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GRACE Phase 2a Medicine > Neurology > Flashcards

Neurology Flashcards

1
Q

What does meningism refer to?

A

set of 3 symptoms:

stiffness of the neck, photophobia, severe headache

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2
Q

Patients with viral or bacterial meningitis generally have?

A

Fever, malaise, rash (typically haemorrhagic in meningococcoal meningitis)

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3
Q

Viral causes of meningitis (HELP Me)

A 
Herpes simplex virus
Enteroviruses
Lymphocytic chorio meningitis virus
Poliovirus
Mumps virus
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4
Q

Bacterial causes of meningitis in neonates?

A

E.Coli, group B streptococcus, listeria monocytogenes

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5
Q

Bacterial causes of meningitis in infants?

A

Neisseria meningitidis, Steptococcus pneumoniae, haemophilius influenzae

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6
Q

Bacterial causes of meningitis in young adults?

A

Neisseria meningitidis, S.pneumoniae

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7
Q

Bacterial causes of meningitis in the elderly

A

S.pneumoniae, Neisseria meningitidis, Listeria monocytogenes

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8
Q

What is encephalitis? Clinical symptoms?

A

inflammation of the cerebral cortex (generally viral)

fatigue, decreased consciousness, fever, fits

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9
Q

Meningo-encephalitis

A

If a patient with encephalitis also has meningism

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10
Q

Viral causes of encephalitis

A

Herpes simplex virus, varicella zoster virus, HIV, mumps, measles, parvoviruses

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11
Q

Procedure to test CSF?

A

lumbar puncture

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12
Q

Lumbar puncture

A

Needle that pierces the dura and arachnoid mater to enter the subarachnoid space

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13
Q

Early signs of meningitis in a lumbar puncture

A

Low glucose, high protein, WCC

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14
Q

Difference between lumbar and epidural?

A

Different needle, epidural, need to stay OUTSIDE the dura, therefore bent and blunt needles used for epidural (not sharp). Once reaches the dura, pushes dura away, can feed tube into needle and inject anaesthesia

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15
Q

If the predominant kind of WBC in the CSF are neutrophils, does this indicate viral or bacterial infection?

A

bacterial (neutrophils are professional phagocytes that respond to bacteria)

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16
Q

Why do you get reduced glucose in the CSF with an inflammatory response to a bacterial infection?

A

neutrophils are metabolically active and use glucose

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17
Q

Why is there increased protein in the CSF in a bacterial infection?

A

Dying bacteria, antibacterial proteins and antibodies all contribute to the elevated CSF

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18
Q

Empirical antibiotics given for CNS bacterial infections?

A

IV cefotaxime, ceftriaxone

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19
Q

Adjunctive therapy alongside antibiotics for CNS infections?

A

IV dexamethasone (corticosteroids) - reduce the risk of long-term neurological complications from some bacterial causes of meningitis

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20
Q

CSF from lumbar puncture with a viral infection?

A

WCC predominantly lymphocytes (not neutrophils), moderately raised protein

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21
Q

Meninges blood supply

A

meningeal vessels (branches of the internal carotid) run in the extradural (epidural) space, bridging veins across the subdural space, circle of Willis lies in the subarachnoid space, there are no vessels deep to the pia mater, the pia forms part of the BBB

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22
Q

Stroke definition

A

Infarction or bleeding to the brain which manifests with sudden-onset focal CNS signs, lasting over 24hours

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23
Q

Risk factors for stroke

A

HTN, DM, age, smoking, heart disease, raised PCV, polycythaemia, clotting disorders, combined oral contraceptive pill

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24
Q

Two types of stroke

A

Ischaemic (85%) - cerebral infarction due to thrombosis or arterial embolism

Haemorrhagic (15%) - subarachnoid or intracranial, blood leaks into brain

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25
Q

Causes of ischaemic stroke?

A

Thrombosis or arterial embolism blocks a blood vessel

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26
Q

Causes of haemorrhagic stroke

A

Trauma, aneurysm rupture, thrombolysis, anticoagulation, carotid artery dissection

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27
Q

Differential diagnosis for stroke?

A

Hypoglycaemia, migraine aura, focal epilepsy, syncope

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28
Q

Clinical presentation of anterior cerebral artery (ACA) ischaemic stroke (DISTAL)

A 
Drowsiness
Incontinence
Sensory leg disturbances
Truncal ataxia
Akinetic mutism
Leg weakness
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29
Q

Clinical presentation of middle cerebral artery (MCA) ischaemic stroke (CHAFD)

A 
Contralateral arm/leg weakness
Hemianopia
Aphasia
Facial droop
Dysphasia
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30
Q

Clinical presentation of posterior cerebral artery (PCA) ischaemic stroke (CCCUPV)

A 
Contralateral homonymous hemianopia
Cortical blindness
Colour naming and discrimination difficulties
Unilateral headache
Prosopagnosia
Visual agnosia
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31
Q

Stroke Ix

A
  1. Urgent CT/MRI (to identify ischaemic or haemorrhagic)
  2. Pulse, BP, ECG - to look AF/MI
  3. FBC - thrombocytopenia, polycythaemia, exclude hypoglycaemia
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32
Q

1st step of stroke Mx

A

Maximise reversible ischaemic tissue - hydration and oxygen

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33
Q

Stroke Mx - ischaemic

A
  1. Thrombolysis - give tissue plasminogen activator (IV altepase) and start antiplatelet therapy
  2. If time of onset is known, give daily aspirin for 2 weeks and lifelong clopidogrel
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34
Q

Stroke Mx - haemorrhagic (MC MARS)

A 
Monitor GCS
Control HTN
Manual decompression of raised ICP or give diuretics
Antiplatelets contraindicated
Reverse anticoagulation
Surgery may be required
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35
Q

Transient ischaemic attack

A

Ischaemic neurological event with symptoms lasting <24hours, without intervention 1 in 12 patients will have a stroke within a week

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36
Q

Risk factors for TIA

A

(same for stroke), age, HTN, DM, smoking, raised PCV, polycythaemia

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37
Q

Causes of TIA?

A
  1. atherothromboembolism (from the carotid)
  2. cardioembolism (microemobil from mural thrombus post-MI, AF)
  3. hyperviscosity (raised PCV, polycythaemia)
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38
Q

Distribution of TIA

A

Anterior circulation (90%) - carotid, posterior (10%) - vertebrobasilar

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39
Q

TIA symptoms - anterior circulation (HOAD)

A

Hemiparesis
Occlusion may cause weak contralateral arm/leg
Amaurosis fugax
Dysphagia

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40
Q

TIA symptoms - posterior circulation (Don’T CHAV)

A

Diplopia, tetraparesis, choking, hemianopia vision loss, ataxia, vertigo/vomiting

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41
Q

Ix for TIA

A

Bloods - FBC (polycythaemia), glucose (hypoglycaemia), cholesterol
Diffusion weighted MRI (if ABCD2 >4)
Carotid artery doppler US
ECG (AF)

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42
Q

Tx for TIA

A
  1. ABCD2 score for stroke risk
  2. Control CDV risk factors (HTN = ACE-i/ARBs, cholesterol = statins)
  3. Antiplatelet drugs - aspirin then clopidogrel
  4. Anticoagulation - e.g. warfarin, if have AF, mitral stenosis
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43
Q

What driving precautions should be taken after TIA?

A

Do not drive for 4 weeks after a TIA

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44
Q

Clopidogrel

A

P2Y12 inhibitor, antiplatelet drug. Works by binding to the P2Y12 receptors on platelets to prevent platelet aggregation

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45
Q

Subarachnoid haemorrhage (SAH)

A

Bleeding in the subarachnoid space (arachnoid and pia mater)

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46
Q

Risk factors for SAH?

A

HTN, age, smoking, previous aneurysmal SAH, FHx

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47
Q

Causes of SAH

A

Berry aneurysm rupture (80%), arteriovenous malformations (15%) - fistula between arterial and venous symptoms causing high blood flow between AVM, idiopathic otherwise

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48
Q

Ix for SAH

A

CT scan
Lumbar puncture (bilirubin, oxyhaemoglobin)
MR angiography

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49
Q

Tx for SAH

A

Immediate referral to neurosurgeon
Re-examine CNS often - BP, GCS
Maintain cerebral perfusion by keeping well hydrated
CCB (nimodipine) to reduce vasospasm
Surgery - endovascular coiling or surgical clipping

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50
Q

Complications of SAH?

A

Re-bleeding, hyponatraemia, cerebral ischaemia due to vasospasm, hydrocephalus

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51
Q

Subdural haemorrhage (SDH)

A

accumulation of blood in the subdural space (between dura and arachnoid) following the rupture of a bridging vein

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52
Q

Who are vulnerable to SDH and why?

A

Alcoholics, those with dementia - brain size < skull, bridging veins more vulnerable to rupture

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53
Q

Causes of SDH

A

Most due to trauma, but can be 9 months previously

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54
Q

Pathophysiology of SDH

A

Bleeding from bridging veins, stops due to low pressure, forms clot, after time clot lyses and increased clot fragments in blood increases osmotic pressure, draws in water which increases ICP, leads to shift of the midline structures to the side, eventual coning

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55
Q

What is meant by coning?

A

As the ICP rises the brain pushes through the foramen magnum

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56
Q

Clinical presentation of SDH

A

Latent period –> headache, drowsiness, unsteadiness, mood change

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57
Q

Ix of SDH

A

CT scan, MRI

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58
Q

Tx for SDH

A

Reverse clotting abnormalities, refer to neurosurgeon, IV mannitol (diuretic) to reduce ICP

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59
Q

Extradural haemorrhage

A

Collection of blood between the dura mater and bone, most commonly due to trauma –> skull fracture –> laceration of the middle meningeal artery

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60
Q

Clinical presentation of extradural haemorrhage

A

Characteristic history of head trauma, followed by brief period of unconsciousness/drowsiness –> lucid interval (hours/days)
Severe headache, nausea, vomiting, confusion, rapid ICP increase, ipsilateral pupil dilates, decreased GCS, coning

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61
Q

Ix for extradural haemorrhage

A

CT scan shows hyperdense haematoma in biconcave shape

Skull X-ray may show fracture that crosses the middle meningeal artery

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62
Q

Tx for extradural haemorrhage

A

ABCDE, IV mannitol (diuretic to reduce ICP), referral to neurosurgery, maintain airway via intubation

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63
Q

Myasthenia gravis

A

Autoimmune condition mediated by antibodies against ACh receptors on the post-synaptic side of the NMJ

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64
Q

Causes of myasthenia gravis

A
  • If <50, more common in women and associated with other autoimmune conditions e.g. SLE, RA
  • If >50, more common in men, and associated with thymus atrophy/cancer
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65
Q

Clinical presentation of Myasthenia gravis?

A

Progressive muscle weakness (order of muscle weakness - extraocular, bulbar, facial, neck, trunk), ptosis (eyelid drooping), displopia, myasthenic snarl when smiling, tendon reflexes present, general respiratory difficulties

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66
Q

Order of progressive muscle weakness in myasthenia gravis? (Every Boy Finds Nice Trousers)

A

Extraocular, bulbar, facial, neck, trunk

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67
Q

Ix for myasthenia gravis

A
  1. Anti-AChR antibodies
  2. Electromyography (EMG) - decrement in muscle AP upon stimulation
  3. CT of thymus
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68
Q

Mx for myasthenia gravis?

A
  1. Symptom control (muscle weakness) - acetylcholinesterases (pyridostigmine)
  2. Immunosuppression (prednisolone)
  3. Thyectomy
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69
Q

Myasthenic crisis

A

Life-threatening weakness of the respiratory muscles during a relapse, monitor the FVC, treat with plasmapheresis (removal of AChR antibodies)

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70
Q

Lambert-Eaton Myasthenic syndrome (LEMS)

A

Autoimmune disorder of NMJ, impaired pre-synaptic release of ACh due to antibodies against the calcium voltage gated ion channels (P/Q subtype)

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71
Q

Risk factor for LEMS

A

Cancer - LEMS is paraneoplastic in 50% cases (in particular small cell cancer of the lungs)

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72
Q

Presentation of LEMS

A

Proximal muscle weakness, depressed tendon reflexes, gait difficulty, autonomic symptoms - dry mouth, constipation, postural hypotension

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73
Q

Ix for LEMS

A

EMG, CT scan/MRI of lungs, serum test for voltage gated calcium channel antibodies

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74
Q

Mx of LEMS

A

Pyridostigmine (improve muscle strength), prednisolone (steroid immunosuppression), IV Ig

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75
Q

What is epilepsy?

A

Condition that occurs due to excessive and uncontrolled neuronal activity in the brain, manifesting in seizures

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76
Q

Seizure criteria to be defined as epileptic?

A

> 2 24hrs apart

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77
Q

Risk factors for epilepsy?

A

FHx, premature babies, abnormal blood vessels in brain, Alzheimers/dementia, drug use

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78
Q

Causes of epilepsy

A
  1. Idiopathic
  2. Cortical scarring - head injury, cerebrovascular disease
  3. Stroke, tumour, Alzheimer’s dementia
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79
Q

Focal/partial seizures

A

Originating in networks often linked to one hemisphere/lobe

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80
Q

generalised seizures

A

originating at some point within and rapidly engaging bilaterally distributed networks leading to simultaneous onset of widespread electrical discharge

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81
Q

Two types of focal/partial seizure

A
  1. Simple/without loss of consciousness

2. Complex/loss of consciousness

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82
Q

Types of generalised seizures

A

Tonic-clonic, absence, atonic, myoclonic, infantile spasms

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83
Q

What is meant by tonic and clonic?

A

tonic = muscles stiffen, clonic = muscles jerk

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84
Q

Symptoms of simple focal seizure?

A

Focal motor, sensory, autonomic or psychic symptoms e.g. deja vu, hallucinations
NO post-ictal symptoms

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85
Q

Mx for focal seizures?

A
  1. carbamazepine, lamotrigine

2. sodium valproate

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86
Q

Symptoms of complex focal seizures?

A

Impaired awareness, post-ictal confusion

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87
Q

Tonic-clonic seizure

A

Muscle stiffening followed by muscle jerking, may be associated with tongue biting, incontinence, groaning.
POST-ICTAL confusion and drowsiness

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88
Q

Mx for tonic-clonic seizures?

A
  1. sodium valproate

2. carbamazepine, lamotrigine

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89
Q

Absence seizures

A

Typically occur in children, brief (<10s) pause, stare into space, then return to normal suddenly, unaware during episode

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90
Q

Mx for absence seizures

A

Sodium valproate

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91
Q

Atonic seizures

A

‘Drop attacks’, sudden lapse in muscle tone, may cause a fall, no loss of consciousness

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92
Q

Mx for atonic seizures

A
  1. Sodium valproate

2. Lamotrigine

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93
Q

Myoclonic seizures (flying saucer seizure)

A

Sudden brief muscle contractions/jerking

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94
Q

Mx for myoclonic seizures

A
  1. Sodium valproate

2. Lamotrigine

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95
Q

Infantile spasms

A

Clusters of full body spasms in infancy, rare disorder

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96
Q

Ix for epilepsy

A
  1. Electroencephalogram (EEG)
  2. MRI
  3. CT
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97
Q

Mx of epilepsy

A
  1. Anti-eplieptic drugs
  2. Psychological therapies e.g. CBT
  3. Surgical intervention
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98
Q

papilloedema

A

optic disc swelling, often a presentation of brain tumours

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99
Q

Why does raised ICP at the start of a brain tumour not cause a problem?

A

Brain is compliant, removes CSF from ventricles –> spinal cord to adjust for increasing ICP due to tumour, but there is a point when no more CSF can be relocated and there is a really sharp rise in ICP –> symptoms –> midline shift of brain

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100
Q

Commonest types of tumours to metastasise to the CNS?

A

Lungs, breast, renal cell carcinoma, melanoma, GI

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101
Q

Gliomas (in order of decreasing malignancy)

A
  1. Astrocytomas (85-90%)
  2. Oligodendrogliomas (5%)
  3. Ependymomas
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102
Q

Most common form of primary brain tumour?

A

gliomas

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103
Q

meningiomas

A

tumours growing from cells in the meninges, often benign

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104
Q

If a pituitary tumour grows large enough and presses on the optic chiasm?

A

Bitemporal hemianopia

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105
Q

Acoustic neuroma

A

tumours of the Schwann cells surrounding the auditory nerve that innervates the inner ear, occurring around the cerebellopontine angle

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106
Q

Risk factors for primary brain tumours?

A

FHx, ionising radiation, vinyl chloride, affluent people, immunosuppression

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107
Q

Common pathway for malignant gliomas?

A

Mutation of IHD-1 –> excessive 2-hydroxyglutarate (glycolysis of glucose) –> triggers genetic instability in glial cells –> inappropriate mitosis –> cancer

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108
Q

Oligodendrgliomas

A

arise from oligodendrocutes, slow growing, grade II, cause seizures, all IHD-1 positive

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109
Q

4 cardinal symptoms of primary brain tumours

A
  1. Raised ICP
  2. Neurological deficits
  3. Epilepsy/seizures
  4. Lethargy/fatigue
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110
Q

Symptoms of raised ICP due to brain tumour? (Prince Died Very Peacefully)

A
  1. progressive headache
  2. drowsiness
  3. vomiting
  4. papilloedema
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111
Q

Frontal lobe neurological deficit symptoms due to primary tumour?

A

hemiparesis, personality change, Broca’s dysphasia, lack of ability to plan

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112
Q

parietal lobe neurological deficit symptoms due to primary tumour?

A

hemisensory loss, dysphasia, reduction in 2 point-discrimination

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113
Q

temporal lobe neurological deficit symptoms due to primary tumour?

A

dysphasia, amnesia

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114
Q

occipital lobe neurological deficit symptoms due to primary tumour?

A

contralateral visual defects

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115
Q

cerebellar neurological deficit symptoms due to primary tumour?

A 
Dysdiadochokinesia
Ataxia
Nystagmus
Intention tremor
Slurred speech
Hypotonia
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116
Q

Ix for primary brain tumorus

A

CT and MRI, bloods, biopsy (via skull burr-hole)

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117
Q

Mx for primary brain tumours

A

Surgery, radiotherapy, chemotherapy (temozolomide), oral dexamethasone (most powerful synthetic steroid which rapidly improves brain performance in all tumours)

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118
Q

Most common type of seizures in primary brain tumours?

A

Focal

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119
Q

Charcot-marie-tooth disease

A

peroneal muscle atrophy, heterogenous group of inherited peripheral neuropathies

120
Q

Clinical presentation of Charcot-Marie-Tooth disease

A
  • High foot arches (pes cavus)
  • ‘Inverted champagne bottle legs’ due to distal muscle wasting
  • Lower limb and hand weakness
  • Foot drop
  • Peripheral sensory loss
121
Q

Gullain-Barré syndrome

A

Acute inflammatory demyelinating polyneuropathy, begins soon after infection, followed by recovery

122
Q

Signs of Gullain-Barré syndrome

A

Symmetrical ascending muscle weakness following infection, reduced reflexes

123
Q

Triggers for Gullain-Barré syndrome

A

Infections such as campylobacter jejuni, HIV, EBC, causes antibody production which can also attack nerves

124
Q

Mx of Gullain-Barré syndrome

A

IV immunglobulin and plasmapheresis

125
Q

Giant cell arteritis (temporal arteritis)

A

Granulmatous arteritis of the aorta and large vessels (affecting the head and neck), particularly affect the temporal artery

126
Q

Pathophysiology of GCA

A

Granulomatous arteritis (arterial inflammation) in skip lesions along the artery, leading to endothelial damage and thus thrombus formation –> obstruction of blood flow –> ischaemia

127
Q

Clinical presentation of GCA

A
  • New onset severe headache
  • Tenderness along the temporal artery
  • Scalp tenderness
  • Visual loss
  • Jaw claudication
128
Q

Ix for GCA

A
  1. Temporal artery biopsy - diagnostic, need large section due to skip lesions
  2. Raised ESR/CRP
  3. Raised platelets
129
Q

Mx of GCA

A
  1. Begin high dose steroids (e.g. prednisolone) IMMEDIATELY

2. Bisphosphonates (osteoporosis prophylaxis)

130
Q

What forms the carpal tunnel? what passes through

A

ligament and carpal bones, nine tendons and median nerve

131
Q

Why does carpal tunnel syndrome occur more often in females?

A

smaller wrists but same size tendons

132
Q

Clinical presentation of CTS?

A
  • Aching pain in hand and arm (especially at night, can wake patient)
  • Paraesthesia in thumb, index and middle fingers, relieved by dangling over the edge of the bed (wake and shake)
133
Q

Ix for CTS

A

Phalen’s test - maximal flexion of wrist for 1 min may induce pain
Tinel’s test - tapping over nerve can induce tingling

134
Q

Mx of CTS

A

Wrist splinting, local steroid injections, decompression surgery

135
Q

Amaurosis fugax?

A

Unilateral vision loss ‘like a curtain descending’, occurs when the retinal artery is occluded

136
Q

How does Paget’s disease of bone affect the skull?

A

Overgrowth of bone can compress and damage the nerve, causing pain, weakness or tingling in an arm or leg or hearing loss

137
Q

Huntington’s disease

A

neurodegenerative disorder that causes chorea, characterised by the lack of GABA (inhibitory neurotransmitter)

138
Q

Effect of lack of GABA in HD?

A

Less inhibition of glutamate release, therefore more thalamic stimulation –> jerky, semi-purposeful movements

139
Q

What is meant by anticipation in HD?

A

The number of CAG repeats in each successive generation = earlier onset disease, more severe disease

140
Q

Pathophysiology of HD?

A

Repeated expression of CAG, >35 repeats = HD, –> mutated huntingtin proteins have tendency to cluster and cause neurodegeneration in the brain therefore

141
Q

Clinical presentation of HD

A

Chorea, muscle rigidity, dysarthria, dysphagia, cognitive symptoms (dementia)

142
Q

Prodromal phase of HD

A

Irritability, confusion, incoordination

143
Q

Medications for HD

A

Antipsychotics, diazepam, dopamine deleting agents (e.g. tetrabenazine)

144
Q

What is Wernicke-Korsaoff syndrome?

A

Acute and reversible encephalopathy due to vitamin B1/thiamine deficiency

145
Q

In which patients is WK syndrome common?

A

Alcohol abusers

146
Q

Classic triad of symptoms in Wernickes encephalopathy?

A

confusion, ataxia and opthalmoplegia

147
Q

Korsakoff’s syndrome?

A

Late manifestation of the condition where Wernicke’s encephalopathy is not treated adequately

148
Q

How does chronic alcohol intake lead to thiamine/B12 deficiency?

A
  • Inadequate intake
  • Decreased absorption
  • Impaired utilisation in the cells
149
Q

Wernicke’s Korsakoff’s syndrome presentation COAT RACK

A

Confusion, ophthalmoplegia, ataxia, thymine deficiency

Retrograde amnesia
Anterograde amnesia
Confabulation
Korsakoff’s psychosis

150
Q

Myopathy

A

Primary disorder of muscles with gradual-onset symmetrical proximal muscle weakness

151
Q

Differences between myopathy and neuropathy

A

Paraesthesia present in NP, not MP
NP = asymmetrical, MP = symmetrical
NP = distal, MP = proximal
Tendon reflexes, NP = diminished, MP = present

152
Q

Muscular dystrophies

A

Progressive degeneration and weakness of specific muscle groups

153
Q

Duchenne’s muscular dystrophy (DMD)

A

Commonest muscular dystrophy, X-linked recessive condition, presents in early childhood and progresses, mutation in dystrophin gene –> absence of dystrophin protein

154
Q

Ix of DMD

A
  • Suspect in any boy that cannot walk by 18 months
  • Serum creatinine kinase (high in DMD)
  • Genetic analysis
  • Muscle biopsy for dystrophin protein
155
Q

Presentation of DMD

A
  • Progressive proximal muscular dystrophy
  • Pseudohypertrophy of calves
  • Delay in motor milestones - inability to run, waddling gait
  • Gower’s sign - climbing up legs using hands when rising from the floor
156
Q

Mx for DMD

A

genetic counselling, physiotherapy, corticosteroids (e.g. prednisolone) may improve muscle strength

157
Q

Where does the spinal cord end? What is this tapered structure called?

A

L1-L2, conus medullaris

158
Q

Cauda equina

A

bundle of nerves that arise from the end of the spinal cord

159
Q

Spinal cord compression (SCC) occurs in 2.5% of patients presenting with?

A

metastatic cancer

160
Q

Most common cause of spinal cord compression (SCC) (85%)

A

Metastases in the osseous vertebral column

161
Q

What can happen to the intervertebral discs –> SCC?

A

Disc herniation - centre of disc moves out through the annulus and puts pressure on the nerve root, causing pain

162
Q

Clinical presentation of SCC?

A

Back pain, motor pain, radicular pain, incontinence and bowel dysfunction

163
Q

Ix for SCC

A

MRI scan

164
Q

Mx of SCC

A

dependent on cause, malignancy (IV dexamethasone to reduce inflammation and oedema), refer to neurosurgery

165
Q

Cauda equina syndrome

A

Medical emergency due to compression/spinal damage at or caudal to L2

166
Q

Most common place of lumbar disc herniation for cauda equina syndrome?

A

L4/5 and L5/S1

167
Q

Causes of cauda equina syndrome?

A

Herniation of lumbar disc, tumour, infection, trauma

168
Q

Presentation of cauda equina syndrome?

A

Absent knee/ankle reflexes, saddle paraesthesia, loss of anal sphincter and bladder control, lower motor weakness

169
Q

Ix for cauda equina syndrom

A

MRI, test lower limb reflexes

170
Q

Mx of cauda equina syndrome

A

urgent referral to neurosurgeon

171
Q

Syncope

A

Essentially fainting - caused by a temporary drop in the amount of blood that flows to the brain
Happens due to a sudden drop in BP, drop in HR, or changes in the amount of blood in areas of your body

172
Q

Thalamus

A

Connection between cortex and brainstem and spinal cord

173
Q

Main protein found in lewy body deposits?

A

alpha synuclein

174
Q

What are lewy bodies?

A

Abnormal deposits/occlusions of protein that form within the brain in neurons affected by Parkinsons, Lewy body dementia, etc.

175
Q

What is Parkinsons disease?

A

Common neurodegenerative disease where the clinical features result from progressive depletion of dopaminergic neurons in the substantia nigra, leading to excessive thalamic inhibition (less refined movement)

176
Q

Differential diagnosis forr PD?

A

Benign essential tremor, Lewy Body dementia

177
Q

Parkinsonian triad (TBH)

A

Tremor, bradykinesia, hypotonia

178
Q

Tremor in PD

A

Worse at rest, improved by voluntary movement, most obvious in hands

179
Q

Bradykinesia in PD

A

Slow to initiate movement and slow actions, decreased amplitude with repetition, hesitant gait (shuffling, hunched forward, no arm swinging), freezing at obstacles/doors, expressionless face

180
Q

Hypotonia in PD

A

cogwheel rigidity

181
Q

Clinical features in Parkinsons disease?

A

Neuropsychiatric symptoms - hallucinations, depression, dementia
Sleep disorders - insomnia
Fatigue
GI and autonomic disorders - drooling, sweating, constipation, dysphagia

182
Q

Dx for PD?

A

Clinical diagnosis, signs invariably worse on one side is indicative, positive response to levodopa therapy

183
Q

Mx for PD

A
  1. Levodopa (combine with dopa-decarboxylase inhibitor)
  2. Dopamine agonists - early onset PD
  3. Monoamine oxidase B inhibitors
184
Q

Enzyme that breaks down dopamine

A

Monoamine oxidase B

185
Q

why does levodopa need to be combined with dopa-decarboxylase inhibitor?

A

So the L-dopa is not converted into dopamine peripherally, therefore more L-dopa is available to cross the BBB

186
Q

SE of levodopa

A

nausea, vomiting, psychosis, hallucinations, wearing off effects

187
Q

SE of dopamine agonists?

A

Impulse control disorders (gambling, hypersexuality, think wheelbarrows), drowsiness, nausea, hallucinations

188
Q

Examples of Parkinsons’s-plus syndromes

A

Dementia with lewy bodies, multiple system atrophy

189
Q

What is benign essential tremor?

A

Common condition in the elderly, fine tremor affecting voluntary muscles, most notable in hands. It is SYMMETRICAL, MORE PROMINENT on voluntary movement, worse with caffeine/stress, improved by alcohol

190
Q

Mx for benign essential tremor

A

Propanolol - non-selective beta blocker

191
Q

Dementia

A

Clinical neurodegenerative condition with progressive decline in several cognitive domains, initial presentation is memory loss over months/years

192
Q

Risk factors for dementia

A

FHx, age, Down’s, high BP, obesity, hyperlipidaemia, DM

193
Q

Alzheimer’s disease

A

neuronal reduction in multiple areas of the brain, neurons affected develop surrounding neurofibrillary tangles, amyloid plaques and produce less ACh

194
Q

Largest genetic risk factor for sporadic Alzheimer’s disease?

A

Apolipoprotein E4 variant

195
Q

Vascular dementia

A

Stepwise deterioration, followed by periods of stability, history of TIAs, presents with vascular pathology

196
Q

Lewy-body dementia

A

Fluctuating condition with variation in alertness and attention, recurrent hallucinations, frequent falls

197
Q

Frontal-temporal dementia

A

Specific degeneration of the frontal and temporal lobes. Loss of motivation, emotional unconcern, behaviour change, selfishness, neglecting personal hygiene, language problems, speaking slowly

198
Q

Clinical presentation of Alzheimers?

A
  1. Persistent, progressive and global cognitive impairment
  2. Memory loss
  3. Irritability, behaviour change
  4. Psychosis
  5. Agnosia
  6. Anosognosia
  7. Planning affected
  8. Verbal difficulty
199
Q

Ix for Alzheimers

A

History, MMSE, exclusion of differentials (e.g. hypothyroidism), bloods, MRI

200
Q

Mx for dementia

A
  1. Treat associated anxiety/depression
  2. BP control
  3. Acetylcholinesterase inhibitors (rivastigmine)
  4. Antiglutamatergic treatment (memantine)
201
Q

Motor neurone disease (MND)

A

umbrella term for neurodegenerative conditions characterised by selected loss of motor neurones (motor cortex, cranial nerve nuclei, anterior horn cells)

202
Q

Muscles spared in MND

A

rectal and bladder sphincters, occulomotor muscles

203
Q

Epidemiology for MND

A

males > females, median age onset - 60

204
Q

Archetypal MND

A

Amyloidosis lateral sclerosis (80%)

205
Q

ALS (UMN and LMN)

A
  • Loss of motor neurons in motor cortex and anterior horn of cord
  • Progressive weakness and UMN signs
  • LMN muscle wasting
  • Split hand sign
  • Cramps
  • Wrist and foot drop
206
Q

UMN lesion signs

A

No/little muscle atrophy, weakness, hyperreflexia, positive Babinski sign, hypertonia

207
Q

LMN lesion signs

A

Muscle atrophy, flaccid paralysis, diminished tendon reflexes, fasciculations, negative Babinski sign

208
Q

Progressive bulbar palsy (LMN)

A
  • Only affects CN 9-12
  • Dysarthria, dysphagia, nasal regurgitation of fluids and choking
  • LMN lesion of tongue and muscles of talking and swallowing
209
Q

Progressive muscular atrophy (LMN)

A

Weakness, muscle wasting, fasciculations, affect distal muscles before proximal

210
Q

Primary lateral sclerosis (UMN)

A

Least common, loss of Betz cells in the motor cortex, mainly UMN signs, marked leg weakness

211
Q

Differentiate between MND and MS

A

MND NO sensory loss

212
Q

Differentiate between MND and myasthenia gravis

A

MND does NOT affect occulomotor muscles

213
Q

Ix for MND

A

clinical diagnosis, MRI, lumbar puncture (exclude inflammatory causes), EMG

214
Q

Tx of MND

A

Riluzole

215
Q

Riluzole

A

used to improve survivla in MND, inhibitor of glutamate release and NMDA receptor antagonist

216
Q

5 types of primary headache? Which is the most common? Most disabling?

A
  1. Migraine
  2. Tension (most common)
  3. Cluster (most disabling)
  4. Sinus
  5. Hormonal
217
Q

Causes of secondary headache?

A

meningitis, SAH, GCA, intracranial haemorrhage, medication over-use

218
Q

Secondary headache red flags - SNOOP

A

Systemic symptoms (illness)
Neurological symptoms
Onset new (>40) or sudden (thunderclap)
Other associated symptoms e.g. papilloedema
Previous headache history with progression or change in attack character

219
Q

Migraine

A

Disorder of recurrent attack, throbbing/pulsatile headache, often preceded by aura and other associated symptoms (nausea, vomiting, visual changes)

220
Q

Migraine aura

A

Visual aura - zig-zags, shimmering, black holes
Sensory aura - paraesthesia, numbness
Motor aura - weakness, dysphasia

221
Q

Migraine presentation

A
  1. Classically visual aura (15-30mins), followed by unilateral throbbing headache within 1hr
  2. Isolated aura w/o headache
  3. Episodic headache w/o aura, unilateral, with nausea, vomiting, photo/phonophobia
222
Q

Prodrome migraine aura

A

Cravings, yawning, mood change

223
Q

Partial triggers of migraine (CHOCOLATE)

A

Chocolate, hangovers, orgasms, caffeine/cheese, OCP, lie-ins, alcohol, travel, exercise

224
Q

Dx of migraines

A

Clinical diagnosis, examine eyes, BP, head and neck, exclusion of SNOOP red flags

225
Q

Mx of migraine

A
  1. Prophylactic treatment - propanolol (beta blocker) or topiramate (anti-convulsant)
  2. During attack - oral triptan (sumatriptan) and NSAIDs
226
Q

presentation of tension headaches

A

bilateral pressure/tightness (band), non-pulsatile, no associated symptoms e.g. aura, vomiting, nausea, variation in duration

227
Q

Mx of tension headaches?

A

Analgesia e.g. paracetamol

228
Q

Cluster headaches

A

Most disabling primary headache, associated with trigeminal neuralgia

229
Q

Cluster headaches - epidemiology

A

More common in males and smokers

230
Q

Presentation of cluster headaches?

A

Unilateral pain around one eye, rapid onset, duration 15mins–>3hrs, episodic clusters, associated symptoms (ptosis, miosis, lacrimation, nasal discharge

231
Q

Mx of cluster headaches?

A

Sumatriptan SC injection

232
Q

Sinus headache

A

Associated with sinusitis, dull constant ache over the frontal and maxillary sinuses, pain worse on bending over

233
Q

Mx for sinus headache

A

analgesics, anti-emetics, ABx

234
Q

Hormonal headache

A

Associated with decreased oestrogen concentration - beginning of periods, withdrawal of HRT

235
Q

Medication over-use headaches

A

Common cause of headache due to overuse of painkillers/triptans taken regularly for headaches, stop medication to resolve

236
Q

Common culprits for medication over-use headaches?

A

Codeine/co-codamol, sumatriptan (NSAIDs = unlikely)

237
Q

Classic triad of meningitis

A

fever, headache, neck stiffness

238
Q

Symptoms of acute bacterial meningitis

A

sudden onset, photophobia, vomiting, deliriousness, drowsiness, papilloedema, non-blanching petechiae and purpuric rash

239
Q

Symptoms of viral meningitis

A

benign, self-limiting

240
Q

Ix for meningitis

A

Blood culture from lumbat puncture (at L4)

241
Q

CSF findings for bacteria (cells protein, glucose)

A

Neutrophils, raised, decreased

242
Q

CSF findings for virus (cells protein, glucose)

A

lymphocytes, normal/slightly raised, normal

243
Q

Mx of meningitis?

A

start ABx immediately if suspected bacterial, confirmed bacterial - IV cefotaxime or ceftriaxone

244
Q

What is encephalitis?

A

infection and inflammation of the brain parenchyma, most affects frontal and temporal lobes (responsible for emotion and memory change)

245
Q

Viral causes of encephalitis?

A

HSV (1+2), varicella zoster, EBV, cytomegalovirus, HIV, mumps, measles

246
Q

Presentation of encephalitis?

A

Fever, headache, brain dysfunction (behavioural change, decreased consciousness, confusion, drowsiness, seizures)

247
Q

Ix for Meningitis

A

Blood culture, lumbar puncture, MRI, PCR CSF

248
Q

Ix for encephalitis

A

CT and MRI scan, CSF analysis, viral serology of blood and CSF

249
Q

Tx for encephalitis

A

Immediately treat with IV acyclovir, anti-seizure medication

250
Q

What is herpes zoster-shingles?

A

Infection caused by the reactivation of the varicella zoster virus (VZV - chicken pox), usually within the dorsal root ganglia

251
Q

Clinical presentation of herpes zoster infection?

A

Pain and paraesthesia in dermatomal distribution, malaise, fever, headache, rash consisting of papules and vesicles restricted to the same dermatome

252
Q

Ix for herpes zoster? Mx?

A

Clinical diagnosis, oral anti-viral therapy (acyclovir), analgesia

253
Q

Where do you get Borrelia from?

A

Ticks

254
Q

Most common bacteria causing meningitis in neonates?

A

Group B strep

255
Q

Most common bacteria causing meningitis in children

A

strep. pneumoniae

256
Q

Most common bacteria causing meningitis in –> 50years

A

N.meningitidis, strep. pneumoniae

257
Q

Most common bacteria causing meningitis in >50

A

strep. pneumoniae

258
Q

Dx of bacterial meningitis

A

cloudy purulent fluid, increased WCC (neutrophils), high protein, low glucose, high lactate

259
Q

When is a lumbar puncture contraindicated?

A

Raised ICP (risk of coning)

260
Q

Empirical ABx for meningitis

A

ceftriaxone, cefotaxime

261
Q

Prodrome phase in encephalitis?

A

fever, headache, nausea, vomiting, fatigue

262
Q

Trigeminal neuralgia?

A

pain syndrome characterised by attacks of facial pain in the area of one or more branches of the trigeminal nerve

263
Q

Px of trigeminal neuralgia

A

Unilateral facial pain, severe/shooting, electric shock like, lasts several seconds, typically shoots from mouth to angle of jaw

264
Q

Bell’s palsy

A

Acute, unilateral facial nerve palsy (peripheral - paralysis of ipsilateral eyelid, facial muscles)

265
Q

Which nerve is damaged following wrist drop?

A

Radial

266
Q

Tx for trigeminal neuralgia?

A

1st line - anticonvulsants e.g. carbamazepine

267
Q

Dx of trigeminal neuralgia?

A

Clinical

268
Q

Uhthoff’s phenomenon

A

Paraesthesia in MS in heat (bath)

269
Q

What lobe is Jacksonian march seizure associated with? What type of seizure is it?

A

Frontal, simple partial

270
Q

What is a Jacksonian march seizure?

A

Phenomenon where a simple partial seizure spreads from the distal part of the limb toward the ipsilateral face, involve a progression of the location of the seizure in the brain, which leads to a “march” of the motor presentation of symptoms

271
Q

Features of seizures in the temporal lobe

A

Motor phenomena, impaired awareness, lip smacking, dysphasia, deja vu, hallucinations

272
Q

Features of seizures in the frontal lobe

A

Motor features, Jacksonian march, motor arrest, dysphasia, speech arrest

273
Q

Features of seizures in the parietal lobe

A

Sensory disturbances, tingling, numbness, pain

274
Q

Features of seizures in the occipital lobe

A

Visual phenomena e.g. spots, lines, flashes

275
Q

Brown-sequard syndrome

A

ipsilateral haemiplegia with contralateral pain and temperature sensation deficits

276
Q

Ix for Brown-sequard

A

MRI (gold standard)

277
Q

Mx of Brown-sequard

A

Surgery to fix the cause, dexamethasone to reduce inflammation

278
Q

Pharmacological therapy for MS

A

Oral prednisolone or IV hydrocortisone

279
Q

What is Gullain-Barre syndrome?

A

Progressive onset of distal limb weakness, symmetrical, ascending

280
Q

Mx of Gullain-Barre syndrome?

A

Vital capacity and ECG monitoring

281
Q

What is neurofibromatosis?

A

Rare genetic disorder that causes typically benign tumours of the nerves, symptoms are variable, manifests itself at birth or in childhood

282
Q

What is neurofibromatosis 1 characterised by?

A

Cafe-au-lait spots concentrated in the groin and armpits (light brown spots), scoliosis, tumours on the brain or spinal cord

283
Q

Cafe-au-lait spots are typical of what?

A

neurofibromatosis

284
Q

Causes of neurofibromatosis?

A

Mutations in the gene that controls production of neurofibromin protein (acts as a tumour suppressor)

285
Q

Sleep stages

A

Non-REM stage 1 (N1), N2, N3, REM (rapid eye movement)

286
Q

Acronym for EEG representations for each sleep stage

A

The Sleep Doctor’s Brain

Theta waves, Sleep spindles and K complexes, Delta waves, Beta waves

287
Q

Sleep stage N1

A

light sleep, jerks

288
Q

Sleep stage N2

A

Deeper sleep (50% of total sleep)

289
Q

Sleep stage N3

A

Deep sleep - night terrors, nocturnal enuresis, sleepwalking

290
Q

REM sleep stage

A

Dreaming, loss of muscle tone, erections

291
Q

Gullain Barre syndrome is typically associated with?

A

Gastroenteritis caused by campylobacter jejuni, cytomegalovirus, or EBV

292
Q

Gullain barre is like what neuropathy but just peripherally?

A

MS, attacks myelin

293
Q

Most likely pathogen causing meningitis in pregnant women?

A

Listeria monocytogenes

294
Q

CI for lumbar puncture?

A

raised ICP, focal neurology, infection at site of LP

295
Q

Prophylactic Abx for meningitis contacts

A

Oral ciprofloxacin

296
Q

Long term prophylaxis for cluster headaches?

A

Verapamil

297
Q

How would you treat raised ICP?

A

IV mannitol

GRACE Phase 2a Medicine (20 decks)

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