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Neurology Flashcards

1
Q

What conditions are associated with SAH?

A

PKD
Ehlers-Danlos
Coarctation of the aorta

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2
Q

What is Kernig’s sign?

A

Hip and knee bent to 90 degrees and positive if pain is caused by straightening the knee.
Demonstrates meningeal irritation.

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3
Q

Where is the blood found in SAH on CT?

A

Interhemispheric fissure
Basal cisterns
Ventricles.

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4
Q

What is looked for on LP for SAH?

A

Xanthochromia.

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5
Q

What four bones meet at the pterion?

A

Frontal
Temporal
Sphenoid
Parietal

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6
Q

What signs on CT may suggest extradural haemorrhage?

A

Midline shift
Compression of the ventricles

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7
Q

What are risk factors for stroke?

A

Diabetes
AF
Valvular
Peripheral vascular disease
Previous TIA
Polycythaemia rubra vera
Carotid artery disease
Hyperlipidaemia
Clotting disorders
COCP
Excess alcohol

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8
Q

What is the visual field defect in stroke?

A

Homonyous hemaniopia

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9
Q

What is Todd’s palsy?

A

Temporary weakness following a seizure (usually of affected limb)

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10
Q

What is a partial seizure?

A

Features focal to one hemisphere e.g. motor region

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11
Q

What airway adjunct would you use in epilepsy?

A

Nasopharyngeal

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12
Q

What are immediate management steps for epileptic fit?

A

Roll patient into recovery position
Move any items away that could cause harm
Call for senior help
Place pillow under head
Oxygen if required.

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13
Q

Is the lateral or medial portion of the retinal field likely to be affected in bitemporal hemaniopia?

A

Medial

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14
Q

How would you assess cranial nerves II, III, IV and VI?

A

Visual acuity
Visual fields
Fundoscopy
Pupillary light reflexes (direct and consensual)
Pupillary accommodation
Eye movements.

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15
Q

What structures are damaged in homonymous hemaniopia?

A

Unilateral damage to optic radiation or visual cortex

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16
Q

What is the mechanism of action of triptans?

A

5-HT receptor agonists which bind to and stimulate serotonin receptors

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17
Q

What is the management of cluster headaches?

A

100% oxygen and subcutaneous/intranasal sumatriptan

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18
Q

What are the pupil changes in cluster headache?

A

Miosis, ptosis, lacrimation

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19
Q

How and when do you treat sinusitis?

A

Post 10 days with steroid nasal spray
Or antibiotics (phenoxymethylpenicillin)

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20
Q

What can trigger trigeminal neuralgia?

A

Touch
Talking
Eating
Shaving
Cold

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21
Q

What are the findings of GCA on biopsy?

A

Multinucleated giant cells

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22
Q

What blood test is characteristically raised in GCA?

A

ESR

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23
Q

When do you use IV medication for GCA as opposed to oral?

A

High dose IV methylprednisolone used when there is eye involvement

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24
Q

What does the artery feel like in GCA?

A

Tender, thickened, pulseless

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25
Q

What medication is given with Levoodpa?

A

Peripheral decarboxylase inhibitor

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26
Q

What is the management for essential tremor?

A

Propranolol
Primidone (barbiturate anti-epileptic)

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27
Q

What medications are used in Parkinson’s?

A

Levodopa + peripheral decarboxylase (e.g. carbidopa, benserazide)
COMT inhibitor (inhibitor of catecholomethyltransferase) e.g. entacapone
Dopamine agonist e.g. bromocriptine, cabergoline, pergolide
Monoamine oxidase-B inhibitors e.g. selegiline, rasagiline

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28
Q

What is the main side effect of Levodopa?

A

Dyskinesia:
Dystonia
Chorea
Athetosis

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29
Q

How is the dyskinesia caused my Levodopa managed?

A

Amantadine (glutamate antagonist)

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30
Q

What is the mechanism of action of COMT inhibitors?

A

Inhibit the enzyme which metabolises Levodopa in the brain so Levodopa has a longer effective duration

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31
Q

What is a notable SE of dopamine agonists?

A

Pulmonary fibrosis

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32
Q

Why are MOAI used in PD?

A

Reduce end of dose worsening of symptoms

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33
Q

What are the Parkinson’s plus syndromes?

A

Multi system atrophy (autonomic dysfunction)
Lewy body dementia (associated with visual hallucinations, delusions, REM sleep disorders, sexual dysfunction, cerebellar dysfunction)
Progressive supranuclear palsy
Corticobasal degeneration (movement disorders in limbs)

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34
Q

Where is CSF contained?

A

Meninges and sucbarachnoid space

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35
Q

What are the most common causes of bacterial meningitis?

A

Neisseria meningitidis (gram negative diplococcus)
Streptococcus pneumonia
Haemophilus pneumoniae
Group B streptococcus (most common in neonates)
Listeria monocytogenes (common in neonates)

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36
Q

What are the viral causes of meningitis?

A

Enteroviruses e.g. coxsackie
Herpes simplex virus
Varicella zoster virus

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37
Q

What are the two tests for meningitis?

A

Kernig’s
Brudzinski’s (lie flat and flex head, positive if patient flexes their hips and knees involuntarily)

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38
Q

What is a faster way to test for meningococcal DNA than blood culture?

A

Meningococcal PCR

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39
Q

Where is a LP inserted?

A

L3/L4 level in the subarachnoid space

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40
Q

What is the management of bacterial meningitis for < 3 months?

A

IV cefotaxime + amoxicillin (covers Listeria)

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41
Q

What is the management of bacterial meningitis for > 3 months?

A

IV ceftriaxone

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42
Q

What is given to reduce the frequency and severity of hearing loss and neurological complications in meningitis?

A

Dexamethasone

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43
Q

What are notifiable diseases

A

Bacterial meningitis and meningococcal septicaemia

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44
Q

What is given as post exposure prophylaxis for meningitis?

A

Single dose ciprofloxacin

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45
Q

What are complications of meningitis?

A

Hearing loss
Seizures
Cognitive impairment
Memory loss
Focal neurological deficits e.g. limb weakness or spasticity

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46
Q

Where does HSV typically infect in encephalitis?

A

Temporal lobes and inferior frontal lobes

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47
Q

Which type of HSV is most common in neonatal encephalitis?

A

Type 2 due to genital herpes contracted during birth

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48
Q

What does a LP show in encephalitis?

A

Lymphocytosis
Elevated protein

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49
Q

What is Todd’s palsy?

A

Temporary weakness, usually of the affected limb, following a seizure

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50
Q

What are infantile spasms known as?

A

West syndrome

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51
Q

What is the characteristic finding of West syndrome on en EEG?

A

Hypsarrhythmia

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52
Q

How is West syndrome treated?

A

ACTH and vigabatrin

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53
Q

What features are suggestive of a pseudo seizure vs a seizure?

A

Pelvic thrusting
Crying after
Don’t occur when the patient is alone
Gradual onset
More common in females

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54
Q

What is a ketogenic diet?

A

Increased fat
Low carbohydrate
Controlled protein

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55
Q

What are the investigations for epilepsy?

A

EEG: electroencephalogram
MRI brain

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56
Q

What are the DVLA rules for epilepsy?

A

6 months no driving if partial seizure or seizure with no changes on imagine
Otherwise 1 year seizure free

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57
Q

What are non-medical management options in epilepsy?

A

Take showers rather than baths
Caution with swimming, heights, traffic, dangerous equipment

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58
Q

What is the management for a tonic clonic seizure?

A

Male: sodium valproate
Female: lamotrigine or levetiracetam

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59
Q

What is the management for a partial seizure?

A

Male: lamotrigine or levetiracetam
Female: lamotrigine or levetiracetam

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60
Q

What is the management for a myoclonic seizure?

A

Male: sodium valproate
Female: levetiracetam

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61
Q

What is the management for a tonic or atonic seizure?

A

Male: sodium valproate
Female: lamotrigine

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62
Q

What is the management for an absence seizure?

A

Male: ethosuximide
Female: ethosuximide

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63
Q

Which anti epileptic medication can exacerbate absence seizures?

A

Carbamazepine

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64
Q

Which anti epileptic medication can cause peripheral neuropathy?

A

Phenytoin

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65
Q

What is the mechanism of action of sodium valproate?

A

Increases the activity of GABA (gamma-aminobutyric acid)

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66
Q

What are the notable side effects of sodium valproate?

A

Teratogenic
Liver damage and hepatitis
Hair loss
Tremor
Reduce fertility

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67
Q

What are the rules for taking sodium valproate in regards to pregnancy?

A

The Valproate Pregnancy Prevention Programme (contraception and annual risk acknowledgement form) as it can cause neural tube defects and developmental delay

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68
Q

How many times is a benzopdiazepine given in status epilepticus?

A

Twice

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69
Q

What are the second line options in status epilepticus?

A

IV phenytoin
IV sodium valproate
IV levetiracetam

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70
Q

What are the third line options in status epilepticus?

A

Phenobarbital
General anaesthesia

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71
Q

What are the doses for medication in status epilepticus?

A

Buccal midazolam (10mg)
Rectal diazepam (10mg)
IV lorazepam (4mg)

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72
Q

What is the pathophysiology of MS?

A

Chronic and progressive autoimmune condition involving demyelination in the CNS. The immune system attacks the myelin sheath of the myelinated neurones (myelin is provided by oligodendoryctes in the CNS).
Inflammation and immune cell infiltration cause damage to the myelin, affecting the electrical signals moving along the neurones

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73
Q

Why do symptoms become gradually more permanent in MS?

A

Re-myelination is incomplete

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74
Q

What is needed for a diagnosis of MS?

A

Demyelinated lesions disseminated in time and space

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75
Q

What are the patterns of disease in MS?

A

Clinically isolated syndrome: first presentation (lesions on MRI suggest they will progress to MS)
Relapsing-remitting
Secondary progressive (used to be relapsing-remitting and now progressive)
Primary progressive

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76
Q

What are risk factors for MS?

A

Genes
EBV
Low vitamin D
Smoking
Obesity

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77
Q

How is optic neuritis investigated?

A

MRI with contrast

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78
Q

What is the pathophysiology of optic neuritis?

A

Demyelination of the optic nerve

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79
Q

What are the key features of optic neuritis?

A

Central scotoma
Pain with eye movement
Impaired colour vision
Relative afferent pupillary defect (affected eye has a decreased response when shining light into it but a normal response when shining light into other eye)

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80
Q

What is an eye movement disorder in MS?

A

Internuclear ophthalmoplegia
Caused by a lesion in the medial longitudinal fasciculus
Impaired adduction of the same side as the lesion and nystagmus in the contralateral eye

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81
Q

What type of limb weakness is in MS?

A

Spastic weakness

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82
Q

What is a sign of MS?

A

Lhermitte’s sign: electric shock sensation that travels down the spine and into the limbs when flexing the neck (indicating disease in the cervical spinal cord in the dorsal column caused by stretching the demyelinated dorsal column)

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83
Q

What is transverse myelitis?

A

A site of inflammation in the spinal cord which results in sensory and motor symptoms below the level of inflammation

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84
Q

What is Romberg’s testing for?

A

Sensory ataxia (could be cause by a lesion in the dorsal columns)

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85
Q

What is the criteria used for MS?

A

McDonald

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86
Q

What is shown on LP for MS?

A

Oligoclonal bands in the CSF

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87
Q

What are the investigations for MS?

A

MRI
LP

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88
Q

What is an example of a medication used long term in MS?

A

Betaferon

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89
Q

How are acute episodes of MS treated?

A

Methylprednisolone

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90
Q

Where does demyelination occur in GBS?

A

Peripheral nervous system

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91
Q

What is the pathophysiology of GBS?

A

Autoimmune
“Molecular mimicry”

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92
Q

What are the infective triggers of GBS?

A

Campylobacter jejuni
EBV
CMV

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93
Q

What are the signs of GBS on examination?

A

Loss of reflexes
Flaccid paresis

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94
Q

What are the CSF findings in GBS?

A

Elevated protein
Normal glucose
Normal WCC

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95
Q

What is the management of GBS?

A

IV immunoglobulins
Plasmapheresis

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96
Q

How is GBS investigated?

A

EMG nerve conduction studies
CSF
Monitor FVC serially for respiratory depression

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97
Q

What are the antibodies in myasthenia graves?

A

Acetylcholine receptor antibodies (bind to post synaptic membrane to block receptors. The more they are used, the more they become blocked)
Muscle specific kinase antibodies (MuSK)
Low density lipoprotein receptor-related protein 4 antibodies

All of these also activate the complement system, leading to cell damage and worsening symptoms

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98
Q

Where does myasthenia graves affect?

A

Neuromuscular junction

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99
Q

Where are the autoantibodies produced in myasthenia gravis?

A

Thymus

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100
Q

What test can confirm if doubt in diagnosis for myasthenia graves?

A

Tensilon/ Edrophonium test:
Give IV edrophonium chloride which blocks cholinesterase inhibitors and should temporarily relieve weakness

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101
Q

What is the management for myasthenia gravis?

A

Anti-cholinesterases: pyridostigmine or rivastigmine
Immunosuppression to decrease production of antibodies: steroids, azathioprine
Thymoma
Plasmapheresis for severe relapsing cases
Rituximab (monoclonal antibody against B cells) when other treatment fails

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102
Q

Which medications worsen myasthenia graves?

A

Antibiotics
CCBs
BB
Lithium
Statin

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103
Q

What is the management of myasthenic crisis?

A

IV Immunglobulins
Plasmapheresis
NIV e.g. BIPAP
Mechanical ventilation
Serial FVC measurements

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104
Q

What is the pathophysiology of MND?

A

Progressive degeneration of UMN and LMN
Relentless and unexplained destruction of upper motor neurones and anterior horn cells in the brain and spinal cord

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105
Q

What are the types of MND?

A

Amyotrophic lateral sclerosis
Progressive bulbar palsy
Progressive muscular atrophy
Primary lateral sclerosis

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106
Q

Does MND have sensory symptoms?

A

No

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107
Q

Does MND have visual symptoms?

A

No

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108
Q

What is the diagnostic tool for MND?

A

El-Escorial diagnostic criteria

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109
Q

What is the medication used in MND?

A

Riluzole (aims to slow progression and increase survival by 2-3 months)

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110
Q

What is the management of MND?

A

Riluzole
Baclofen for muscle spasticity
Antimuscarinic for excess saliva
Benzodiazepines for breathlessness worsened by anxiety
Advanced directives

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111
Q

Which condition is MND associated with?

A

Pick’s disease (frontotemporal dementia)

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112
Q

What do most patients die of in MND?

A

Respiratory failure or pneumonia as a result of bulbar palsy (impairment of CN 9, 10, 11 and 12)

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113
Q

What are the microscopic changes in Alzheimer’s?

A

Cortical plaques due to deposition of type A-beta amyloid protein and intraneuronal neurofibrillary tangles caused by abnormal aggregation of the tau protein
Hyperphoshorylation of the tau protein

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114
Q

What is the macroscopic change in Alzheimer’s?

A

Widespread cerebral atrophy involving the cortex and hippocampus

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115
Q

What are the biochemical changes in Alzheimer’s?

A

Deficit of acetylcholine

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116
Q

What are cognitive assessment tools?

A

6 item cognitive impairment test (6CIT)
10 point cognitive screener (10-CS)
Mini mental state examination <24/30

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117
Q

What medications are used in Alzheimer’s?

A

Acetylcholinesterase inhibitors: donepezil, galantamine and rivastigmine (mild or moderate)
Memantine (second line or mono therapy in severe)

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118
Q

When is donepezil CI?

A

Relatively in bradycardia

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119
Q

What is the SE of donepezil?

A

Insomnia

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120
Q

What does the facial nerve supply parasympathetic supply to?

A

Submandibular and sublingual salivary glands
Lacrimal glands

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121
Q

What causes bilateral UMN lesions?

A

Rare:
Pseudobulbar palsies
MND

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122
Q

What are common causes of facial nerve palsy?

A

Bell’s palsy
Ramsay Hunt syndrome
Otitis media
Otitis externa
HIV
Diabetes
Sarcoidosis
MS
GBS
Acoustic neuroma
Parotid tumour
Cholesteatoma
Basal skull fracture

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123
Q

Who is given Aciclovir in shingles?

A

If presenting within 72 hours to reduce risk of post hepatic neuralgia

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124
Q

Who is eligible for the shingles vaccination?

A

> 70

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125
Q

What is the most malignant brain tumour?

A

Glioblastoma multiforme

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126
Q

What do meningiomas cause?

A

“Mass effect”

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127
Q

Which cancers most commonly spread to the brain?

A

Lung
Breast
Renal cell carcinoma
Melanoma

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128
Q

How does raised ICP cause papilloedema?

A

The sheath around the optic nerve is connected with the subarachnoid space
The raised CSF pressure flows into the optic nerve sheath, increasing the pressure around the optic nerve behind the optic disc, causing the optic disc to bulge forwards

129
Q

What does papilloedema show on fundoscopy?

A

Blurring of the optic disc margin
Elevated optic disc
Loss of venous pulsation
Engorged retinal veins
Haemorrhages around the optic disc
Paton’s lines (creases or folds in the retina around the optic disc)

130
Q

What is Cushing’s reflex?

A
  1. Bradycardia
  2. Hypertension
  3. Irregular respirations
131
Q

What is the management of raised ICP?

A

Mannitol or hypertonic saline
Intubation/hyperventilation (decreased CO2)

132
Q

What is coning?

A

Herniation of cerebellar tonsils through the foramen mangnum leads to compression of the brainstem and respiratory arrest

133
Q

What is the management of a brain abscess?

A

Surgery: craniotomy and the abscess cavity is debrided
IV abx 3rd generation cepahlosporin (ceftriaxone) + metronidazole
Intracranial pressure management: dexamethasone

134
Q

What is shown on a CT head in a brain abscess?

A

Ring enhancing lesion

135
Q

What causes congenital hydrocephalus?

A

Spina bifida
Infection during pregnancy e.g. mumps, rubella

136
Q

What causes acquired hydrocephalus?

A

Illness
Injury e.g. head injury or brain tumour

137
Q

What is the triad of normal pressure hydrocephalus?

A
  1. Abnormal gait
  2. Urinary incontinence
  3. Dementia
    Symptoms come on gradually
138
Q

What shows on imaging for normal pressure hydrocephalus?

A

Ventriculomegaly in the absence of or out of proportion to sulcal enlargement

139
Q

What is the management of hydrocephalus?

A

Ventriculo-peritoneal shunt
Endoscopic third ventriculostomy

140
Q

What causes idiopathic intracranial hypertension?

A

Unknown
Secondary to venous sinus thrombosis
Drugs: tetracyclines, nitrofurantoin, vitamin A, isotretionoin, danazol, somatropin.

141
Q

What is a sixth nerve palsy?

A

Abducens controls lateral rectus so abducens palsy causes esotropia (eye deviated inwards)

142
Q

What are the investigations for idiopathic intracranial hypertension?

A

CT: shows no SOL
LP: increased opening pressure

143
Q

What is the management of idiopathic intracranial hypertension?

A

Weight loss
Acetozolamide
Topiramate
Therapeutic LP
Surgery: optic nerve sheath decompression and fenestration to prevent optic nerve damage
Lumboperitoneal or ventriculoperitoneal shunt

144
Q

What visual field defect does a pituitary tumour cause?

A

Bitemporal hemianopia due to compression of optic chiasm

145
Q

What is the management of pituitary tumours?

A

Trans sphenoidal surgery
Radiotherapy
Bromocriptine to block excess prolactin
Somatostatin analogues e.g. octreotide to block excess growth hormone

146
Q

Where is the Huntington’s generation found?

A

Huntington protein chromosome 4

147
Q

How does Huntington’s present?

A

Begins with cognitive, psychiatric or mood problems followed by movement disorders:
Chorea
Dystonia
Rigidity
Eye movement disorders
Dysarthria
Dysphagia

148
Q

What medication is used for chorea symptoms in Huntington’s?

A

Tetrabenazine

149
Q

What is the most common cause of death in Huntington’s?

A

Aspiration pneumonia
Suicide

150
Q

What are the SE of NSAIDs?

A

Gastritis with dyspepsia
Stomach ulcers
Exacerbation of asthma
Hypertension
Renal impairment
CAD, HF, strokes

151
Q

How do you convert oral morphine to oral codeine/tramadol?

152
Q

How do you convert oral morphine to oxycodone?

A

x0.6666666

153
Q

How do you convert oral morphine to diamorphine?

154
Q

What is a buprenorphine 5mcg patch equivalent to in morphine?

155
Q

What is a 12cmg fentanyl patch equivalent to in morphine?

156
Q

What questionnaire is used to determine the likelihood of neuropathic pain?

A

The DN4 questionnaire >4=likely

157
Q

What types of medication are gabapentin and pregablin?

A

Anticonvulsant

158
Q

What is the terminal end of the spinal cord called?

A

Conus medullaris

159
Q

What is the most common primary cancer to metastasise to brain?

160
Q

What are the ascending spinal tracts?

A

Spinothalamic tracts
Dorsal column

161
Q

What is the descending spinal tract?

A

Corticospinal

162
Q

What do the spinothalamic tracts carry?

A

Anterior: crude touch
Lateral: pain and temperature

163
Q

Do dorsal roots carry afferent or efferent?

A

Afferent (away from stimulus towards CNS and brain)

164
Q

Do dorsal roots carry sensory or motor?

165
Q

Where do the spinothalamic tracts decussate?

A

At the spinal cord level

166
Q

Where do the dorsal columns decussate?

A

Brainstem (medulla)

167
Q

What do the dorsal columns carry?

A

Fine touch, vibration, proprioception

168
Q

Where do the corticospinal tracts decussate?

A

Lateral: brainstem (medulla oblangata)
Anterior

169
Q

What do corticospinal tracts carry?

170
Q

How does a complete cord lesion present?

A

Complete loss of function (motor/sensory) below the level of the lesion

171
Q

How does Brown Sequard syndrome present?

A

Ipsilateral weakness (UMN signs below the lesion (spastic paralysis) and LMN weakness (flaccid paralysis) at the level of the lesion): corticospinal tracts cross at the brainstem
Ipsilateral proprioception/vibration loss: dorsal columns cross at the medulla
Contralateral pain/temperature loss: spinothalamic cross at the level of the spinal cord
Horner’s syndrome is the lesion is above T1

172
Q

What is ventral cord syndrome also known as?

A

Anterior cord syndrome
Damage to the anterior 2/3 of the spinal cord

173
Q

How does anterior cord syndrome present?

A

Bilateral weakness
Bilateral loss of pain and temperature
Autonomic dysfunction (abnormal BP)
Bladder dysfunction

174
Q

What causes anterior cord syndrome?

A

Ischaemia of the anterior spinal artery:
Thromboembolism
Truama
Hypotension
Aortic disease as damaging the arterial supply to the anterior spinal artery e.g. aortic aneurysm, thrombosis, dissection

175
Q

What is dorsal cord syndrome also known as?

A

Posterior cord syndrome

176
Q

What is mainly carried in the dorsal/posterior cord?

A

Ascending tracts

177
Q

How does posterior cord syndrome present?

A

Gait ataxia
Abnormal vibration sense and paraesthesia
If large, may involve the lateral and corticospinal tracts leading to weakness

178
Q

What are the causes of posterior cord syndrome?

A

Inflammatory e.g. MS
Syphilis
Ischaemia e.g. posterior cord syndrome
Malignancy
Metabolic e.g. subacute degeneration of the cord due to Vitamin B12 deficiency
Hereditary e.g. Friedreich ataxia

179
Q

What often causes central cord syndrome?

A

Hyperextension injury of the neck within the cervical spine
Most commonly a trauma, caused by a fall in the elderly where there is simultaneous compression of the anterior and posterior cord

180
Q

Which cords does central cord syndrome affect?

A

Medial aspect of the corticospinal and the crossing fibres of the spinothalamic

181
Q

How does central cord syndrome present?

A

Weakness: upper extremities > lower extremities
Pain and temperature loss: usually located at the level of the lesion in a cape like distribution affecting the upper back and upper extremities
Neck pain: commonly due to mechanism of injury
Normal vibration and proprioception (dorsal columns)
Urinary retention may occur.

182
Q

What is a syringomyelia?

A

Fluid filled cyst within the spinal cord

183
Q

What is a radiculopathy?

A

A narrowing where the nerve root exits the spine

184
Q

What causes a radiculopathy?

A

Stenosis
Bone spurs
Disc herniation
Disc degeneration
Age related spondylosis (cervical)

185
Q

Where does cervical radiculopathy most commonly affect?

186
Q

What is sciatica also known as?

A

Lumbar radiculopathy

187
Q

Which nerve root is biceps jerk?

188
Q

Which nerve root is triceps jerk?

189
Q

Which nerve root is ankle jerk?

190
Q

Which nerve root is sensation for thumb?

191
Q

Which nerve root is sensation for middle finger?

192
Q

Which nerve root is sensation for dorsum of foot/big toe?

193
Q

Which nerve root is sensation for ankle, lateral aspect of foot, sole and little toe?

194
Q

Which nerve root is myotome for biceps?

195
Q

Which nerve root is myotome for triceps?

196
Q

Which nerve root is myotome for dorsiflexion (stand on heels)?

197
Q

Which nerve root is myotome for plantar flexion (stand on toes)?

198
Q

In which nerve roots is the knee reflex affected?

199
Q

In which nerve roots is there a positive femoral stretch test?

200
Q

In which nerve roots is there a positive sciatic stretch test?

201
Q

Which nerve root is sensation for anterior thigh?

202
Q

Which nerve root will cause weak hip flexion, knee extension and hip adduction?

203
Q

Which nerve root is sensation for anterior aspect of knee and medial malleolus?

204
Q

Which nerve root will cause weak knee extension and hip adduction?

205
Q

What are the nerve roots of the spinal cord?

A

C1-C7
T1-T12
L1-L5
S1-S5

206
Q

Which nerve root is upper cervical flexion?

207
Q

Which nerve root is upper cervical extension?

208
Q

Which nerve root is cervical lateral flexion?

209
Q

Which nerve root is shoulder girdle elevation?

210
Q

Which nerve root is shoulder abduction?

211
Q

Which nerve root is elbow flexion?

212
Q

Which nerve root is elbow extension (biceps)?

213
Q

Which nerve root is thumb extension (triceps)?

214
Q

Which nerve root is finger adduction?

215
Q

Which nerve root is hip flexion?

216
Q

Which nerve root is knee extension?

217
Q

Which nerve root is ankle dorsiflexion?

218
Q

Which nerve root is great toe extension?

219
Q

Which nerve root is ankle plantar flexion?

220
Q

Which nerve root is bladder and rectum motor supply?

221
Q

Which nerve root is sensation to heel?

222
Q

Which nerve root is sensation to top of foot?

223
Q

Which nerve root is sensation to medial malleolus?

224
Q

Which nerve root is sensation to inguinal ligament?

225
Q

How does a common perineal nerve lesion present?

A

Foot drop
Weakness of foot dorsiflexion
Weakness of foot eversion
Weakness of extensor hallucis longus
Sensory loss over the dorsum of the foot and the lower lateral part of the leg
Wasting of the anterior tibial and perineal muscles

226
Q

What does the sciatic nerve divide into?

A

Tibial and common perineal nerves

227
Q

What are examples of brachial plexus injury?

A

Erb-Duchenne paralysis: C5,C6
Winged scapula
May be caused by breech presentation

Klumpke’s paralysis: T1
Loss of intrinsic hand muscles
Due to traction

228
Q

Which roots does the radial nerve supply?

A

C5-T1 (continuation of posterior cord of brachial plexus)

229
Q

How does a radial nerve lesion present?

A

Wrist drop (Saturday night palsy)
Sensory loss to small area between the dorsal aspect of the 1st and 2nd metacarpals
Paralysis of tricep (loss of elbow extension)

230
Q

Which nerve roots are the ulnar nerve?

231
Q

How does an ulnar nerve lesion present?

A

Motor to the adductor pollicis and hypothenar muscles
Wasting and paralysis of intrinsic hand muscles
Sensory to the medial 1.5 fingers (palmar and dorsal aspect)
“Claw hand”: hyperextension of the metacarpophalangeal joints and flexion at the distal and proximal interphalangeal joints of the 4th and 5th digits
Radial deviation of the wrist

232
Q

How do you treat normal pressure hydrocephalus?

A

Ventriculoperitoneal shunting

233
Q

What causes normal pressure hydrocephalus?

A

Reduced CSF absorption at the arachnoid villi

234
Q

What are the risk factors for carpal tunnel?

A

Idiopathic
Pregnancy
Oedema e.g. heart failure
Lunate fracture
Rheumatoid arthritis

235
Q

What are the symptoms of carpal tunnel?

A

Pain/pins and needles in thumb, index, middle finger
Unusually the symptoms may ‘ascend’ proximally
Patient shakes his hand to obtain relief, classically at night.

236
Q

What are the signs of carpal tunnel?

A

Weakness of thumb abduction (abductor pollicis brevis)
Wasting of thenar eminence (not hypothenar)
Tinel’s sign: tapping causes paraesthesia
Phalen’s sign: flexion of wrist causes symptoms.

237
Q

What is the management of carpal tunnel?

A

6 week trial of conservative:
Wrist splints at night
Corticosteroid injection.

If persistent:
Surgical decompression: flexor retinaculum division.

238
Q

What are the verbal points in GCS?

A

Orientated in time/place/person
Confused
Inappropriate words
Incomprehensible sounds
None

239
Q

What are the motor points in GCS?

A

Obeys command
Localises pain
Normal flexion to pain (withdraws)
Abnormal flexion to pain (decorticate response)
Extends to pain (decerebrate response)
None

240
Q

What is dysphonia?

A

Difficulty with speech volume

241
Q

What are tests for cognitive state?

A

AVPU
AMT 0-10 (abbreviated mental test)
MMSE 0-30
MOCA (Montreal cognitive assessment)
ACE-R 0-100 (Addenbrooke’s cognitive examination)

242
Q

Which cranial nerve supplies lateral rectus?

243
Q

Which cranial nerve supplies superior oblique?

244
Q

What is the motor component of trigeminal nerve?

A

Muscles of mastication and jaw jerk

245
Q

Which muscles does the accessory nerve supply?

A

Sternocleidomastoid and trapezius

246
Q

Which nerve root level is the clavicle?

247
Q

Which are the phrenic nerve roots?

248
Q

Which nerve root is the sternum?

249
Q

What is the neurotransmitter from UMN to LMN?

250
Q

What are UMN?

A

Neurones with originate in the cerebral cortex and terminate in the brainstem/spinal cord when it synapses with LMN

251
Q

Where does the corticospinal tract terminate?

A

Ventral horn

252
Q

Which of the corticospinal tracts decussates in the medulla and which remained ipsilateral descending into the spinal cord?

A

Lateral decussates
Anterior remains ipsilateral

253
Q

What are the two corticospinal tracts?

A

Lateral
Anterior

254
Q

What are LMN?

A

Cell body lies within the ventral horn of the brainstem nuclei of the cranial nerves. Terminate on the muscle fibres

255
Q

What is a motor unit?

A

LMN + muscle fibre

256
Q

What causes mononeuritis multiplex?

A

Vasculitis (Wegener’s, polyarteritis nodosa, RA)
Inflammation
Sarcoidosis

257
Q

How do the antibodies in Lambert-Eaton myasthenia syndrome work?

A

Against voltage gated sodium channels
Less acetylcholine across the synapse

258
Q

Which malignancy is Lambert-Eaton myasthenia syndrome associated with?

A

Small cell lung cancer

259
Q

How does Lambert-Eaton myasthenia syndrome present?

A

Proximal muscle weakness
Autonomic dysfunction (dry mouth, blurred vision, impotence, dizziness)
Reduced or absent tendon reflexes

260
Q

How do you differentiate Lambert-Eaton myasthenia syndrome from myasthenia graves?

A

In Lambert-Eaton myasthenia syndrome, symptoms improve after periods of muscle contraction

261
Q

How is Lambert-Eaton myasthenia syndrome treated?

A

Amifampridine blocks voltage gated potassium channels in the presynaptic membrane which prolonged the depolarisation of the cell membrane and assist calcium channels in carrying out their action

Other:
Pyridostigmine
Immunosuppressant (prednisolone)
IV immunoglobulins
Plasmapheresis

262
Q

How is Charcot-Marie-Tooth disease inherited?

A

Autosomal dominant

263
Q

What are the causes of peripheral neuropathy?

A

A lcohol
B 12 deficiency
C cancer e.g. myeloma and CKD
D diabetes and drugs (isoniazid, amiodarone, leflunomide, cisplatin)
E very vasculitis

264
Q

What is a characteristic feature of Charcot-Marie-Tooth disease?

A

Peripheral neuropathy
Inverted champagne bottle legs

265
Q

How is neurofibromatosis type 1 inherited?

A

Autosomal dominant
Chromosome 17, codes for a protein called neurofibromin which is a tumour suppressor gene

266
Q

What is the diagnostic criteria for neurofibromatosis type 1?

A

“CRABBING”
C afe au last spots (>15mm is significant)
R elative with the condition
A xillary or inguinal freckling
BB bony dysplasia such as bowing of a long bone or sphenoid wing dysplasia
I ris hamaatomas (Lisch nodules, yellow-brown spots on the iris)
N eurofibromas
G lioma of the optic pathway

267
Q

Which neurofibromas are significant?

A

2 or more
A single plexiform neurofibroma

268
Q

What GI malignancy can neurofibromatosis type 1 cause?

A

GI stromal tumour (type of sarcoma)

270
Q

How is neurofibromatosis type 2 inherited?

A

Autosomal dominant
Chromosome 22, codes for a protein called merlin which is a tumour suppressor protein important in Schwann cells

271
Q

What is the key feature of neurofibromatosis type 2?

A

Bilateral acoustic neuromas

272
Q

What signs are present in complex regional pain syndrome?

A

Intermittent swelling
Colour changes
Temperature changes
Skin flushing
Abnormal sweating

273
Q

What type of pain is complex regional pain syndrome?

A

Neuropathic

274
Q

What is needed for a diagnosis of chronic fatigue syndrome?

A

3 months of disabling fatigue affecting mental and physical function >50% of the time in the absence of other disease which may explain symptoms

275
Q

What brain chemical is lacking in narcolepsy?

A

Hypocretin (orexin) that regulates wakefulness
Immune system thought to attack the cells that produce it

276
Q

How is narcolepsy managed?

A

Stimulant: modafininl, dexamphetamine, methylphenidate, pitolisant

277
Q

What can trigger narcolepsy?

A

Hormones e.g. puberty, menopause
Stress
Infection

278
Q

What is cataplexy?

A

The sudden loss of muscle tone while a person is awake

279
Q

What are types of myopathy?

A

Steroid myopathy
Statin myopathy
Metabolic and endocrine myopathies
Myotonic dystrophy (myotonia = prolonged muscle contractions after use)

280
Q

What sign is positive in myopathies?

A

Gower’s sign: use their hands and arms to “walk” up their own body from a squatting position due to lack of hip and thigh muscle

281
Q

What is Becker’s muscular dystrophy?

A

Milder form of Duchenne’s

282
Q

How is Duchenne’s muscular dystrophy inherited?

A

X-linked recessive
Females are carriers but not affected
No male to male transmission

283
Q

What are symptoms of Duchenne’s muscular dystrophy?

A

Proximal muscle weakness
Often have very bulky muscles at first (psuedohypertrophy) and then muscle wasting later on
Scoliosis later on

284
Q

How is Duchenne’s muscular dystrophy diagnosed?

A

Genetic testing

285
Q

How is Duchenne’s muscular dystrophy managed?

A

Supportive: physiotherapy, wheelchair
Corticosteroids are best treatment (prednisolone): prolong life
Manage congestive HF and arrhythmias
NIV for respiratory failure

286
Q

Which cranial nerves does a pseudobulbar palsy affect?

A

UMN CN 4, 5, 7

287
Q

Which cranial nerves does a bulbar palsy affect?

A

LMN CN 9, 10, 11, 12

288
Q

What causes a bulbar palsy?

A

Brainstem stroke
Tumour
MND
Neurosyphilis

289
Q

What causes a psuedobulbar palsy?

A

Cerebral stroke or haemorrhage involving both hemispheres

290
Q

What are symptoms of bulbar and psuedobulbar palsy?

A

Difficulty swallowing (dysphagia)
Vocal cord muscle spasms that change your voice (dysphonia)
Slowed, slurred speech (dysarthria)

291
Q

How do you differentiate between psuedobulbar and bulbar palsy?

A

Bulbar is LMN, psueodbulbar is UMN
In bulbar palsy, emotions are not affected.

292
Q

What are causes of dysphagia?

A

Neurological:
Myasthenia gravis
Bulbar palsy
Pseudobulbar palsy
Syringobulbia
Wilson’s
PD
Stroke

Non-neurological:
Cancer
Benign stricture
Pharyngeal pouch
Achalasia
Oesophageal spasm
Systemic sclerosis

293
Q

What is suggestive of a motility disorder e.g. achalasia/CNS?

A

Difficulty swallowing both solids and liquids from the start

294
Q

What makes you suspect a bulbar palsy cause for dysphagia?

A

Difficulty to make the swallowing movement, especially if they cough on swallowing

295
Q

How do you investigate dysphagia?

A

CXR
Barium swallow
Upper GI endoscopy

296
Q

What does DANISH stand for?

A

Dysdiadokinesia, dysmetria (past pointing)
Ataxia
Nystagmus (horizontal = ipsilateral)
Intention tremor
Slurred speech
Hypotonia

297
Q

Who can confirm brain death?

A

Two doctors at two separate times
Must have 5 years post grad experience
One must be a consultant
Neither can be from transplant team

298
Q

How is brain death confirmed?

A

Fixed, unresponsive pupils
No corneal reflex
Absent oculi-vestibular reflex (caloric test where there is no eye movement when ice cold water injected to the ear)
No response to supraorbital pressure
No cough or gag reflex
No observed respiratory effort in response to disconnection from ventilator for 5 minutes

299
Q

When can brain death be confirmed?

A

Deep coma of known aetiology
Reversible causes excluded
No sedation
Normal electrolytes

300
Q

What are the types of cerebral palsy?

A

Spastic (70%): UMN affected in the periventricular white matter (pyramidal or corticospinal). Can be hemiplegic, quadriplegic or diplegic
Ataxic hypotonic (10%): cerebellum affected
Dyskinetic (10%): basal ganglia and substantia nigra are affected (extrapyramidal)
Mixed (10%)

301
Q

What causes cerebral palsy?

A

Antenatal (80%): genetic syndromes, rubella, CMV
hypo-ischaemic injury at birth (10%)
Postnatal (10%): intraventricular haemorrhage in prems, trauma, NAI, hydrocephalus, kernicterus due to hyperbilirubinaemia

302
Q

What is the pathophysiology of cerebral palsy?

A

Non-progressive lesion of motor pathways in the developing brain

303
Q

What are symptoms of cerebral palsy?

A

Movement issues
Posture trouble
Epilepsy (30%)
Squints (30%)
Visual impairment
Speech and language disorders due to hearing problems
Behaviour problems
Learning difficulties
Feeding problems
Joint contractures
Hip subluxation
Scoliosis

304
Q

Which limb is usually worse in hemiplegic CP?

305
Q

What is diplegia spastic CP?

A

All four limbs affected
Legs worse so arm function appears relatively normal
Walking is abnormal

306
Q

What is a developmental sign for CP?

A

Hand preference before 12 months
Persistent primitive reflexes beyond 6 months

307
Q

What are signs of spastic CP?

A

Increased limb tone
Brisk deep tendon reflexes
Extensor plantar response (positive Babinski)
Increased tone may suddenly yield under pressure (clasp knife)

308
Q

How is tuberous sclerosis inherited?

A

Autosomal dominant
TSC1 gene on chromosome 9 which codes for hamartin
TSC2 gene on chromosome 16 which codes for tuberin
Hamartin and tubers interact with each other to control the size and growth of cells

309
Q

What is the characteristic sign of tuberous sclerosis?

A

Hamartomas (benign tissue growths) affecting:
Skin
Brain
Lungs
Heart
Kidneys
Eyes

310
Q

What are the skin features of tuberous sclerosis?

A

Ash leaf spots (depigmented areas)
Shagreen patches (thickened, dimpled, pigmented patches of skin)
Angiofibromas (small skin-coloured or pigmented papule that occur over the nose and cheeks)
Ungual fibromas: circular painless lumps that slowly grow from the nail bed and displace the nail
Cafe-au-lait spots
Poliosis: isolated patch of white hair on the head, eyebrows, eyelashes or beard

311
Q

What are the neurological features of tuberous sclerosis?

A

Epilepsy
Learning disability
Brain tumours

312
Q

What are the signs of CP?

A

Abnormal limb tone (head and trunk hypo and limbs hyper)
Abnormal limb and trunk posture
Delayed motor milestones
Feeding difficulties: slow, gagging, vomiting, promoter incoordination
Abnormal gait

313
Q

What are the signs of ataxic CP?

A

Symmetrical
Early trunk and limb hypotonia
Poor balance
Delayed motor development
Ataxic gait
Intention tremor
Cerebellar signs

314
Q

What is quadriplegic CP?

A

All 4 limbs affected
Arms usually worse
Trunk involved: extensor posturing, poor head control, low central tone
Seizures
Microcephaly
Learning difficulties

315
Q

What is hemiplegic CP?

A

Bad side
Unilateral involvement of arm and leg
Arm usually worse
Face spared
Tip toe walking
Fisting and flexion of the affected arm

316
Q

What are signs of dyskinetic CP?

A

Athetoid movements: slow, involuntary, writhing movements, dystonia, choreoathetosis
Oromotor problems
Fluctuating tone
Involuntary movements
Intellect unimpaired

317
Q

Does the dorsal column run posteriorly or anteriorly in the spinal cord?

A

Posteriorly

Finals (11 decks)

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