziness) not typical 
Emboli may pass to the retinal artery, causing amaurosis fugax (one eye's vision is progressively lost)
99
Q 
Transient Ischaemic Attack 
Differential diagnoses (4)
A

Hypoglycaemia
Migraine aura (symptoms spread over seconds, often visual)
Focal epilepsy (symptoms spread over seconds, often twitching/jerking)
Retinal bleeds

100
Q

Transient Ischaemic Attack

Investigations (6)

A 
Bloods: FBC, U&amp;E, ESR, glucose, lipids, clotting 
CXR
ECG: exclude MI/AF
Echo: valvular disease 
Carotid doppler
CT/MRI
101
Q

Transient Ischaemic Attack

Treatment (4)

A

Immediate anti-platelet: aspirin or clopidogrel
Carotid endarterectomy: if >70% stenosis
Anticoagulation eg. warfarin: if cardiac emboli eg. AF
Control cardiovascular risk factors: antihypertensives, statin, diabetic control, stop smoking

102
Q

Subarachnoid Haemorrhage

Aetiology (3)

A

Berry aneurysm rupture (80%): usually at junction of posterior communicating artery with the internal carotid artery or anterior communicating artery with anterior cerebral artery or MCA bifurcation, berry aneurysms are associated with polycystic kidneys, coarctation, Ehlers-Danlos
Arterio-venous malformation
No cause is found in <15%

103
Q 
Subarachnoid Haemorrhage
Risk factors (5)
A 
Smoking 
Alcohol misuse 
Hypertension 
Bleeding disorders 
Post-menopausal
104
Q

Subarachnoid Haemorrhage

Signs + symptoms (8)

A 
Sudden (thunderclap) occipital headache 
Vomiting 
Collapse 
Seizures 
Coma 
Neck stiffness
Terson's syndrome: retinal,macular and vitreous bleeds 
Kernig's sign: severe stiffness of hamstrings causes inability to straighten leg when hip flexed to 90 degrees
105
Q 
Subarachnoid Haemorrhage
Differential diagnoses (4)
A

Meningitis
Migraine
Intracerebral bleeds
Cortical vein thrombosis

106
Q

Subarachnoid Haemorrhage

Investigations (6)

A 
CT: detects 90% in first 48h 
LP: if CT -ve and no contraindications 12h after headache onset, CSF is bloody early then becomes xanthochromic (yellow) due to breakdown of haemoglobin to bilirubin 
FBC: leucocytosis 
Clotting: raised prolonged INR and PT 
U&amp;E: hyponatraemia 
Troponin: elevated
107
Q

Subarachnoid Haemorrhage

Treatment (4)

A

Immediate neurosurgery referral
Maintain cerebral perfusion by keeping well hydrated and aim SBP >160 (only treat BP if very severe)
Nimodipine: reduces vasospasm
Endovascular coiling > surgical clipping

108
Q

Subarachnoid Haemorrhage

Complications (4)

A

Rebleeding commonest cause of death, usually in first few days
Cerebral ischaemia due to vasospasm and causes permanent CNS defect
Hydrocephalus due to blockage of arachnoid granulations
Hyponatraemia is common but shouldn’t be managed with fluid restriction

109
Q

Intracranial Venous Thrombosis

Dural venous sinus thrombosis (3)

A

Most commonly sagittal/transverse sinus thrombosis
Symptoms come on gradually over days/weeks
Thrombosis within a dural venous sinus may extend into the cortical veins and cause infarction within a venous territory

110
Q

Intracranial Venous Thrombosis

Cortical vein thrombosis (5)

A

Often causes venous infarcts
Stroke-like focal symptoms that develop over days
May have an associated thunderclap headache
Seizures are common and focal
Usually occurs with sinus thromboses

111
Q

Intracranial Venous Thrombosis

Aetiology (4)

A

Common: pregnancy, OCP, head injury, dehydration, recent LP
Systemic: hyperthyroidism, heart failure, SLE, nephrosis, ketoacidosis
Infections: meningitis, TB, cerebral abscess, septicaemia
Drugs: androgens, antifibrinolytics, infliximab

112
Q

Intracranial Venous Thrombosis

Signs + symptoms (4)

A

Sagittal sinus: headache, vomiting, seizures, reduced vision, papilloedema
Transverse sinus: headache +/- mastoid pain, seizures, papilloedema, focal CNS signs
Sigmoid sinus: cerebellar signs, lower cranial nerve palsies
Cavernous sinus: often due to spread from facial pustules/folliculitis, headache, oedematous eyelids, fever

113
Q 
Intracranial Venous Thrombosis
Differential diagnoses (3)
A

Subarachnoid haemorrhage
Meningitis
Encephalitis

114
Q

Intracranial Venous Thrombosis

Investigations (3)

A

Must rule out SAH and meningitis
CT/MRI venography: absence of sinus
Lumbar puncture: raised opening pressure indicates venous thrombosis if there is a persistent headache and SAH is excluded

115
Q

Intracranial Venous Thrombosis

Treatment (2)

A

LMWH then warfarin once INR 2-3

Fibrinolytics eg. streptokinase

116
Q

Subdural Haemorrhage

Aetiology (3)

A

Trauma (can be delayed)
Intracranial hypotension
Dural metastases

117
Q

Subdural Haemorrhage

Pathology (3)

A

Bleeding from bridging veins between cortex and venous sinuses (vulnerable to deceleration injury)
Blood accumulates between arachnoid and dura matter
Gradually increases ICP shifting midline sutures away from side of clot

118
Q 
Subdural Haemorrhage
Risk factors (3)
A

Elderly (cerebral atrophy makes bridging veins vulnerable)
Falls (epilepsy, alcohol)
Anticoagulation

119
Q

Subdural Haemorrhage

Signs + symptoms (7)

A 
Fluctuating level of consciousness 
Headache 
Personality change 
Unsteadiness 
Increased ICP 
Seizures 
Localising neurological symptoms (eg. unequal  pupils, hemiparesis) occur late after injury
120
Q

Subdural Haemorrhage

Investigations (1)

A

CT shows crescent cell shaped haematoma over 1 hemisphere +/- midline shift

121
Q 
Subdural Haemorrhage
Differential diagnoses (3)
A

Stroke
Dementia
CNS masses (eg. tumours, abscess)

122
Q

Subdural Haemorrhage

Treatment (2)

A

Irrigation and evacuation with Burr-hole craniostomy 1st line
Craniotomy 2nd line if clot has organised

123
Q

Extradural Haemorrhage

Aetiology (1)

A

Fractured temporal or parietal bone causing laceration of middle meningeal artery and vein, typically after trauma to a temple (blood accumulates between bone and dura)

124
Q

Extradural Haemorrhage

Signs + symptoms (3)

A

Lucid interval: head injury with no loss of consciousness, may last a few hours –> days
Subsequent features: reduced GCS (from rising ICP), severe headache, vomiting, confusion, fits +/- hemiparesis with brisk reflexes and upgoing plantars
Bleeding continues: dilation of ipsilateral pupil, GCS decreases more, bilateral limb weakness

125
Q

Extradural Haemorrhage

Investigations (2)

A

CT: biconvex/lens shaped haematoma

Skull X-ray may show fracture lines across course of middle meningeal vessels

126
Q

Extradural Haemorrhage

Treatment (1)

A

Craniotomy with clot evacuation +/- bleeding vessel ligation

127
Q

Delirium

Epidemiology (3)

A

20-30% hospital inpatients
50% post-op
85% of patients in last weeks of life

128
Q

Delirium

Aetiology (10)

A

Systemic infection: pneumonia, UTI
Intracranial infection: encephalitis, meningitis
Drugs: opiates, anti-convulsants, sedatives, levodopa
Withdrawal: alcohol, drugs
Metabolic: uraemia, high/low Na, high/low glucose
Hypoxia: resp/cardiac failure
Vascular: stroke, MI
Increased ICP: head injury, SOL
Epilepsy: post-ictal state
Nutritional: thiamine/B12 deficiency

129
Q

Delirium

Symptoms (8)

A 
Impaired attention 
Anterograde memory impairment 
Disorientation in time, place or person 
Fluctuating levels of arousal 
Disordered sleep/wake cycle 
Disorganised thinking (rambling/incoherent) 
Perceptual distortions eg. illusions, hallucinations 
Mood changes
130
Q

Delirium

Signs (7)

A 
Acute onset and fluctuant 
Disturbed consciousness 
Change in cognition 
Delusions 
Emotional disturbance 
Sleep/wake cycle disturbance 
Psychomotor function disturbance
131
Q

Delirium

Investigations (3)

A

4AT (>4 = possible delirium/cognitive impairment, 1-3 = possible cognitive impairment, 0 = both unlikely)
FBC, U&E, LFT, glucose
Septic screen: urine dipstick, CXR, blood cultures

132
Q

Delirium

Treatment (2)

A

Exclude and treat possible triggers (sepsis, blood glucose, medications, retention/constipation)
Drug management not usually necessary but if disruptive may need haloperidol for sedation

133
Q

Dementia

Aetiology (5)

A 
Alzheimer's disease (50%)
Vascular dementia (25%)
Lewy body dementia (15-25%) 
Fronto-temporal dementia 
Others: alcohol and drug abuse, repeated head trauma, Whipple's disease, Huntington's
134
Q 
Dementia
Reversible causes (7)
A 
Hypothyroidism 
B12/folate deficiency 
Syphilis 
Subdural haemorrhage 
Parkinsons 
HIV 
Normal pressure hydrocephalus
135
Q

Dementia

Investigations (4)

A

MMSE/MOCA
Bloods: FBC, ESR, U&E, Ca, LFT, TSH, B12, folate
CT/MRI: vascular damage, haemorrhage, structural pathology
Functional imaging: FDG, PET, SPECT

136
Q 
Dementia
Diagnostic criteria (3)
A 
Present for >6 months
Functional decline in ADLs
Memory impairment +1 of: 
-dysphagia (expressive/receptive) 
-dyspraxia (motor skills) 
-dysgnosia (difficulty recognising objects) 
-dysexecutive functioning
137
Q

Alzheimer’s Disease

Aetiology (2)

A

Accumulation of B-amyloid peptide results in neuronal damage, tangles, increased amyloid plaques + loss of acetylcholine
Usually temporal lobes affected first

138
Q 
Alzheimer's Disease 
Risk factors (7)
A 
1st degree relative affected 
Down's syndrome 
Vascular risk factors: high BP, AF, diabetes 
Smoking 
Alcohol
Reduced physical and cognitive activity 
Depression and loneliness
139
Q

Alzheimer’s Disease

Signs + symptoms (7)

A

Enduring, progressive and global cognitive impairment (unlike other dementias which may affect certain domains but not others)
Reduced visuospatial skill (get lost)
Reduced memory
Reduced verbal abilities
Reduced executive functioning
Anosognosia (lack of insight into the problems caused by the disease)
Later on: irritability, mood disturbance, behavioural change (eg. disinhibition), psychosis

140
Q

Alzheimer’s Disease

Treatment (2)

A

Acetylcholinesterase inhibitors eg. donepezil, galantamine, rivastigimine- SE: D+V, cramps, incontinence, dizziness, insomnia
Antiglutamatergic: memantine (NMDA antagonist) for late stage disease- SE: hallucinations, confusion, hypersexuality

141
Q

Vascular Dementia

Aetiology (1)

A

Cumulative effects of many small strokes

142
Q 
Vascular Dementia 
Risk factors (5)
A 
Diabetes 
Previous strokes 
Hypertension 
Peripheral vascular disease 
Ischaemic heart disease
143
Q

Vascular Dementia

Signs + symptoms (2)

A

Stepwise deterioration

Often predominant executive dysfunction and gait abnormalities

144
Q

Lewy Body Dementia

Signs + symptoms (7)

A 
Fluctuating cognitive impairment 
Detailed visual hallucinations 
Parkinsonism later 
Amnesia not prominent 
REM sleep disorder 
Falls + syncope 
Frontal-executive and visuospatial defects
145
Q

Fronto-Temporal Dementia

Signs + symptoms (5)

A

Younger onset
Behavioural disorder (personality change)
Early preservation of episodic memory and spatial orientation
Disinhibition
Speech disorder

146
Q

Parkinson’s Disease

Aetiology of Parkinsonism (2)

A

Idiopathic (Parkinson’s Disease)

Drugs (neuroleptics, prochloperazine)

147
Q

Parkinson’s Disease

Pathology (3)

A

Mitochondrial DNA dysfunction causes degeneration of dopaminergic neurones in substantia nigra
Reduced input to striatum
Reduced dopamine levels

148
Q

Parkinson’s Disease

Signs + symptoms (7)

A

Tremor: worse at rest, pill-rolling of thumb over fingers
Rigidity: with tremor gives cogwheel rigidity
Bradykinesia: slow initiation of movement and slow repetitive actions
Postural instability
REM sleep disorders
Reduced sense of smell
Poor executive functioning

149
Q

Parkinson’s Disease

Treatment (6)

A

Levodopa + co-beneldopa (dopa-decarboxylase inhibitor), but efficacy reduces over time
Dopamine agonists eg. ropinirole can delay starting levodopa
Anticholinergics can help tremor but cause confusion in the elderly
MAO-B inhibitors eg. selegiline, as alternative to dopamine agonists
COMT inhibitors
Deep brain stimulation

150
Q

Multiple Sclerosis

Aetiology (5)

A

Discrete plaques of demyelination at multiple CNS sites due to T-cell mediated immune response
Demyelination heals poorly, causing relapsing and remitting symptoms
Prolonged demyelination causes axonal loss and clinically progressive symptoms
Lack of sunlight and vit D exposure
Genetic

151
Q

Multiple Sclerosis

Presenting signs + symptoms (5)

A 
Usually monosymptomatic 
Unilateral optic neuritis (pain on eye movement and rapid reduction in central vision) 
Limb paraesthesia 
Brainstem/cerebellar: ataxia, diplopia 
May worsen with heat and exercise
152
Q

Multiple Sclerosis

Progresssive signs + ymptoms (9)

A

Sensory: pins + needles, reduced vibration sense
Motor: spastic weakness, myelitis
GU: erectile dysfunction, retention, incontinence
GI: swallowing disorder, constipation
Eyes: diplopia, hemianopia, pupillary defect
Cerebellum: trunk/limb ataxia, intention tremor, falls
Cognitive/visuospatial decline: amnesia, mood disturbed
Transverse myelitis: loss of motor, sensory, autonomic reflex and sphincter function below level of lesion
L’hermitte’s sign: neck flexion causes electric shock in trunk and limbs

153
Q

Multiple Sclerosis

Poor prognostic signs (4)

A

Older male
Motor signs at onset
Many relapses early on
Many MRI lesions and axonal loss

154
Q

Multiple Sclerosis

Investigations (4)

A

McDonald criteria
MRI
CSF: oligoclonal bands of IgG on electrophoresis that are not present in serum suggests CNS inflammation
Bloods: FBC, TFT, B12, U&E to exclude other causes

155
Q 
Multiple Sclerosis 
Differential diagnoses (5)
A 
SLE 
HIV 
Tumour 
Stroke 
Vasculitis
156
Q

Multiple Sclerosis

treatment of acute relapses (2)

A

Steroids: IV methylprednisolone (don’t use more than 2x/year)
Plasma exchange if severe

157
Q 
Multiple Sclerosis 
Ongoing treatment (3)
A

Interferons (IFN-1B + IFN-1a): reduce relapses by 30% in active relapsing remitting disease and reduce lesion accumulation
Monoclonal antibodies: eg. alemtuzumab, natalizumab for relapsing remitting
Azathioprine for relapsing remitting

158
Q

Multiple Sclerosis

Palliation (3)

A

Spasticity: baclofen, diazepam
Tremor: botulinum injection
Urgency/frequency: self catheterisation

159
Q

Space Occupying Lesions

Primary brain tumours (7)

A

Astrocytoma: low grade tumour of CNS supporting cells, low grade diffuse tumours tend to occur in young people
Glioblastoma multiforme: high grade tumour of CNS supporting cells, may arise from pre-existing astrocytoma, v. aggressive, most common adult brain tumour
Oligodendroglioma: arise rom myelin sheath
Ependymoma: ventricular tumour in children
Medulloblastoma: neuroectoderm tumour that tends to occur in children in the brainstem
Primary CNS lymphoma: usually diffuse large B cell
Meningioma non-invasive but locally advanced, arise from arachnoid cells

160
Q

Space Occupying Lesions

Secondary brain tumours (3)

A

Lung
Breast
Melanoma

161
Q

Space Occupying Lesions

Signs + symptoms (4)

A

Increased ICP: headache worse on waking, lying down, bending forward or with coughing, vomiting, papilloedema
Seizures
Evolving focal neurology: VIth nerve palsy commonest due to long intracranial course
Subtle personality change

162
Q

Space Occupying Lesions

Investigations (3)

A

CT
MRI good for posterior fossa masses
Consider biopsy

163
Q

Space Occupying Lesions

Treatment (3) Prognosis (1)

A

Treatment:
- Benign: surgical excision unless inaccessible
- Malignant: surgical excision and adjuvant radiotherapy
- Lone chemo-radiotherapy if inoperable
Prognosis:
- <50% 5 year survival

164
Q

Space Occupying Lesions

Localising the lesion (5)

A

Temporal lobe: dysphasia, contralateral homonymous hemianopia, amnesia
Frontal lobe: hemiparesis, personality change, Broca’s dysphasia
Parietal lobe: hemisensory loss, dysphasia
Occipital lobe: contralateral visual field defects
Cerebellar: DANISH- Dysdiadokinesis (inability to perform rapidly alternating movements), Ataxia, Nystagmus, Intention tremor, Slurred speech, Hypotonia

165
Q

Bell’s Palsy

Definition (1)

A

Idiopathic facial nerve palsy

166
Q

Bell’s Palsy

Other causes of VIIth nerve palsy (7)

A 
Ramsay Hunt syndrome 
Lyme disease
Meningitis 
Stroke 
Tumour 
MS
Guillain-Barre
167
Q

Bell’s Palsy

Signs + symptoms (8)

A 
Abrupt onset 
Complete unilateral facial weakness 
Ipsilateral numbness/pain around ear 
Reduced taste 
Drooling 
Food trapped between gum and cheek 
Speech difficulties 
Ask to wrinkle forehead and close eyes forcefully (under bilateral cortical control so spared in uMN lesion)
168
Q

Bell’s Palsy

Investigations (2)

A

Blood: ESR, glucose, increased Borrelia antibodies in Lyme disease (indistinguishable from Bell’s clinically), increased VZV antibodies in Ramsay Hunt
MRI: space occupying lesion, stroke, MS

169
Q

Bell’s Palsy

Treatment (3)

A

Prednisolone within 72h of onset
May need plastic surgery if eye closure remains a problem and to straighten drooping face
Botulinum toxin can augment facial symmetry

170
Q 
Mononeuropathies
Definition (2)
A

Lesions of individual peripheral/cranial nerves, usually caused by trauma or entrapment (eg. tumour), except for carpal tunnel syndrome
Mononeuritis multiplex is when 2+ nerves are affected, causes tend to be systemic eg. AIDS, RA, diabetes

171
Q 
Mononeuropathies
Median nerve (5)
A

C6-T1
Nerve of precision grip
LOAF: 2 Lumbricals, Opponens pollicis, Abductor pollicis brevis, Flexor pollicis brevis
Trauma (lacerations) or carpal tunnel
Weakness of abductor pollicis brevis and sensory loss over radial 3.5 fingers and palm

172
Q 
Mononeuropathies
Ulnar nerve (3)
A

C7-T1
Vulnerable to elbow trauma
Wasting/weakness of medial wrist flexors, interossei and medial two lumbricals (claw hand), hypothenar wasting

173
Q 
Mononeuropathies
Radial nerve (5)
A

C5-T1
Nerve that opens the fist
Damaged by compression against the humerus
Wrist and finger drop
Muscles: BEST- Brachioradialis, extensors, Supinator, Triceps

174
Q 
Mononeuropathies
Phrenic nerve (3)
A

C3-5 (C3, 4, 4 keeps the diaphragm alive)
Consider phrenic nerve palsy if orthopnoea with raised hemidiaphragm on CXR
Causes: lung cancer, myeloma, thymoma, thoracic surgery, MS, HIV

175
Q 
Mononeuropathies
Sciatic nerve (3)
A

L4-S3
Damaged by pelvic tumours/fractures to pelvis/femur
Lesions affect hamstrings and all muscles below the knee (foot drop), with loss of sensation below the knee

176
Q

Mononeuropathies

Common peroneal nerve (5)

A 
L4-S1
Originates from sciatic nerve just above knee, often damaged as it winds round the fibular head 
Foot drop 
Weak ankle dorsiflexion/eversion 
Sensory loss over dorsum of foot
177
Q 
Mononeuropathies
Tibial nerve (4)
A

L4-S3
Originates from sciatic nerve just above knee
Lesions lead to inability to stand on tiptoe (plantar flexion), invert foot, flex toes
Sensory loss over the sole

178
Q

Polyneuropathies

Definition (1)

A

Disorders of peripheral/cranial nerves, distribution is symmetrical and widespread, often with distal weakness and sensory loss (‘glove and stocking’)

179
Q

Polyneuropathies

Aetiology (5)

A

Metabolic: diabetes and renal failure (mostly sensory)
Vasculitides: RA, Wegener’s
Inflammatory: Guillain-Bare syndrome (mostly motor)
Infections: leprosy (mostly sensory), HIV, syphilis
Alcohol

180
Q

Polyneuropathies

Signs + symptoms of sensory neuropathy (5)

A

Numbness
Pins and needles/burning
Affects extremities 1st (glove and stocking distribution)
Difficulty handling small objects like buttons
Trauma/joint deformity

181
Q

Polyneuropathies

Signs + symptoms of motor neuropathy (5)

A 
Often progressive 
Weak/clumsy hands 
Difficulty walking (falls, stumbling) 
Difficulty breathing 
LMN lesion signs
182
Q

Polyneuropathies

Signs + symptoms of cranial neuropathy (2)

A

Swallowing/speaking difficulties

Diplopia

183
Q

Polyneuropathies

Signs + symptoms of autonomic neuropathy (5)

A 
Sympathetic and parasympathetic neuropathies may be isolated or part of generalised sensorimotor peripheral neuropathy 
Postural hypotension 
Erectile dysfunction 
Reduced sweating 
Constipation and urinary retention
184
Q

Guillain-Barre Syndrome

Pathology (4)

A

Acute inflammatory demyelinating polyneuropathy
Triggered by Campylobacter jejuni, CMV, HIV, EBV
Trigger causes antibodies which attack nerves but very often no cause is found
May advance quickly and cause paralysis, unlike other neuropathies, proximal muscles are more affected (trunk, respiratory, cranial nerves)

185
Q

Guillain-Barre Syndrome

Signs + symptoms (4)

A

A few weeks after infection a symmetrical ascending muscle weakness starts (progression over days-weeks)
Pain common
Autonomic dysfunction: sweating, tachycardia, BP changes, arrhythmias
Areflexia

186
Q

Guillain-Barre Syndrome

Investigations (2)

A

Nerve conduction studies: slow conduction

CSF: high protein, normal WCC

187
Q

Guillain-Barre Syndrome

Treatment (3)

A

Ventilate with respiratory involvement
IV immunoglobulin
Plasma exchange

188
Q

Guillain-Barre Syndrome

Prognosis (3)

A

85% make complete or near complete recovery
10% unable to walk 1 year
Mortality 10%

189
Q

Motor Neuron Disease

Definition (2)

A

Cluster of major degenerative diseases characterised by selective loss of neurons in motor cortex, cranial nerve nuclei and anterior horn cells
Upper and lower motor neurons are affected but there is no sensory loss/sphincter disturbance

190
Q

Motor Neuron Disease

Classification (4)

A

ALS: loss of motor neurons in motor cortex and the anterior horn of the cord, so weakness and UMN signs + LMN signs
Progressive bulbar palsy: only affects cranial nerves IX-XII (LMN lesion of tongue and muscles of talking/swallowing, can also be caused by Guillain-Barre, myasthenia
Corticobulbar palsy: UMN lesion of muscles of swallowing/talking, due to bilateral lesions (increased jaw jerk, slow speech, also see in MS/stroke)
Progressive muscular atrophy: anterior horn lesion only, thus no UMN signs

191
Q

Motor Neuron Disease

Signs + symptoms (7)

A 
Stumbling spastic gait 
Foot drop 
Proximal myopathy 
Weak grip 
Shoulder abduction 
UMN signs 
LMN signs
192
Q

Motor Neuron Disease

Treatment (3)

A

Antiglutamatergic drugs may prolong life
Treat symptoms such as drooling, dysphagia, spasticity, joint pain
Non-invasive ventilation

193
Q

Duchenne Muscular Dystrophy

Pathology (1)

A

X-linked recessive mutation in dystrophin gene results in near-total loss of dystrophin (muscles get replaced by fibroadipose tissue)

194
Q

Duchenne Muscular Dystrophy

Signs + symptoms (4)

A

Boys aged 1-6
Waddling, clumsy gait
Gower’s manoeuvre: on standing, he uses his hands to climb up his legs
Wheelchairs required by 9-12

195
Q

Duchenne Muscular Dystrophy

Investigations (2)

A 
CK increases (measure in all boys not walking by 1.5 years) 
Muscle biopsy (abnormal fibres surrounded by fat and fibrous tissue)
196
Q

Duchenne Muscular Dystrophy

Prognosis (3)

A

Prednisolone slows decline in muscle strength and function in short term
Mechanical ventilation improves longevity
Median age at death 31 years

197
Q

Myasthenia Gravis

Pathology (3)

A

Autoimmune disease mediated by antibodies to acetylcholine receptors (AChR)
Interfering with the neuromuscular transmission via depletion of working post-synaptic receptor sites
Both B+T cells implicated

198
Q

Myasthenia Gravis

Signs + symptoms (5)

A 
Increasing muscular fatigue 
Muscle groups affected in order: extraocular --> bulbar (swallowing, chewing) --> face --> neck etc. 
Ptosis 
Diplopia 
On counting to 50 the voice fades
199
Q

Myasthenia Gravis

Associations (2)

A

If under 50 commoner in women and associated with other autoimmune diseases and thymic hyperplasia
If over 50 commoner in men and associated with thymic atrophy/tumour

200
Q

Myasthenia Gravis

Investigations (3)

A

Anti-AChR antibodies
Neurophysiology
CT thymus

201
Q

Myasthenia Gravis

Treatment (3)

A

Symptom control: anticholinesterase
Immunosuppression: treat relapses with prednisolone (may combine with azathioprine/methotrexate)
Thymectomy

202
Q

Spinal Cord Injury

Aetiology (5)

A 
Most due to trauma, especially RTAs
Falls in elderly population 
Tumours 
Prolapsed discs 
Inflammatory disease
203
Q

Spinal Cord Injury

Assessment (8)

A

ATLS principles
Log-roll technique for movement
C-spine immobilisation
Prevent and treat hypotension (due to neurogenic shock)
Restore intravascular volume (don’t overload)
Monitor and treat symptomatic bradycardia
Monitor and regulate temp.
Perform serial neurological examinations

204
Q

Spinal Cord Injury

Root lesion tests (10)

A 
C5: shoulder abduction 
C6: elbow flexion 
C7: elbow extension 
C8: finger flexion (grip) 
T1: finger abduction 
L2: hip flexion 
L3: knee extension 
L4: ankle dorsiflexion 
L5: great toe extension 
S1: ankle plantarflexion
205
Q

Spinal Cord Injury

Consequences (5)

A

Injury to cervical spine causes tetraplegia but injury above level of phrenic nerve (C3-5) results in paralysis of diaphragm
Thoracic spine: paraplegia
Lumbar spine: cauda equina
Respiratory insufficiency: from neurological dysfunction and associated trauma
Hypotension below lesion (sympathetic interruption and resultant neurogenic shock- low BP + HR)

206
Q

Spinal Cord Injury

Treatment (5)

A 
Early transfer to spinal injuries unit 
Steroids 
Early surgical decompression and stabilisation 
Traction for cervical injuries 
Anticoagulation: v high risk of VTE
207
Q

Brown-Sequard Syndrome

Definition (1)

A

Hemisection (lesion in one half) of spinal cord

208
Q

Brown-Sequard Syndrome

Aetiology (1)

A

Penetrating injuries

209
Q

Brown-Sequard Syndrome

Signs + symptoms (4)

A

Ipsilateral UMN weakness below lesion (severed corticospinal tract causing spastic paraparesis, brisk reflexes, extensor plantars)
Ipsilateral paralysis
Ipsilateral loss of proprioception and vibration (1 dorsal column severed)
Contralateral loss of pain and temp. (severed spinothalamic tract which is crossed over)

210
Q

Spinal Shock

Definition (1)

A

Transient physiological loss of function, often due to haemorrhage

211
Q

Spinal Shock

Signs + symptoms (5)

A

Anaesthesia
Flaccid paralysis below the level
Urinary retention
Over time flexion at hip and knee may be induced by stimuli (cold) and reflexes return
Overall, temporary loss of sensory and motor function tends to recover

212
Q

Spinal Cord Compression

Aetiology (5)

A 
Bone displacement 
Disc prolapse 
Local tumour (secondary malignancy- breast, lung, prostate) 
Abscess 
Haematoma
213
Q

Spinal Cord Compression

Signs + symptoms (6)

A

Spinal/root pain
Leg weakness
LMN signs at level of lesion
UMN signs and sensory changes below lesion (spastic weakness, brisk reflexes, upgoing plantars, loss of coordination, joint position sense and vibration sense)
Joint position and vibration affected on same side
Pain and temp affected on other side

214
Q 
Spinal Cord Compression 
Differential diagnoses (5)
A 
Transverse myelitis 
MS 
Trauma 
Guillain-Barre
Cord vasculitis (eg. syphilis)
215
Q

Spinal Cord Compression

Investigations (4)

A

MRI
Biopsy/surgical exploration may be needed to identify nature of mass
Bloods: FBC, ESR, syphilis serology, U&E, LFT, PSA
CXR: primary lung malignancy or secondaries

216
Q

Spinal Cord Compression

Treatment (2)

A

If malignancy: IV dexamethasone while considering chemo/radio +/- decompressive laminectomy
If epidural abscess: surgical decompression and antibiotics

Med Student Finals (23 decks)

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