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Neurological conditions Flashcards

1
Q

What is dementia?

A

A syndrome consisting of progressive impairment of multiple areas of the brain, resulting in loss of skills, cognitive function and social understanding.

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2
Q

What are the some types of dementia?

A 
Alzheimer's - temporo-parietal. 
Fronto-temporal.
Vascular
Lewy body
Creutzfeldt-Jacob disease.
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3
Q

What are some characteristics of Alzheimer’s?

A

Early memory disturbance
Language and visuospatial problems
Personality and drive preserved til later as it does not start in frontal lobe.

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4
Q

What is Alzheimer’s disease?

A

Disease in which connections between nerve cells are lost due to a build up of protein plagues and tangles. Also a reduction in some chemical messengers of the brain.

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5
Q

What are some characteristics of vascular dementia?

A

Location within brain and therefore symptoms dependent on where the mini strokes occur.
Stepwise progression.

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6
Q

What are the characteristics of fronto-temporal dementia?

A

Early change in personality and behaviour.
Often an eating habit change.
Early dysphasia.
Memory and visuospatial preserved until later stages.

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7
Q

What is the generalised treatment for dementia?

A

Non-pharmalogical - support services,OT, social work etc.

Pharmaological - treatment for insomnia, behaviour and depression.

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8
Q

What is the specialised treatment for Alzheimer’s?

A

Cholinesterase inhibitors e.g donepezil, rivastigmine, galantamine.

NMDA antagonists - memantine.

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9
Q

What is Parkinsonism?

A

Clinical syndrome with bradykinesia and at least one other of Rigidity, Tremor or Postural instability. Involves a pathology within the basal ganglia.

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10
Q

What are some causes of Parkinsonism?

A 
Idiopathic
Drug induced
Vascular
Multiple system atrophy
Progressive supra nuclear palsy.
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11
Q

How is Parkinson’s disease diagnosed?

A 
Clinical signs:
Bradykinesia
Postural instability.
Tremor
Rigidity
Slow progression rate
Good response to dopamine treatment
Asymmetric rest tremor.
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12
Q

What is the early treatment for Parkinson’s?

A

Levadopa
COMT inhibitors - Entacapone
Dopamine agonists - Ropinirole, Pramipexrole, Rotigotine.
MAO-B inhibitors - Selegiline, Rasagiline, Safiniamide.
Often used in combination with one another.

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13
Q

What are some drug induced complications of Parkinson’s?

A

Levadopa wears off causing motor fluctuations.
Dyskinesias (involuntary movements) also due to levodopa.
Psychiatric - hallucinations, impulse control.

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14
Q

What are some non drug induced and non motor complications of Parkinson’s?

A 
Depression (20% of cases)
Dementia (50% after 10yrs)
Blood pressure control
loss of bladder/bowel control 
Difficulty speaking and swallowing
Balance issues.
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15
Q

What is the late stage treatment of Parkinson’s?

A

Aim to prolong levodopa half life : MAO-B inhibitors, COMT inhibitors, slow release levodopa. Oral dopamine agonists, continuous infusion of amamorphine, duadopa.

Deep brain stimulation

Allied health professionals +/- care package.

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16
Q

What is the difference between primary and secondary headaches?

A

Secondary headaches had an identifiable cause whereas primary headaches do not.

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17
Q

What are some examples of primary headaches?

A

Tension type
Migraine
Cluster

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18
Q

What are some causes of secondary headaches?

A 
Tumour
Meningitis
Vascular disorders 
Systemic infection
Head injury
Drug induced.
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19
Q

What are some characteristics of Tension Type headaches?

A 
Tame
Tightening or pressing 
Two sides - bilateral
No Triggers/associated features
Tasks - not disabling.
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20
Q

What is the treatment for tension type headaches?

A

Aspirin or Paracetamol
NSAIDs
Preventative treatment rarely required but tricyclic antidepressants.

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21
Q

What are some characteristics of migraine?

A 
Disabling
Chronic with episodic attacks 
Many triggers 
Stages of attack
Complex changes within the brain. 
More common in woman than men.
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22
Q

What are some triggers of migraine?

A 
Dehydration
Stress
Sleep disturbances 
Diet
Hunger
Environmental stimuli
Changes in oestrogen levels in women.
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23
Q

What are the stages of a migraine attack?

A

Premonitory symptoms - mood changes, fatigue, muscle pain, food cravings.
Aura - not always present. Transient neurological symptoms. May involve motor, visual, sensory or speech systems.
Early headache - dullness, nasal congestion, muscle pain
Advanced headache- nausea, unilateral, throbbing, photophobia, phonophobia, osmophobia
Postdrome - fatigue, cognitive changes, muscle pain.

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24
Q

What defines a chronic migraine?

A

Headache for 15 or more days of the month of which 8 or more are migraine, for more than 3 months.

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25
Q

What is the treatment for migraine?

A

Aspirin
NSAIDs
Triptans

Preventative treatment: Propranolol, Candesartan
Anti-epileptics - topiramate, valproate, gabapentin
tricyclic antidepressants
venlafaxine.

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26
Q

What are Trigeminal autonomic cephalalgias?

A

Primary headaches with Trigeminal pain and autonomic signs.

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27
Q

What are some examples of Trigeminal autonomic cephalalgias?

A

Cluster headaches
Paroxysmal hemicrania
Short lasting Unilateral Neuralgiform heartache with conjunctival injection and tearing (SUNCT)
Short lasting Unilateral Neuralgiform headache with Autonomic symptoms (SUNA).

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28
Q

What are some characteristics of cluster headaches?

A 
Unilateral
Temporal/ orbital pain 
Rapid onset and cessation. 
15min - 3hrs duration
Severe pain - worst you've ever had. 
Ipsilateral autonomic symptoms. 
Often come in bout with periods of remission.
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29
Q

What are some characteristics of Paroxysmal Hemicrania?

A 
Unilateral 
Severe
Rapid onset and cessation. 
2-30mins duration
Ipsilateral autonomic symptoms. 
Absolute response to Indometacin.
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30
Q

What are some characteristics of SUNCT?

A 
Unilateral
Supra orbital, orbital and temporal pain
Severe
Stabbing or pulsating pain.
10-240s duration 
Rapid onset and cessation
Cutaneous triggers - wind, cold, touch chewing. 
Conjuctival injection and lacrimation.
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31
Q

What are some characteristics of Trigeminal Neuralgia?

A 
Unilateral
Mandibular or maxillary pain 
5-10 secs duration
Stabbing pain
Cutaneous triggers - wind, cold, touch, chewing. 
Refractory period. 
Autonomic symptoms Uncommon.
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32
Q

What is the treatment for cluster type headaches?

A

Headache - Subcutaneous sumatriptan or nasal zolmaetriptan. Oxygen.

Headache bouts - Occipital depomedrone injection or oral prednisone.

Preventative - verapamil, lithium, methysergide, topiramate.

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33
Q

What is the treatment for paroxysmal hemicrania?

A

No abortive treatment.

Preventative- Indometacin, COX-II inhibitors, Topiramate

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34
Q

What is the treatment for SUNCT/SUNA?

A

No abortive treatment.

Preventative - Lamotrigine, Topiramate, Gabapentin, Carbamazepine.

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35
Q

What is the treatment for Trigeminal neuralgia?

A

No abortive treatment.
Preventative - Oxcarbazepine, Carbamazepine.
Surgical intervention - Glycerol ganglion injection, Steriotactic radiosurgery, decompressive surgery.

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36
Q

What features predict sinister headache?

A 
New daily headaches
Returning patient
Sudden onset (thunderclap) 
Change in headache pattens or type
Associated head trauma.
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37
Q

What is a thunderclap headache?

A

High intensity headache reaching maximum intensity within less than a minute. Can be primary or secondary.

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38
Q

What is intracranial hypotension?

A

Low intracranial pressure. Usually due to a CSF leak.

Headache gets worse when upright posture/standing and better when lying down.

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39
Q

What is the treatment for intracranial hypotension?

A

Bed rest, fluids, analgesia, caffeine.

IV caffeine, epidural blood patch.

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40
Q

What is giant cell arteritis?

A

Arteritis of large arteries. Usually presents with a new headache in patients over 50yrs. Headache usually diffuse and persistent. Scalp tenderness, jaw claudication and visual disturbance.

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41
Q

What is the treatment for giant cell arteritis?

A

High dose prednisolone and temporal artery biopsy arranged.

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42
Q

What is syncope?

A

Fainting due to temporary loss of blood flow to the brain.

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43
Q

What are the 3 categories of syncope?

A

Reflex - change in vagal tone e.g taking blood, cough.

Orthostatic - change in blood pressure e.g. dehydration, medication, endocrine, autonomic nervous system.

Cardiogenic - e.g arrhythmia, aortic stenosis.

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44
Q

What is a typical patient history of syncope?

A 
Light headed
Clammy
Vision blacking out
Fully orientated quickly
Possible urinary incontinence
Feels better sitting than standing.
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45
Q

What is a typical witness account of syncope?

A 
Looked a bit pale. 
Few brief jerks
Brief loss of consciousness
Rapid recovery
if tongue bite usually tip of tongue.
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46
Q

What is a typical patient history of cardiogenic syncope?

A 
Begins on exertion
Chest pain
Palpitations
Shortness of breath
Recovers fairly quickly
Clammy/sweaty.
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47
Q

What is a typical witness account of cariogenic syncope?

A 
Suddenly went floppy
Looked grey/ashen white
Seemed to stop breathing
Unable to feel a pulse
May be a few brief jerks
Rapid recovery.
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48
Q

What are some assessments of cariogenic syncope?

A 
Family history
Heart sounds
Pulse
ECG- look for heart block, QT ratio
Possible referral to cardiology
May need 24hr ECG, ECHO, prolonged monitoring.
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49
Q

What is epilepsy?

A

The tendency to recurrent seizures.

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50
Q

What are some causes of provoked seizures?

A 
Alcohol withdrawal
Drug withdrawal
Head injury
24hrs of stroke
24hrs of neurosurgery
Severe electrolyte disturbance
Eclampsia
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51
Q

What are the 2 basic classifications of seizures?

A

Generalised and Focal.

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52
Q

What are some examples of generalised seizures?

A 
Absence seizures
Generalised tonic-clonic seizures
Myoclonic seizures
Juvenile myoclonic epilepsy
Atonic seizures
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53
Q

What are some examples of Focal seizures?

A

Simple partial seizures
Complex partial seizures
Secondary generalised
Or by localisation of onset e.g temporal lobe.

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54
Q

What are some characteristics of primary generalised seizures?

A

No warning
<25yrs
May have family history
Generalised abnormality on EEG.

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55
Q

What are some characteristics of focal epilepsies?

A

May get an aura
Any age
Focal abnormality of EEG
MRI may show cause.

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56
Q

What is a typical patient history of a Generalised Tonic Clonic Seizure?

A 
Unpredictable, tend to cluster
May have a vague warning
Irritability before they occur
Lateral tongue biting
Incontinence
Muscle Pain
May have Past MH of complications at birth, trauma, meningitis, brain injuries.
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57
Q

What is a typical witness account of a Generalised Tonic Clonic Seizure?

A 
Groaning sound
Tonic - rigid stage followed by generalised jerking in all 4 limbs.
Eyes open - staring and rolling upwards
Foaming at mouth
Groggy for 15-30mins afterwards.
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58
Q

What are some characteristics of Absence seizures?

A

Mainly in children
Sudden arrest of activity for a few secs - brief staring, may have eyelid fluttering.
Restart what they were doing afterwards.
May be provoked by hyperventilation or photic stimulation.

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59
Q

What are some characteristics of Juvenile Myoclonic Epilepsy?

A

Mainly in Adolescence.
Can be provoked by alcohol, sleep deprivation.
Can be a mixture of Absence and GTC seizures.
Often early morning myoclonus - drop things, brief jerks in limbs.

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60
Q

What is a typical history of a complex partial seizure?

A 
Rising feeling in stomach
Funny smell/taste
De ja vu
No recollection of the event. 
Disorientated for a spell afterwards.
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61
Q

What is a typical witness account of a complex partial seizure?

A

Sudden arrest in activity
Staring blankly into space
Automatisms - lip smacking, repetitive picking at clothes.

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62
Q

What investigation can help when there is uncertainty about diagnosis of seizures/epilepsy?

A

Video-telemetry - 5days of video and EEG monitoring.

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63
Q

What is the first line of treatment for primary generalised epilepsies?

A

Sodium Valproate
Lamotrigine
Levetiracetam

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64
Q

What is the first line of treatment for focal and secondary generalised seizures?

A

Lamotrigine
Carbamazepine
Levetiracetam

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65
Q

What is the first line of treatment for absence seizures?

A

Ethosuximide

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66
Q

What is the first line of treatment for treating acute seizures?

A

Lorazepam
Midazolam
Diazepam

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67
Q

What are some side effects of therapy?

A

Phenytoin - arrhythmias, hepatitis, medication interactions.

Sodium Valproate- tremor, weight gain, ataxia, nausea, drowsiness, hepatitis, avoid in woman of childbearing age.

Carbamazepine - ataxia, drowsiness, blurred vision, low serum sodium, skin rash.

Lamotrigine- skin rash, difficulty sleeping.

Levetiracetam- irritability, depression.

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68
Q

What is status epilepticus?

A

Prolonged or recurrent tonic-clonic seizures persisting for more than 30mins with no recovery period between seizures. Usually occurs in patients with no history of epilepsy.

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69
Q

What is the first line treatment for Status Epilepticus?

A

Midazolam
Lorazepam
Diazepam

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70
Q

What is the 2nd line treatment for Status Epilepticus?

A

Phenytoin
Valproate
and sometimes Leviteracetam.

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71
Q

What is a pseudoseizure or non epileptic attack?

A

A series of movements or behaviours that resemble a seizure but have no abnormal electrical activity in the brain.

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72
Q

What is a typical history of a pseudoseizure?

A 
May occur at times of stress or at rest.
Will give lots of detail of others reaction instead of their own. 
May recall what people said during it.
May be prolonged- waxing and waining.
Dissociation.
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73
Q

What is a typical witness account of a pseudoseizure?

A

Tracking eye movements
May be some verbalisation
Pelvic thrusting, tremor, asynchronous movements
Waxing and waining

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74
Q

What are the signs of an upper motor lesion?

A

Weakness
Increased reflexes
Increased tone
Babinski response (plantar)

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75
Q

What are the signs of a lower motor lesion?

A 
Weakness
Atrophy (muscle wastage)
Decreased reflexes
Decreased tone
Fasciculations
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76
Q

What is the transition point between upper and lower motor lesions?

A

Anterior horn cell.

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77
Q

At what level does the spinal cord terminate?

A

L2

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78
Q

What is myelopathy?

A

Neurological deficit due to compression of the spinal cord. Upper motor neurone.

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79
Q

What is radiculopathy?

A

Compression of the nerve root resulting in dermatomal and myotomal deficits. Lower motor neurone.

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80
Q

What is a disc prolapse?

A

Acute herniation of a intervertebral disc causing compression of spinal roots or the spinal cord.

Tends to be acute onset and in younger patients. Less movement in thoracic region so not common there.

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81
Q

How does disc prolapse usually present?

A

Acute pain down leg or arm.
Numbness and weakness in distribution of nerve root involved.
Investigate with MRI.

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82
Q

How is disc prolapse managed?

A

Rehabilitation.
Nerve root inject to temporarily numb nerve.
Lumbar/cervical discectomy.

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83
Q

What is Cauda Equina syndrome?

A

The bundle of nerves (caudal equina) at end of spine become damaged and compressed. It is a medical emergency.

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84
Q

What are the symptoms of Cauda Equina syndrome?

A 
Bilateral sciatica (pain in both legs)
Urinary dysfunction and loss of bladder and bowel control. 
Saddle anaesthesia - loss of sensation in bottom, perineum and inner surface of thighs.
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85
Q

How is Cauda Equina syndrome managed?

A

Urgent MRI within 4hrs.

Emergency lumbar discectomy.

86
Q

What is cervical spondylosis?

A

General term degenerative change in the cervical spine leading to nerve root and spine compression.
Patients can present with myelopathy, radiculopathy or both.
Gradual onset of usually months to years.

87
Q

What is lumbar spinal stenosis?

A

The spinal canal narrows, compressing the nerves at the lumbar vertebral level.

88
Q

How does lumbar spinal stenosis present?

A

Pain down both legs - spinal claudication.

Worse on walking/standing, relieved on sitting down/bending forward.

89
Q

How is lumbar spinal stenosis managed?

A

Lumbar laminectomy.

90
Q

What triad of symptoms indicates an epidural abscess?

A

Pyrexia
New back pain
Focal neurology - weakness, bladder problems.

91
Q

What are the risk factors for epidural abscess?

A

Diabetes
IV drug abuse
Chronic renal failure
Alcoholism

92
Q

What organisms commonly cause an epidural abscess infection?

A

Staph aureus.
E.coli
Streptococcus

93
Q

How is an epidural abscess managed?

A

Urgent surgical intervention

Long term IV antibiotics

94
Q

What are the risk factors for osteomyelitis?

A 
IV drug abuse
Diabetes
Chronic renal failure
Alcoholism
AIDS.
95
Q

What is Stroke?

A

Sudden onset of focal neurological symptoms caused by either ischemia or haemorrhage, lasting more than 24hrs.

85% are ischemic.

96
Q

What is a Transient Ischemic Attack (TIA)?

A

Sudden onset of focal neurological symptoms caused by either ischemia or haemorrhage, that RESOLVES WITHIN 24hrs.

97
Q

What are some common causes of ischaemic stroke?

A

Atherosclerosis
Cardioembolic e.g atrial fibrillation
Small artery occlusion
Thromboembolism.

98
Q

What are some common causes of haemorrhagic stroke?

A

Primary intracerebral haemorrhage.
Subarachnoid haemorrhage
Arteriovenous malformation

99
Q

What are some risk factors for stroke?

A 
Previous stroke
Increasing age
Male > female
Family history
Smoking
Hypertension
Cardiac problems 
Diabetes
100
Q

What are small end arteries at risk of?

A

Lacunar ischaemic stroke and deep haemorrhagic stroke due to their high pressure. Common sites include brainstem, basal ganglia and subcortical areas.

101
Q

What are the symptoms of Anterior cerebral artery occlusion?

A

Contra-lateral paralysis of foot and leg, sensory loss over foot and leg.
Impairment of gait and stance.

102
Q

What are the symptoms of middle cerebral artery occlusion?

A

Contralateral paralysis of face/arm/leg, sensory loss of face/arm/leg.
Homonymous hemianopia.
Gaze paralysis to the opposite side.
Aphasia if stroke is in dominant hemisphere.
Unilateral neglect and agnosia for half of external space if non dominant stroke.

103
Q

What are some examples of agnosias typically present in right hemisphere strokes?

A

Visual agnosia
Sensory agnosia
Anosagnosia (denial of hemiplegia (paralysis down 1 side))
Prosopagnosia (failure to recognise faces).

104
Q

What are some lacunar stroke syndromes?

A

Devoid of cortical signs - e.g no dysphasia, neglect, hemianopia.

Pure motor stroke
Pure sensory stroke
Dysarthria - clumsy hand syndrome.
Ataxic hemiparesis.

105
Q

What are some symptoms of posterior cerebral artery occlusion?

A 
Brainstem dysfunction:
Coma, vertigo, nausea, vomiting, cranial nerve palsies, ataxia. 
Hemiparesis, hemisensory loss
Crossed sensori-motor deficits
Visual field deficits.
106
Q

What are the aims of acute ischaemic stroke therapies?

A

Restore blood supply
Prevent extension of ischaemic damage.
Protect vulnerable brain tissue.

107
Q

How is ischaemic stroke managed?

A 
Urgent CT/MRI. 
Antiplatelets - aspirin 
Thrombolysis - alteplase
Thrombectomy
Admit to stroke unit
108
Q

What are the different classifications of stroke?

A

Total Anterior Circulation Stroke TACS

Partial Anterior Circulation Stroke PACS

stroke LACS

Posterior Circulation Stroke POCS.

109
Q

What is TPA?

A

Tissue Plasminogen Activator

110
Q

What are some investigations fr stroke?

A 
Routine blood tests
CT/MRI
ECG
ECHO
Carotid doppler
Cerebral angiogram
Hyper-coagulable blood screen.
111
Q

What is the secondary prevention for stroke?

A 
Anti-hypertensives
Anti-platelets
Lipid lowering agents - statins
Warfarin for AF
Carotid endarterectomy. 
Aspirin for 2 weeks after. 300mg.
112
Q

What is myasthenia gravis?

A

Autoimmune neuromuscular disease mediated by antibodies attaching to nicotinic acetylcholine receptors on the post synaptic neuromuscular junction.

113
Q

How does myasthenia gravis present?

A 
Slowly increasing or relapsing muscle fatigue.
Ptosis, diplopia.
Reflexes are normal.
Weakness
Normal sensation.
114
Q

What are the investigations for myasthenia gravis?

A

Antibodies- AChreceptor antibodies, anti-muscarinic antibodies.
CT to exclude thyoma.
Single fibre EMG - jitter.

115
Q

What is Brown-Sequard Syndrome?

A

Damage to one half of the spinal cord resulting in paralysis and loss of proprioception on ipsilateral side and loss of temperature and pain on the contralateral side.

116
Q

What is Meningitis?

A

Infection of the protective membranes (meninges) that cover brain and spinal cord.

117
Q

What are the symptoms of meningitis?

A 
Headache
Neck stiffness
Photophobia
Nausea/vomiting
Fever
Rash that does not go away when a glass is rolled over it
Seizures
118
Q

What is the classical triad for meningitis?

A

Headache
Neck Stiffness
Altered mental state

119
Q

What organisms commonly cause meningitis?

A

Bacterial - meningococcus and pneumococcus.

Viral - enteroviruses.

120
Q

What is Encephalitis?

A

Inflammation/infection of brains tissue.

121
Q

What are the symptoms of Encephalitis?

A

Flu-like prodrome 4-10days.

Progressive headache associated with fever.

Cerebral dysfunction - confusion, abnormal behaviour, memory disturbance, depressed conscious level.

Seizures.
Focal symptoms/signs.

122
Q

What are the 2 important antibodies involved Auto-immune Encephalitis?

A

Anti-VGKC (Voltage Gated Potassium Channel) :

  • frequent seizures
  • amnesia
  • altered mental state

Anti-NMDA receptor

  • flulike prodrome
  • prominent psychiatric features
  • altered mental state and seizures
  • progresses to a movement disorder and coma.
123
Q

What are the investigations for Meningitis?

A

Blood cultures
Lumbar Puncture - CSF culture/microscopy
No need to image if no contraindications of LP.

124
Q

What are the investigations for Encephalitis?

A

Blood cultures
Imaging (CT +/- MRI)
Lumbar Puncture
EEG.

125
Q

What are the contraindications for Lumbar Puncture?

A

Focal neurological deficit, not including cranial nerve palsies.

New onset seizures.

Papilloedema.

GCS < 10

Severe immunocompromised state.

126
Q

What are the CSF findings in Bacterial meningitis?

A

Opening pressure - increased.

Cell count - High, mainly neutrophils.

Glucose - Reduced

Protein - High

127
Q

What are the CSF findings for viral meningitis and encephalitis?

A

Opening pressure - Normal /increased.

Cell count - High, mainly lymphocytes.

Glucose - Normal

Protein - Slightly increased.

128
Q

What is the commonest cause of Encephalitis in Europe?

A

Herpes Simplex Virus.
Nearly always type 1.
Treated with Aciclovir

129
Q

What are enteroviruses?

A

Large family of RNA viruses. Transmission through the intestine, faecal oral route.

E.g polioviruses, coxsackieviruses, echoviruses.

130
Q

What are some other, rarer causes of Encephalitis?

A

Arbovirus encephalitide e.g West Nile virus, St Louis encephalitis.

131
Q

What is a Brain Abscess?

A

Localised area of pus within the brain.

132
Q

What are the symptoms of a Brain Abscess?

A 
Fever
Headache
Focal Symptoms/signs
Signs of raised intracranial pressure - papilloedema, depressed conscious level. 
Meningism
133
Q

What are some causes of Brain Abscess?

A

Penetrating head injury
Spread from adjacent infection e.g dental, sinusitis, otitis media.
Blood borne infection e.g bacterial endocarditis.
Neurosurgical procedure.

134
Q

What are the investigations for Brain Abscess and Empyema?

A

CT/MRI
Blood cultures
Biopsy - drainage of pus.
Investigation of source.

135
Q

What organisms are commonly present within Brain Abscesses?

A

Often a mixture of organisms.

70% cases have streptococci, especially penicillin-sensitive group e.g strep anginosus, intermedius, constellates.

Anaerobes present in 40-100% cases e.g bactericides, prevotella.

136
Q

What is the management of Brain Abscesses?

A

Surgical drainage if possible.
Penicillin or ceftriaxone to cover streps.
Metronidazole for anaerobes.

137
Q

What is the organism responsible for Lyme’s Disease?

A

Spirochaete - Borrelia burgdorferi.

3 stage disease:
1 - expanding rash at site of bite.
2- early disseminated infection
3- chronic infection with neurological and musculoskeletal involvement.

138
Q

What is Poliomyelitis?

A

Infection by poliovirus types 1,2 or 3.
Usually asymptomatic.
Infects anterior horn cells of lower motor neurones.
Asymmetric, flaccid paralysis especially in legs.
No sensory features.

139
Q

What is Botulism?

A

Infection from clostridium botulinum, anaerobic spore forming gram positive bacillus.
Neurotoxin that binds to presynaptic membranes and prevents ACh release.

Descending symmetrical flaccid paralysis.

140
Q

What is Creutzfeldt-Jakob disease (CJD)?

A

Fatal, degenerative brain disorder due to the build up of Prions (transmissible proteinaceous particles) in cells causing tissue damage.

Symptoms include memory loss, poor coordination, behavioural changes.
1 year prognosis.

141
Q

What is Guillan- Barré syndrome?

A

Rapid onset muscle weakness caused by the immune system damaging the peripheral nervous system.

142
Q

What is Multiple Sclerosis?

A

Chronic Inflammatory condition of the Central Nervous System characterised by multiple plaques of demyelination that spreads throughout body over time.
Most commonly affects young people.

143
Q

What is demyelination?

A

Autoimmune process activated by T cells crossing the BBB causing acute inflammation of the myelin sheath. Lesions or plaques appear on MRI. Progresses to axonal loss which appears as black holes on MRI.

144
Q

What are the symptoms of a Relapse attack of MS?

A 
Optic neuritis
Sensory symptoms
Limb weakness
Diplopia
Vertigo
Ataxia
Bilateral spinal cord symptoms 
\+/- bladder involvement.
145
Q

What is Optic neuritis?

A 
Subacute visual loss
Pain on moving eye
Disturbed colour vision
Swelling of optic disc
Optic atrophy
Relative sensory pupillary defect.
146
Q

What is myelitis?

A

Inflammation of the spinal cord.

Sensory level often with a band of hyperaesthesia (hypersensitivity).

147
Q

What is Clinically Isolated Syndrome (CIS)?

A

A single episode of demyelination symptoms. No further episodes.

148
Q

What are some Progressive phase symptoms of MS?

A 
Fatigue
Temperature sensitivity
Stiffness/spasms
Imbalance
Slurred speech
Dysphagia
Bladder/bowel involvement
Diplopia (double vision)
Visual loss
Cognitive dementia
Emotional lability (changes)
149
Q

How is MS diagnosed?

A

Clinically - Poser’s criteria

MRI - Macdonald’s criteria.

150
Q

What are the different types of MS?

A

Relapsing- remitting 85%
Secondary progressive
Primary progressive - presents in later years.

151
Q

What are some poor prognostic signs for MS?

A 
Male 
Increasing age
Multifocal symptoms 
Motor signs at onset
Axonal loss
Many MRI lesions.
152
Q

How is an Acute relapse of MS treated?

A

Oral Prednisolone
Rehabilitation
Symptomatic treatment

153
Q

What is the symptomatic treatment for MS patients?

A

Spasticity - muscle relaxants/anti-spasmodics e.g baclofen.
Dysaethesia - Amitriptyline, gabapentin
Urinary - Anti-cholinergics, catheterisation
Constipation - laxatives
Sexual dysfunction - sildenafil
Vision - carbamazepine

154
Q

What are some disease modifying agents used in MS treatment?

A

Injections of beta-interferons, glatiramer acetate.
Oral - teriflunomide, dimethyl fumarate.
Biologics - Natalizumab, Fingolimod tablets, Alemtuzumub.

155
Q

What are the symptoms of Cord Compression?

A

Deep, local spinal pain
Stabbing, radicular pain in dermatomal distribution.
LMN weakness at lesion level.
Progressive UMN weakness and sensory loss below the lesion.
Bladder hesitancy, painless retention.
Faecal incontinence or constipation.

156
Q

What are the signs of cord compression?

A

Look for motor, reflex and sensory level.
LMN signs at level, UMN signs below level.
Tone and reflexes are usually reduced acute cord compression.

157
Q

What are some causes of cord compression?

A 
Trauma
Infection - epidural abscess, TB.
2ndry malignancy  - Breast, thyroid, bronchus, kidney, prostate. 
Disc prolapse. 
Haematoma - warfarin. 
Intrinsic cord tumour
Myeloma.
158
Q

What investigations would you carry out for a suspected cord compression?

A

MRI - definitive modality.

CXR to look for primary malignancies.

159
Q

What is the treatment for Cord compression?

A

Neurosurgical emergency!
Malignancy - dexamethasone IV, chemo, radiotherapy.
Abscess - antibiotics and surgical decompression.

160
Q

What is Cauda Equina Syndrome?

A

Compression of all nerve roots within the lumbar spine, usually due to a disc prolapse.

161
Q

What are the symptoms of Cauda Equina Syndrome?

A 
Bilateral Sciatica - pain in both legs. 
Saddle Anaesthesia (think saddle, horses, equine)
Urinary dysfunction - painless retention.
162
Q

What is the treatment for Cauda Equina Syndrome?

A

Emergency lumbar discectomy to remove some of the disc so the nerves are no longer being compressed.

163
Q

What is Spondylosis?

A

Degenerative change in spinal structure due to trauma and/or ageing. Intervertebral disc prolapse or vertebral collapse. Osteophytes (bone spurs) may form as a result.
may also lead to myelopathy and/or radiculopathy.

164
Q

How does Spondylosis present?

A

Usually asymptomatic

Cervical:

  • Neck stiffness
  • Stabbing/ dull arm pain
  • Upper limb motor and sensory disturbance according to compression level.
  • tingling
Lumbosacral:
- Severe pain on sneezing/coughing
- Lower back strain/pain
Sciatica - shooting radicular pain down bottom and thigh. 
- limited spinal flexion
- Pain on straight leg raise.
165
Q

What is the treatment for Spondylosis?

A

Conservative - analgesia, rest, stiff collar, physio.

Medical - transforminal steroid injection.

Surgical - Decompression - laminectomy, discectomy.

166
Q

What is spinal Stenosis?

A

Generalised narrowing of the lumbar spinal canal due to developmental predisposition +/- facet joint osteoarthritis.

167
Q

How does Spinal Stenosis present?

A

Spinal claudication - aching/heavy bottom and lower limb pain on walking. Rapid onset that may cause numbness.

Pain eased by leaning forwards.
Pain on spine extension.
Negative straight leg raise.

168
Q

What is the treatment for spinal stenosis?

A

Corsets
NSAIDs
Epidural steroid injection
Canal decompression surgery - lumbar laminectomy.

169
Q

What is Bell’s palsy?

A

Entrapment of Facial nerve (CNVII) in the narrow facial canal, causing inflammatory oedema.

170
Q

What is a common cause of Bell’s palsy?

A

Herpes Simplex Virus type 1

171
Q

What are the features of Bell’s palsy?

A

Sudden onset (e.g overnight).

Complete unilateral facial weakness within 24-72hrs.

  • failure to close eye
  • Bell’s sign - eyeball rolls up on attempted closure.
  • Drooling, speech difficulty.

Numbness or pain around ear.

Reduced sense of taste.

Hyperacusis - disabling hearing condition.

172
Q

What investigations would you carry out for Bell’s palsy?

A

Cranial nerve examination.
Serology - infective agent
MRI
LP

173
Q

What is the treatment for Bell’s palsy?

A

Prednisolone within 72hrs, 10 day course.
Valaciclovir if zoster is expected.
Protect eye with eye drops, dark glasses, tape closed at night.
Plastic surgery in extreme cases of no recovery. (Usually better within 9 months).

174
Q

What is Ramsay Hunt Syndrome?

A

Recativation of Varicella Zoster Virus (chickenpox/shingles) in the geniculate ganglion of CNVII.

175
Q

What are the features of Ramsay Hunt Syndrome?

A

Preceding ear pain or stiff neck.
Vesicular rash in auditory canal.
Ipsilateral facial weakness
Ageusia (loss of taste function of the tongue).
Hyperacusis (everyday sounds that cause distress).
May also have CNVIII involvement - vertigo, tinnitus, deafness.

176
Q

What is the treatment for Ramsay Hunt Syndrome?

A

Valaciclovir and Prednisolone within 72hrs.

177
Q

What is Motor Neurone Disease?

A

Progressive neurological disorders that destroy the motor neurones; the cells that control essential voluntary muscle activity.

178
Q

What is Amyotrophic Lateral Sclerosis (ALS)?

A

Type of Motor Neuron Disease.
Progressive, ultimately fatal disorder that disrupts signals to all voluntary muscles.
Most common form of MND is adults. 40-60years.

179
Q

What are some characteristics of ALS?

A

Both upper and motor neurones affected.
Usually limb- bulbar- respiratory order of symptoms.
LMN signs = fasciculations, wasting, weakness.
UMN signs = Increased tone (spasticity) and brisk reflexes.

180
Q

What is the prognosis of ALS?

A

3-5 years after symptom onset.

2-3 years after diagnosis.

181
Q

How is ALS diagnosed?

A

Unique combination of UMN and LMN signs

Electromyography (EMG)

182
Q

What is the treatment for ALS?

A

Supportive - PEG feed, non invasive ventilation, physio, OT, care.
Riluzole - reduces neurotransmitter glutamate.
Anticipatory and palliative care.

183
Q

What are some types of congenital muscular diseases?

A

Muscular dystrophies
Congenital myopathies
Channelopathies
Enzymes/ mitochrondria

184
Q

What are some types of acquired muscular diseases?

A

Metabolic - Ca, K
Endocrine - thyroid, adrenal, vit D
Inflammatory muscle disorders.
Iatrogenic - medication; steroids, statins.

185
Q

What are some examples of muscular dystrophies?

A 
Duchenne's MD
Becker's MD
Facioscapulohumeral MD
Myotonic dystrophy
Limb-girdle MD
186
Q

What are some characteristics of muscular dystrophies?

A

Young to older onset.
Progressive
Cell degeneration (high creatinine kinase)

187
Q

What are some examples of muscle channelopathies?

A

Familial Hypokalemic Periodic Paralysis.
Hyperkalaemic Periodic Paralysis.
Paramyotonia congenita.
Myotonia congenita.

188
Q

What are some examples of inflammatory muscle disease?

A

Polymyositis

Dermatomyositis

189
Q

What is the treatment for Myasthenia Gravis?

A

Symptomatic - Acetylcholinesterase inhibitors e.g pyridostigmine
Immunosuppression - prednisolone, steroid saving agent e.g azathioprine.
Immunoglobulin/plasma exchange.
Thymectomy.

190
Q

What are some types of peripheral nerve disease?

A

Root disease
Individual peripheral nerve e.g compressive, vascular.
Generalised peripheral neuropathy e.g motor/sensory/both +/- autonomic symptoms.

191
Q

What are some causes of Generalised Peripheral neuropathy?

A 
Hereditary
Alcohol
Diabetes
Toxic - drugs
Infections - Lyme's, HIV, leprosy
Paraneoplastic malignancy
Inflammatory demyelinating e.g Guillain-Barre syndrome, Chronic inflammatory demyelinating polyneuropathy.
192
Q

What are the signs and symptoms of peripheral nerve disease?

A

Root - myotomal wasting & weakness, reflex change, dermatomal sensory change.

Individual nerve - wasting & weakness of innervated muscle, specific sensory change.

Generalised peripheral neuropathy - sensory and motor symptoms usually starting distally and moving proximally.

193
Q

What are some investigations for peripheral nerve disease?

A 
Blood tests
Genetic analysis
Nerve conduction studies
Lumbar puncture
Nerve biopsy
194
Q

What is Hydrocephalus?

A

Excess CSF within the intracranial space and inter ventricular spaces within brain causing ventricular dilation.

195
Q

What is communicating hydrocephalus?

A

Non- obstructive hydrocephalus usually caused by a problem with CSF reabsorption. Results in ventricular dilation and raised intracranial pressure.

196
Q

What is non-communicating hydrocephalus?

A

Obstruction within the CSF pathway causing hydrocephalus.

197
Q

What are the symptoms of raised intracranial pressure?

A 
Nausea
Vomiting
Headache
Papilloedema
Gait disturbance
6th nerve palsy
Upgaze difficulty
198
Q

What are some causes of communicating hydrocephalus?

A

Infection e.e bacterial meningitis
Subarachnoid haemorrhage
Post-operative
Head trauma

199
Q

What are some causes of non-communicating hydrocephalus?

A 
Aqueductal stenosis
Tumours
Cysts
Infection
Haemorrhage
Congenital malformations
200
Q

What is the earliest radiological sign of hydrocephalus?

A

Dilated temporal horns of the lateral ventricles. Third ventricle will then become ballooned (looks like snowman).

201
Q

What is the treatment for Hydrocephalus?

A

Surgical - Extra ventricular drain (EVD) for acute.

  • Ventriculo-peritoneal shunt
  • lumbar-peritoneal shunt
  • ventriculo-atrial shunt
  • removal of obstructing lesion
  • third ventriculostomy
202
Q

What is Normal Pressure Hydrocephalus?

A

Excess CSF within intracranial space and ventricles, without an increase in intracranial pressure.

203
Q

What is the classical triad for Normal Pressure Hydrocephalus?

A

Wet - urinary incontinence
Wobbly - gait disturbance (wide stance, short, shuffling steps).
Wacky - quickly progressing dementia.

204
Q

What is the treatment for Normal Pressure Hydrocephalus?

A

Ventriculo-peritoneal shunt as quickly as possible.
good prognosis if treated quickly.
Dementia is symptom least likely to improve.

205
Q

What are the signs of Brown-sequard syndrome?

A

Ipsilateral:

  • reduced vibration
  • reduced proprioception
  • weakness

Contralateral:

  • reduced pain sensation
  • reduced temperature sensation
206
Q

What is a spinal cord stroke?

A

Disruption of the blood flow to the spinal cord. Usually the anterior spinal artery and is usually mid thoracic region.

207
Q

What is the treatment of spinal cord stroke?

A

Maintain BP
Reverse hypovolaemia/arrhythmia
OT and physio
Manage vascular risk factors

208
Q

What is an intracranial haemorrhage?

A

Accumulation of blood within the rigid skull causing an in crease in intracranial pressure. Results in compression of the brain which in turn leads to reduced conscious level.
Death will occur due to herniation of the cerebellar tonsils into foramen magnum.

209
Q

What are some characteristics of Extradural haemorrhage?

A

Bleeding between dura mater and skull.
Accumulating blood strips the dura from the skull.
Middle meningeal artery common cause at the period of skull.
Lucid interval may occur.

210
Q

What are some characteristics of Subdural haemorrhage?

A

Bleeding beneath the dura mater but above the arachnoid.
Common cause is bridging veins.
Blood accumulates slowly due to being under venous pressure.
Normally caused by a fall - rotational motion.
Lucid interval may occur.

211
Q

What are some characteristics of Subarachnoid haemorrhage?

A

Bleeding beneath arachnoid matter but above brain.
Berry aneurysm is common cause - rupture of cerebral artery.
Associated with bruising to the brain.
Thunderclap headache and hypertension are risk factors.

212
Q

What is Diffuse traumatic axonal injury?

A

Scattered lesion in white matter tracts and grey matter over a wide spread area.
Caused by trauma.
Diagnosis by microscopy of brain tissue.
Commonly vehicular collisions or falls from height.
Victims are comatose.

Neurology (10 decks)

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