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Year 6 > Neurology > Flashcards

Neurology Flashcards

1
Q

Define aphasia and list the 4 types

A

A disorder where a person has difficulty with their language and speech - the 4 types are:
1) Wernicke’s (receptive)
2) Broca’s (expressive)
3) Conduction
4) Global

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2
Q

What is Wernicke’s aphasia?

A

Due to a lesion of the superior temporal gyrus (supplied by the inferior division of the left MCA) - speech remains fluent but nonsensical - comprehension is impaired

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3
Q

What is Broca’s aphasia?

A

Due to a lesion of the inferior frontal gyrus (supplied by the superior division of the left MCA) - speech is non-fluent, laboured and halting w/ impaired repetition - comprehension is normal

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4
Q

What is Conduction aphasia?

A

Classically due to a stroke affecting the arcuate fasciculus (conneection between Wernicke’s and Broca’s areas) - speech is fluent but repetition is poor, aware that they are making mistakes - comprehension is normal

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5
Q

What is Global aphasia?

A

Large lesion affecting the superior temporal gyrus, inferior frontal gyrus and arcuate fasciculus - severe expressive and receptive aphasia

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6
Q

Define an Arnold-Chiari malformation

A

This is the downwards herniation of the cerebellar tonsils through the foramen magnum - may be congenital or acquired through trauma

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7
Q

Arnold-Chiari malformation features

A

Non-communicating hydrocephalus (CSF outflow obstruction), headache, syringomyelia

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8
Q

Define ataxia

A

Poor muscle control resulting in uncoordinated movements

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9
Q

Define Ataxia telangiectasia

A

An autosomal recessive primary immunodeficiency

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10
Q

Ataxia telangiectasia features

A

Cerebellar ataxia, telangiectasia, IgA deficiency, typically presents in early childhood w/ abnormal movements

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11
Q

Define Autonomic dysreflexia

A

A clinical syndrome which occurs in pts who have a spinal cord injury at, or above T6 spinal level. In response to a noxious stimulus below the level of the spinal cord injury (commonly faecal impaction or urinary retention), there is massive reflex sympathetic discharge. This results in vasoconstriction and hypertension. However, due to the lesion in the spinal cord, this sympathetic response cannot be regulated by the brain.

Above the level of injury, where neural connections are intact, parasympathetic activity via vagal stimulation tries to counteract this by causing vasodilation and bradycardia. However, this compensatory mechanism is only effective above the level of injury and cannot offset the hypertensive crisis occurring below it.

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12
Q

Autonomic dysreflexia features

A

Characterised by extreme hypertension, flushing and sweating above the level of the cord lesion, agitation, haemorrhagic stroke if HTN not treated

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13
Q

Autonomic dysreflexia management

A

Removal/control of the stimulus and treatment of any life-threatening HTN and/or bradycardia

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14
Q

Bell’s palsy features

A

Facial nerve palsy that DOES NOT spare the forehead, post-auricular pain, altered taste, dry eyes, hyperacusis

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15
Q

Bell’s palsy managment

A

All pts should receive oral prednisolone w/in 72 hours of symptom onset, eye care to avoid exposure keratopathy (prescribe artificial tears and eye lubricant, tape eye closed at bedtime), consider adding antivirals - if no improvement after 3 weeks then refer to ENT

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16
Q

Define Erb-Duchenne paralysis

A

Damage to the C5/6 roots in the brachial plexus (commonly by breech presentation) - causes winged scapular

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17
Q

Define Klumpke’s paralysis

A

Damage to T1 at the brachial plexus (usually due to traction) - causes a loss of intrinsic hand muscles

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18
Q

Brain abscess management

A

Surgery (craniotomy performed and the abscess cavity is debrided), IV abx (cephalosporin + metronidazole), dexamethasone to control ICP

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19
Q

Define Brown-Sequard syndrome

A

A lateral hemisection of the spinal cord

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20
Q

Brown-Sequard features

A

Ipsilateral weakness below the lesion, ipsilateral loss of proprioception and vibration sensation, contralateral loss of pain and temp (spinothalamic)

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21
Q

Define cataplexy

A

The sudden and transient loss of muscular tone caused by a strong emotion (ranging from buckling knees to collapse) - related to narcolepsy

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22
Q

Cerebellar syndrome features

A

DANISH = Dysdiadochokinesia, dysmetria, ataxia, nystagmus, intention tremor, speech disturbance, hypotonia

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23
Q

Causes of Cerebellar syndrome

A

Inherited (Freidreich’s ataxia, ataxia telangiectasia), cerebellar haemangioma, stroke, alcohol, MS, hypothyroidism, drugs (anti-epileptics, lead poisoning), paraneoplastic secondary to lung cancer

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24
Q

Define cerebral perfusion pressure

A

The net pressure gradient causing blood flow to the brain. A sharp rise in CPP may cause in a rise in ICP, a fall in CPP may result in cerebral ischaemia - calculated using:

CPP = mean arterial pressure - intracranial pressure

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25
Q

Where does CFS fill?

A

The space between the arachnoid and pia mater (subarachnoid space)

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26
Q

Where is CSF produced?

A

70% by ependymal cells in the choroid plexus, 30% by blood vessles

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27
Q

CSF circulation

A

1) Lateral ventricles
2) 3rd ventricle
3) Cerebral aqueduct
4) 4th ventricle
5) Subarachnoid space
6) Reabsorbed into venous system via arachnoid granulations into superior sagittal sinus

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28
Q

Define Charcot-Marie-Tooth disease

A

The most common hereditary peripheral neuropathy - predominantly causes motor loss

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29
Q

Charcot-Marie-Tooth disease features

A

Foot drop (may have a Hx of frequent sprained ankles), high-arched feet (pes cavus), hammer toes, distal muscle weakness/atrophy, hyporeflexia, Stork leg deformity

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30
Q

Cluster headache investigations

A

Most pts will have an MRI w/ gadolinium contrast to look for underlying brain lesions

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31
Q

Cluster headache management

A

Acute = 100% O2, subcutaneous triptans
Prophylaxis = verapamil

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32
Q

Common peroneal nerve lesion features

A

Most common feature is foot drop - other features include: weakness of foot dorsiflexion/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 peroneal muscles

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33
Q

Where do common peroneal nerve lesions occur?

A

Most commonly occurs at the neck of the fibula

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34
Q

Oculomotor nerve palsy features

A

Ptosis, ‘down and out’ eye, fixed dilated pupil

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35
Q

Trochlear nerve palsy features

A

Defect in downwards gaze - vertical diplopia

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36
Q

Trigeminal nerve lesions features

A

They may cause: trigeminal neuralgia, loss of corneal reflex (afferent), loss of facial sensation, paralysis of mastication muscles, deviation of jaw to weak side

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37
Q

Abducens nerve palsy features

A

Defective eye abduction - horizontal diplopia

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38
Q

Facial nerve lesions features

A

May cause: flaccid paralysis of upper and lower face, loss of corneal reflex (efferent), loss of taste, hyperacusis

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39
Q

Vestibulocochlear nerve lesions features

A

Hearing loss, vertigo, nystagmus

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40
Q

Glossopharyngeal nerve lesions features

A

May result in: hypersensitive carotid sinus reflex, loss of gag reflex (afferent)

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41
Q

Vagus nerve lesions features

A

May result in: uvular deviation away from the side of the lesion, loss of gag reflex (efferent)

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42
Q

Accessory nerve lesions features

A

Weakness in turning head and raising shoulders on contralateral side

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43
Q

Hypoglossal nerve lesions features

A

Tongue deviates towards the side of the lesion

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44
Q

Which nerves innervate the afferent an efferent arms of the corneal reflex?

A

Afferent = Ophthalmic nerve
Efferent = Facial nerve

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45
Q

Which nerves innervate the afferent an efferent arms of the jaw jerk reflex?

A

Mandibular nerve (CN V) for both

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46
Q

Which nerves innervate the afferent an efferent arms of the gag reflex?

A

Afferent = glossopharyngeal
Efferent = vagus

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47
Q

Which nerves innervate the afferent an efferent arms of the pupillary light reflex?

A

Afferent = optic
Efferent = oculomotor

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48
Q

Define Degenerative cervical myelopathy

A

Cord compression in the cervical spine due to disk degeneration and ligament hypertrophy

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49
Q

Degenerative cervical myelopathy features

A

Signs on cord compression, +ve Hoffman’s sign

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50
Q

What is Hoffman’s sign?

A

A reflex test to assess for cervical myelopathy. It is performed by gently flicking one finger on a patient’s hand. A positive test results in reflex twitching of the other fingers on the same hand in response to the flick

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51
Q

Degenerative cervical myelopathy management

A

Urgent referral to neurosurgery for decompressive surgery

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52
Q

5 drugs which cause peripheral neuropathy

A

Amiodarone, isoniazid, vincristine, nitrofurantoin, metronidazole

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53
Q

Define Muscular dystrophy

A

An X-linked recessive condition resulting in a mutated dystrophin (where actin binds to the muscle membrane)

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54
Q

What are the 2 types of muscular dystrophy and what does the mutation cause?

A

Duchenne = frameshift mutation so both binding sites are lost, more severe
Becker = non-frameshift insertion so both binding sites are preserved, more mild

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55
Q

Duchenne muscular dystrophy features

A

Progressive proximal muscular weakness from 5 years, calf pseudohypertrophy, Gower’s sign (child uses arms to stand from squat position), 30% have IQ impairment

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56
Q

Becker’s muscular dystrophy features

A

Progressive proximal muscle weakness from aged 10

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57
Q

How can you distinguish between a neuropathy and a myopathy?

A

Myopathy = usually has proximal weakness (as this is where the bulky muscles are, so the weakness is more obvious), no sensory deficits, normal reflexes, no fasciculations, EMG shows decreased action potential duration/amplitude

Neuropathy = usually has distal weakness (length dependent), mixed motor and sensory deficits, reflex changes, fasciculations, EMG shows increased action potential duration/amplitude

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58
Q

West Syndrome features

A

Salaam attacks which last 1-2 secs and may repeat up to 50 times, progressive mental handicap, onset at the beginning of life, EEG = hypsarrhythmia

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59
Q

Typical absence seizures features

A

Suddenly stopping, staring blankly, automatisms, lasts 2-30 seconds, recover quickly, no warning, often many in a day, onset 4-8 years, EEG = 3Hz, generalised, symmetrical

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60
Q

Typical absence seizures management

A

Sodium valproate, ethosuximide

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61
Q

Lennox-Gastaut syndrome features

A

Atypical absenses, falls, jerks, 90% have moderate IA impairment, may be an extension of infantile spasms, onset 1-5 years, EEG = slow spike

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62
Q

Juvenile monoclonal epilepsy (Janz syndrome) features

A

Infrequent generalised seizures often upon waking/sleep deprived, daytime absences, sudden shock-like myoclonic seizers, onset in teenage years

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63
Q

Juvenile monoclonal epilepsy management

A

Sodium valproate

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64
Q

Focal temporal lobe seizure features

A

An aura for up to 2 mins which may or may not progress into an abscence seizure w/ automatisms - this then may (rarely) progress to a generalised tonic-clonic.

Aura symptoms = Deja Vu, sudden intense feelings of joy/fear/anxiety, a rising sick feeling from the stomach, audio/gustatory/olfactory hallucinations

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65
Q

Focal frontal lobe seizure features

A

Head/leg movements, posturing, post-ictal weakness, Jacksonian march (clonic movements traveling proximally)

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66
Q

Focal parietal lobe seizure features

A

Paraesthesia

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67
Q

Focal occipital lobe seizure features

A

Floaters/flashes

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68
Q

Generalised tonic-clonic seizures management

A

Males = sodium valproate
Females = lamotrigine or levetiracetam

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69
Q

Focal seizures management

A

1st line =lamotrigine or levetiracetam
2nd line = carbamazepine

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70
Q

Absence seizures management

A

1st line = ethosuximide
2nd line = Males = sodium valproate, Females = lamotrigine or levetiracetam
NOTE - carbamazepine may exacerbate absence seizures

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71
Q

Myoclonic seizures management

A

Males = sodium valproate
Females = levetiracetam

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72
Q

Tonic/atonic seizures management

A

Males = sodium valproate
Females = lamotrigine

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73
Q

When do you start treatment for epilepsy?

A

After a second seizure, or after a first with obvious EEG signs

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74
Q

Essential tremor features

A

Postural tremor (worse if arms outstretched) which usually affects both upper limbs, improves w/ alcohol and rest

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75
Q

Essential tremor management

A

Propranolol - Primidone if can’t take beta blockers

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76
Q

Which artery is usually responsible for an extradural haematoma

A

Middle meningeal artery

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77
Q

Extradural haematoma features

A

Hx of head trauma w/ LOC, followed by a lucid interval and then a second LOC, fixed and dilated pupil (due to compression of the oculomotor nerve from uncal herniation)

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78
Q

Extradural haematoma CT appearance

A

Biconvex (lemon), hyperdense collection limited by the suture lines

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79
Q

Extradural haematoma management

A

Craniotomy and evacuation of the haematoma

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80
Q

Causes of facial nerve palsy (unilateral and bilateral)

A

Bilateral = sarcoidosis, GBS, Lyme disease, bilateral acoustic neuromas, Bell’s palsy

Unilateral = as above, Ramsay-Hunt syndrome, parotid tumours, HIV, MS, diabetes mellitus, stoke

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81
Q

Which cause of facial palsy spares the forehead?

A

UMN lesions

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82
Q

Define Foot drop

A

A gait abnormality where the pt has difficulty lifting the front of the foot due to weakness in the dorsiflexors

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83
Q

Causes of foot drop

A

Common peroneal nerve lesion (most common), L5 radiculopathy, sciatic nerve lesion, superficial or deep peroneal nerve lesions, stroke

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84
Q

Trochlear nerve palsy features

A

Vertical diplopia, inability to adduct the eye, subjective tilting of objects, head tilt, eye upwards and outwards when looking forwards

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85
Q

Guillain-Barre syndrome pathophysiology

A

Cross-reaction resulting in the formation of anti-ganglioside antibodies (anti-GM1) usually triggered by Campylobacter jejuni infection - leads to demyelination

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86
Q

Guillain-Barre syndrome features

A

Initially pt commonly experience back/leg pain

Characteristically causes progressive, symmetrical weakness of all the limbs, in an ascending pattern

Also causes hyporeflexia, resp muscle weakness, CN involvement, autonomic involvement (urinary retention and diarrhoea) but causes very few sensory signs

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87
Q

Guillain-Barre syndrome investigations

A

Lumbar puncture (rise in protein w/ a normal WCC found in 66%), nerve conduction studies (decreased motor neve conduction velocity due to demyelination)

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88
Q

Define Miller-Fisher syndrome

A

A variant of Guillain-Barre syndrome due to anti-GQ1b antibodies (still commonly after Campylobacter infection)

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89
Q

Miller-Fisher syndrome features

A

DECENDING paralysis, ophthalmoplegia, areflexia, ataxia - eye muscles are typically affected first

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90
Q

Guillain-Barre syndrome management

A

No cure, treatment is to aid recovery and symptoms - Plasmapheresis or IVIg, gabapentin/amitriptyline/pregabalin

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91
Q

Define Holmes-Adie pupil

A

An enlarged pupil that reacts slowly to light and near stimulus - due to damage to parasympathetic chain

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92
Q

Holmes-Adie pupil features

A
  • Anisocoria = unequal size of pupils
  • Tonic pupillary response = when exposed to light the affected pupil demonstrates slow and prolonged constriction followed by gradual re-dilation
  • Vermiform movements = undulating movements seen under slit-lamp biomicroscopy
  • Accommodation reflex dysfunction = blurriness of near vision
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93
Q

Holmes-Adie syndrome features

A

Holmes-Adie pupil + other neuro features (e.g. a/hyporeflexia esp of Achilles tendon)

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94
Q

Define Horner’s syndrome

A

Unilateral ptosis, myosis and anydrosis due to disruption to the sympathetic chain

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95
Q

Define Huntington’s disease

A

An A.dominant trinucleotide repeat disorder resulting in the degeneration of cholinergic and GABAergic neurones in the striatum of the basal ganglia - death usually occurs w/in 20 years of onset of symptoms

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96
Q

Huntington’s disease features

A

Chorea, personality changes, intellectual impairment, dystonia, saccadic eye movements - usually develop after 35

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97
Q

Huntington’s disease investigations

A

Genetic testing (1st line), neuroimaging to support diagnosis (CT or MRI may show caudate nucleus atrophy)

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98
Q

Huntington’s disease management

A

Neuro management = Tetrabenazine for chorea, antipsychotics for psychosis and chorea, levodopa for bradykinesia/rigidity

Other management = SALT for dysphagia, psychiatric for depression, physiotherapists for mobility, dietitians for nutrition, social workers

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99
Q

Risk factors for raised ICP

A

Female, obesity, pregnancy, medication (COCP, tetracyclines, retinoids, lithium, thyroxine, nitrofurantoin)

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100
Q

Idiopathic intracranial hypertension features

A

Headache, transient visual obscurations, pulsatile tinnitus, photopsia, back pain, retrobulbar pain

Papilledema, visual field loss, 6th nerve palsy, relative afferent pupillary defect

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101
Q

Idiopathic intracranial hypertension investigations

A

All pts should be referred urgently for neuroimaging to rile out secondary causes

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102
Q

Idiopathic intracranial hypertension management

A

Conservative = WL, stop causative agents, regular visual field testing

Medical = Acetazolamide for all pts w/ visual field loss, loop diuretics may be used in refractory cases, repeat LPs

Surgical = Optic nerve sheath fenestration for pts who lose vision despite maximum medical management, Ventriculoperitoneal shunt

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103
Q

Define Idiopathic intracranial hypertension

A

Raised ICP w/out a clear secondary cause on investigations

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104
Q

Define Lambert-Eaton syndrome

A

An autoimmune disorder that usually occurs as a paraneoplastic syndrome seen in SCLC (and breast and ovarian cancer to a lesser extent), but can occur on its own - it’s caused by an antibody directed against the presynaptic voltage-gated Ca channels in the peripheral nervous system

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105
Q

Lambert-Eaton syndrome features

A

Weakness which decreases with muscle use, hyporeflexia, autonomic dysfunction

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106
Q

Lambert-Eaton syndrome investigations

A

EMG shows incremental response to repetitive electrical stimulation

107
Q

Lambert-Eaton syndrome management

A

Treat underlying cancer, immunosuppression (pred, azathioprine)

108
Q

Migraine management

A

Acute = Triptans (oral for adults, nasal for 12-17) +/- NSAIDs or paracetamol

Prophylactic = Propranolol, topiramate (avoid in women of child bearing age), amitriptyline

109
Q

Migraine complications

A

Acute = status migrainosus (severe, debilitating attack lasting more than 62 hrs despite treatment), migrainous infarction (causes an ischaemic stroke), persistent aura w/out infarct (aura lasting more than 1 week after headache resolves)

Chronic = chronic migraines, medication overuse headaches, transformed migraine (AKA chronic daily headache)

Migraine with aura is linked to an increased risk of venous thromboembolism

110
Q

Motor Neurons Disease features

A

A mix of UMN and LMN signs, fasciculations, the absence of sensory signs, wasting of the small muscles of the hand or tibialis anterior

Classically doesn’t affect the external ocular muscles, no cerebellar signs, abdominal reflexes preserved, sphincter dysfunction is a last sign, usually presents after 40

111
Q

Motor Neurons Disease investigations

A

Clinical diagnosis, but nerve conduction studies will show normal motor conduction - EEG will show a reduced number of action potentials w/ increasing amplitude

MRI is done to exclude cervical cord compression and myelopathy

112
Q

Motor Neurons Disease management

A

Riluzole = prevents stimulation of glutamate re4ceptors, mainly used in ALS, prolongs life by about 3 months

Supportive care

113
Q

Motor Neurons Disease subtype examples

A

Amyotrophic lateral sclerosis (ALS) = starts w/ muscle twitching and weakness - most common subtype

Progressive muscular atrophy = causes a lot of muscle wasting

Bulbar palsy

114
Q

Motor Neurons Disease prognosis

A

50% of pts die w/in 3 years

115
Q

Define Multiple Sclerosis

A

An inflammatory demyelinating disease, clinically defined as 2 episodes of neurological dysfunction separated in anatomical location and time

116
Q

Multiple Sclerosis calssification

A

Relapsing-remitting = relapses are followed by periods of neurological stability, relapses last days-months, remits last months-years, ~85% of MS cases

Primary progressive = steady progressive worsening of neuro symptoms from the onset

Secondary progressive = steady progressive worsening of neuro symptoms after an initial relapsing-remitting pattern

117
Q

Multiple Sclerosis features

A

Optic neuritis, fatigue, neuropathic pain, altered sensation, Lhermitte’s phenomenon (shock-like sensation radiating down the spine induced by neck flexion), muscle spasticity/stiffness/weakness, mobility issues, bowel and bladder dysfunction, sexual dysfunction, cognitive impairment, speech and swallowing issues

118
Q

Multiple Sclerosis investigations

A

Neuro bloods, MRI brain, MRI spine (in primary progressive), CSF analysis (oligoclonal bands)

119
Q

Multiple Sclerosis indications for drug management

A

RRMS + 2 relapses in past 2 years + able to walk 100m unaided

SPMS + 2 relapses in past 2 years + able to walk 10m (aided or unaided)

120
Q

Multiple Sclerosis management

A

Steroids in acute relapse, natalizumab, ocrelizumab, beta-interferon

121
Q

Define Multiple system atrophy

A

A fatal neurodegenerative disorder defined chiefly by autonomic dysfunction and parkinsonism - is an alpha-synucleinism

122
Q

Multiple system atrophy features

A

Autonomic dysregulation is the key feature (urinary incontinence, erectile dysfunction, orthostatic hypotension, constipation)

Parkinsonism that usually has a poor response to Levodopa

REM sleep behaviour disorder

Onset is between 30 and 75

123
Q

Multiple system atrophy investigations

A

Primarily a clinical diagnosis, can only be confirmed on post-mortem

MRI brain will show putaminal, pontine and middle cerebellar peduncle atrophy

124
Q

Multiple system atrophy management

A

Levodopa response poor so manage parkinsonism w/ physio, Midodrine for orthostatic hypotension, desmopressin for incontinence, long-term catheters for retention

125
Q

Define Narcolepsy

A

A chronic neuro disorder due to the loss of hypocretin-producing neurons in the hypothalamus, which regulate wakefulness and sleep

126
Q

Narcolepsy features

A

Type 2 = excessive daytime sleepiness resulting in sleep attacks (sudden and involuntary episodes of sleep) which last from minutes to an hour, sleep paralysis, hypnagogic (when falling asleep) and hypnopompic (when waking up) hallucinations

Type 1 = as above + cataplexy (sudden loss of muscle tone triggered by a strong emotion e.g. laughter or anger) - also have low levels of orexin in their CSF

127
Q

Narcolepsy management

A

CNS stimulants (Modafinil, dexamphetamine, methylphenidate), anti-depressants for cataplexy (SSRIs, clomipramine, venlafaxine), good sleep hygiene, scheduled naps

128
Q

Define Neuromyelitis optica

A

A spectrum of rare AI demyelinating CNS conditions that primarily affect the optic nerve and spinal cord - due to anti-apuaporin-4 antibodies (located on brain, spine and optic nerve)

129
Q

Neuromyelitis optica features

A

Hallmark presentation is of attacks of optic neuritis and/or transverse myelitis but can also present w/: Area postrema syndrome (intractable hiccups, N&V w/ no other neuro problems), pruritus (due to inflammation of spinothalamic tract, pain

130
Q

Optic neuritis features

A

Sub/acute loss of vision, retrobulbar and peri-ocular pain that is exacerbated by eye movements, photopsia’s exacerbated by eye movements, visual field loss, relative afferent pupillary defect

131
Q

Define Transverse myelitis

A

Horizontal inflammation through a cross-section of the spinal cord

132
Q

Optic neuritis investigations

A

Visual acuity test, colour vision test, testing for RAPD, fundoscopy (may show swelling of the optic nerve), testing eye movements, MRI w/ gadolinium contrast (will show optic nerve enhancements)

133
Q

Optic neuritis management

A

High-dose IV methylprednisolone for 3 days, followed by oral prednisolone taper over 11 days

134
Q

Neuromyelitis optica diagnostic criteria

A

At least 1 core clinical symptom (optic neuritis, Area postrema syndrome or transverse myelitis)

+ve Aquaporin-4 antibodies

Alternative diagnosis exclusion (primarily MS)

135
Q

Transverse myelitis features

A

Pain, weakness in affected limbs, sensory deficits, bladder and bowel problems

136
Q

Neuromyelitis optica management

A

Acute = IV methylprednisolone for 5 days, plasma exchange therapy if unresponse to steroids

Prophylaxis = Oral prednisolone + immunosuppressive drug (azathioprine, mycophenolate mofetil or monoclonal abs)

137
Q

Neurofibromatosis Type 1 features

A

Cafe-au-lait spots (>6, 15 mm in diamemter), axillary/groind freckles, peripheral neurofibromas, iris hamartomas, scoliosis, pheochromcytomas

138
Q

Neurofibromatosis Type 2 features

A

Bilateral vestibular schwannomas, multiple intracranial schwannomas/meningiomas/ependymomas

139
Q

Define Normal pressure hydrocephalus

A

A neurological disorder due to accumulation of CSF in the ventricles causing them to enlarge - this occurs w/out an increase in ICP

140
Q

Normal pressure hydrocephalus features

A

A triad of gait disturbance, cognitive impairment and urinary incontinence (wet, wobbly and weird)

141
Q

Normal pressure hydrocephalus management

A

Ventriculoperitoneal shunt insertion

142
Q

Parkinson’s disease features

A

Resting tremor (4-6 Hz frequency), muscle rigidity (cogwheel), bradykinesia, postural instability, hypomimia, dysphagia

143
Q

Parkinson’s disease management

A

Levodopa (a dopamine precursor which is converted both in the CNS and periphery) + carbidopa (dopamine decarboxylase inhibitor which reduces the amount of levodopa converted in the periphery)

Monoamine oxidase B inhibitors

Dopamine agonist

Supportive care

144
Q

Key prognostic factors in Parkinson’s disease

A

Early-onst PD (before 50) progresses more slowly than late-onset

Pts presenting w/ tremor have a slower progression than pts presenting w/ bradykinesia and rigidity

Cognitive impairment is associated w. faster disease progression

145
Q

Define Paroxysmal hemicrania

A

A trigeminal autonomic cephalgia which causes attacks of severe unilateral headache (orbital, supraorbital or temporal regions) associated w/ autonomic features which last less than 30 min and occur multiple times in a day

146
Q

Paroxysmal hemicrania features

A

Presents very similarly to cluster headaches

147
Q

Paroxysmal hemicrania management

A

Completely treated by a therapeutic dose of 150 mg indomethacin (an NSAID) - this is how you can differentiate it from cluster headaches

148
Q

Progressive supranuclear palsy features

A

Impairment of vertical gaze (down gaze worse than up gaze), parkinsonism, falls, slurring of speech, cognitive impairment

149
Q

Define Psychogenic non-epileptic seizures

A

A type of seizures that are not caused by abnormal electrical activity in the brain, but by psychological factors (e.g. stress or emotional events) - Pts typically have a Hx of trauma or other psych disorders

150
Q

How do you distinguish Psychogenic non-epileptic seizures from epileptic seizures?

A

PNES has an absence of ictal autonomic symptoms (tachycardia, HTN, hypersalivation), gradual onset and offset, emotional triggers, pelvic thrusting during seizure

151
Q

Causes of peripheral neuropathy

A

Predominately motor loss = Guillain-Barre syndrome, porphyria, lead poisoning, Charcot-Marie-Tooth, chronic inflammatory demyelinating polyneuropathy, diphtheria

Predominately sensory loss = diabetes, uraemia, leprosy, alcoholism, B12 def (SCDC), amyloidosis

152
Q

Radial nerve motor innervation

A

Main nerve = triceps, anconeus, brachioradialis, extensor carpi radialis

Posterior interosseous branch = supinator, extensor muscles of the forearm (excluding carpi radialis), abductor pollicis longus

153
Q

Radial nerve sensory innervation

A

Sensation of the dorsal aspect of the proximal phalanges of the first 3.5 fingers

154
Q

What is the most common pattern of radial nerve injury?

A

Wrist drop (commonly from a mid-humeral fracture)

155
Q

What is Cushing’s triad of raised ICP?

A

Widening pulse pressure, bradycardia., irregular breathing

156
Q

Raised ICP management

A

Head elevation to 30 degrees, IV mannitol (osmotic diuretic)m controlled hyperventilation (aims to reduce pCO2 thus reducing vasoconstriction of the cerbral arteries and reducing ICP), repeat LPs (e.g. in IIH), ventriculoperitoneal shunts (e.g. for hydrocephalus), treat underlying cause

156
Q

Raised ICP features

A

Headache, vomiting, reduced conciosness, papilloedema, Cushing’s triad

157
Q

Ankle jerk reflex nerve roots

A

S1-S2

158
Q

Knee jerk reflex nerve roots

A

L3-L4

159
Q

Biceps tendon reflex nerve roots

A

C5-C6

160
Q

Triceps tendon reflex nerve roots

A

C7-C8

161
Q

Brachioradialis (supinator) reflex nerve roots

A

C5-C6

162
Q

Define Restless leg syndrome

A

A syndrome of spontaneous, continuous LL movements that may be associated w/ paraesthesia

163
Q

Restless leg syndrome features

A

Akathisia of LL (symptoms initially occur at night, but as condition progresses they occur during the day), paraesthesia, periodic limb movements of sleep (PLMS), symptoms worse at rest

164
Q

Restless leg syndrome management

A

Simple measures (walking, stretching, massaging), treat any iron def, dopamine agonists are 1st line (Pramipexole, ropinirole), benzos, gabapentin

165
Q

Define Reye’s syndrome

A

A severe, progressive encephalopathy accompanied by fatty infiltration of the liver, kidneys and pancreas - affects children typically after they have taken aspirin

166
Q

Define spastic paraparesis

A

An UMN pattern of weakness of the lower limbs

167
Q

Causes of spastic paraparesis

A

Demyelination, cord compression, parasagittal meningioma, tropical spastic paraparesis, transverse myelitis, syringomyelia, hereditary, osteoarthritis of C spine

168
Q

ACA stroke features

A

Contralateral hemiparesis and sensory loss - LL > UL

169
Q

MCA stroke features

A

Contralateral hemiparesis and sensory loss - UL > LL

Contralateral homonymous hemianopia

Aphasia

170
Q

PCA stroke features

A

Contralateral homonymous hemianopia w/ macular sparing

Visual agnosia

171
Q

Define Weber’s syndrome

A

A midbrain stroke due to issues w/ the supplying branches of the PCA

172
Q

Weber’s syndrome features

A

Ipsilateral CN III palsy (below the decussation for this)

Contralateral weakness of UL and LL (above the decussation for this)

173
Q

Define Lateral medullary syndrome

A

AKA Wallenberg syndrome - a stroke brainstem, specifically the lateral part of the medulla oblongata, due to issues in the posterior inferior cerebellar artery

174
Q

What is the role of the Medulla oblongata?

A

Contains the:
- Respiratory centre = controls ventilation
- Cardiovascular centre = controls HR
- Vasomotor centre = controls BP
- Reflex centres for vomiting, coughing, sneezing and swallowing

Location of the decussation of the corticospinal tracts

Nuclei for CN 9-12

175
Q

What are the 3 parts of the brain stem?

A

Midbrain (top)
Pons
Medulla oblongata (bottom)

176
Q

What is the role of the Pons?

A

Links the medulla to the rest of the brain

Coordinates autonomic functions

Part of the reticular activating system

Nuclei for CN 5-8

177
Q

What is the role of the midbrain?

A

Tegmentum (anterior surface):
- Reticular formation (part of the reticular activating system)
- Processes pain signals
- Autonomic function
- Nuclei of CN 3 and 4
- Conduit for spinothalamic and corticospinal tracts
- Contains the Red nucleus (involved in motor coordination)
- Contains the substantia nigra (has cells which produce dopamine)

Tectum (posterior surface):
- Process visual signals and sends them to the occipital lobe
- Process auditory signals and sends them them to the temporal lobe

178
Q

What is the reticular activating system?

A

Nerve bundles which regulate wakefulness and sleep-wake transitions - it does this my altering brain electrical activity and releasing hormones

179
Q

Lateral medullary syndrome (PICA stroke) features

A

Ipsilateral facial pain and temp sensation loss
Contralateral limb/torso pain and temp sensation loss
Ataxia
Nystagmus

180
Q

Anterior inferior cerebellar artery stroke (lateral pontine syndrome) features

A

Ipsilateral facial paralysis and deafness
Contralateral limb/torso pain and temp sensation loss
Ataxia
Nystagmus

181
Q

Define Amaurosis fugax

A

Temporary loss of vision in one eye which returns to normal - usually due to transient loss of blood flow to the back of the eye

182
Q
A
183
Q

Retinal/ophthalmic artery stroke features

A

Amaurosis fugax

184
Q

Basilar artery stroke features

A

Locked-in syndrome

185
Q

Lacunar stroke features

A

Isolated hemiparesis +/- limb ataxia
Isolated hemisensory loss

186
Q

What are the basal ganglia?

A

Several structures in the centre of the brain which primarily help coordinate voluntary movement (approves or rejects motor signals to filter out unnecessary/incorrect signals)

Also play a role in processing risk, habit forming and addiction

187
Q

Acute ischaemic stroke management

A

Aspirin 300mg orally or rectally ASAP after exclusion of haemorrhagic

Thrombolysis with alteplase or tenecteoplase if fit the criteria

Thrombectomy to those who fit the criteria

Clopidogrel long-term for secondary prevention (unless A.fib, then give DOAC)

188
Q

Criteria for thrombolysis in an acute ischaemic stroke

A

Standard criteria:
- Haemorrhagic stroke has definitively been excluded
- Administered w/in 4.5 hours of symptom onset

Consider if:
- Between 4.5-9 hours of symptom onset (or 9 hours since mid point of sleep and have woken w/ stroke symptoms)
AND
- There is evidence from a CT/MR perfusion or MRI of the potential to salvage brain tissue

BP should be lowered to 186/110 before thrombolysis

189
Q

Absolute contraindication for stroke thrombolysis

A
  • Previous intracranial haemorrhage
  • Seizure at onset of stroke
  • Intracranial neoplasm
  • Suspected subarachnoid haemorrhage
  • Stroke or traumatic brain injury w/in 3 months
  • Lumbar puncture w/in 7 days
  • GI haemorrhage w/in 3 weeks
  • Active bleeding
  • Oesophageal varices
  • Uncontrolled HTN > 200/120
190
Q

Criteria for thrombectomy in an acute ischaemic stroke

A

If w/in 6 hours in people w/ a confirmed occlusion of the proximal anterior circulation

This criteria extents to w/in 24 hours if CT/CR demonstrates salvageable brain tissue

191
Q

Define Anterior Spinal Artery Infarcts

A

An ischaemic stroke occurring in the anterior 2/3rds of the spinal cord - typically due to disruption of the blood flow from the anterior spinal artery

192
Q

Causes of anterior spinal artery infarcts

A
  • Damage to the aorta - aneurysm repair, dissection
  • Atherosclerosis
  • Cardiac arrest
  • Cardiac emboli
  • Vasculitis
  • Shock
193
Q

Anterior Spinal Artery Infarct features

A

Present w/ a unique pattern of neurological deficits, with the dorsal columns being preserved:

  • loss of pain sensation
  • loss of temp sensation
  • motor function impairment
  • loss of autonomic function
194
Q

Anterior Spinal Artery Infarcts Investigations

A

MRI - shows hyperdense signals on T2-weiggted imaging of the anterior 2/3rds of the spinal cord

195
Q

Causes of autonomic neuropathy

A

DM, neurodegenerative conditions, infections, AI diseases, amyloidosis

196
Q

Autonomic neuropathy features

A

Cardiovascular system = orthostatic hypotension, resting tachycardia, silent MI’s

GI system = dysphagia, gastroparesis, constipation, diarrhoea

Genitourinary system = bladder dysfunction, ED, reduced vaginal lubrication

Thermoregulatory system = anhidrosis, hyperhidrosis

197
Q

Define Cervical spondylosis

A

Age-related degeneration of the spinal cord leading to nerve impingements

198
Q

Cervical spondylosis features

A

Neck pain, radiculopathies (flaccid paresis), myelopathy (sensory changes and spastic paresis), bladder and bowel disturbance

198
Q

Cervical spondylosis management

A

Non-surgical = Physio, NSAIDs, cervical collars and traction

Surgical = anterior cervical decompression (discectomy, corpectomy), posterior decompressions (laminoplasty, laminectomy) and fusions

199
Q

Types of diabetic neuropathy

A

Distal symmetrical sensory neuropathy (most common), small-fibre predominant neuropathy, diabetic amyotrophy, mononeuritis multiplex, autonomic neuropathy

200
Q

Distal symmetrical sensory neuropathy features

A

Sensory loss in glove and stocking distributions, typically affecting touch, vibration and proprioception (dorsal column predominant)

Results from the loss of large sensory fibres due to DM

201
Q

Small-fibre predominant neuropathy features

A

Deficits in pain and temp sensation (spinothalamic predominant) in a glove and stocking distributions, often accompanied by episodes of burning pain

Results from the loss of small sensory fibres due to DM

202
Q

Diabetic Amyotrophy features

A

Severe pain around the thighs and hips, along w/ proximal weakness

Due to inflammation of the lumbosacral or cervical plexus due to DM

203
Q

Define Charcot arthropathy

A

AKA neuropathic arthropathy - a chronic, progressive conditions characterised by painful/painless bone and joint destruction in limbs which have lost sensory innervation

Primarily affects pts w/ peripheral neuropathy (most commonly DM)

204
Q

Charcot arthropathy features

A

6D’s:
- Destruction of bone and joints
- Deformity
- Degeneration
- Dense bones (sclerosis)
- Debris of bone fragments
- Dislocation

Typically affects the tarsometatarsal joints

205
Q

Charcot arthropathy management

A

Conservative = prolonged off-loading (special footwear or plaster casts) to allow healing, use of orthotics long term

Medical = bisphosphonates, neuropathic pain agents, topical anaesthetics

Surgical = resection of bony prominences to prevent ulcer formation, correction of severe deformities, amputations if severe infections

206
Q

Haemorrhagic stroke management

A

Acute:
- Neurosurgical evaluation for potential surgical interventions (e.g. decompressive hemicraniectomy)
- Admission to neuro ICU or stroke unit
- BP control < 140/80

Long-term:
- Rehabilitation
- Secondary prevention

207
Q

Define Internuclear ophthalmoplegia

A

An ocular movement disorder arising from a lesion in the medial longitudinal fasciculus, affecting coordination of horizontal gaze

208
Q

Internuclear ophthalmoplegia features

A

Impaired adduction in the ipsilateral eye during horizontal gaze

Nystagmus in the abducting eye

Some pts may retain the ability to converge on near targets

209
Q

Define Jugular foramen syndrome

A

A disorder resulting from a unilateral lesion of the glossopharyngeal, vagus and accessory CN’s, which transverse the jugular foramen

210
Q

Jugular foramen syndrome features

A

Ipsilateral weakness of the Trapezius and sternocleidomastoid muscles

Deviation of the uvula and soft palate towards the unaffected side

Dysphagia and changes in voice

Hoarseness and loss of gag reflex

Sensory loss in the distribution of the glossopharyngeal nerve

211
Q

How does hyperventilation help to reduce raised ICP?

A

Hyperventilation reduces pCO2, which causes vasoconstriction of the cerebral arteries - causes a rapid reduction in ICP

212
Q

What is the difference between medical and surgical 3rd nerve palsy?

A

Medical = no pupil involvement

Surgical = pupil involvement - this is due to external compression of the oculomotor nerve which compresses the parasympathetic (constrictive) fibres that run on the outside of the nerve, causing pupil dilation

213
Q

Define Meralgia paraesthetica

A

Compression of the lateral femoral cutaneous nerve (usually under the inguinal ligament) - a purely sensory nerve which supplies the outer aspect of the thigh

214
Q

Meralgia paraesthetica features

A

Neuropathic pain, numbness, paraesthesia in the distribution of the lateral femoral cutaneous nerve

Symptoms may be exacerbated by standing, walking or hip extension

No motor loss

215
Q

Meralgia paraesthetica management

A

Conervative = WL, wearing loss clothes, over-the-counter analgesia, physio

Medical = pregabalin or gabapentin

Interventional = local steroids or nerve blocks

Surgical = decompression of the nerve (rare)

216
Q

Define Mononeuritis multiplex

A

A type of peripheral neuropathy characterised by simultaneous or sequential involvement of individual con-contiguous nerve trunks, evolving over days to years

217
Q

Mononeuritis multiplex features

A

Asymmetrical patterns of neuropathic pain and weakness

218
Q

Mononeuritis multiplex causes

A
  • DM
  • Vasculitis = polyarthritis nodosa, granulomatosis w/ polyangiitis, eosinophilic granulomatosis w/ polyangiitis
  • AI = RA, SLE
  • Infections = leprosy, Lyme’s disease, Parvovirus B19, HIV
  • Sarcoid
219
Q

Define Myotonic dystrophy

A

A multi-system, trinucleotide repeat disorder that affects specific chloride channels in the muscles

220
Q

Myotonic dystrophy features

A

Face = frontal balding, myopathic face (long and thin), bilateral ptosis, cataracts

Speech = dysarthria due to myotonic tongue and phalangeal muscles

Neck = wasting of sternocleidomastoid

Hands = Distal muscle wasting and weakness, slow relaxing grip and percussion myotonia

Internal features = metabolic syndrome, cardiomyopathy/arrhythmias, testicular atrophy

221
Q

Cortico-basal degeneration features

A

Parkinsonism, spontaneous activity by an affected limb, akinetic rigidity

222
Q

Define Bulbar palsy

A

A subtype of LMN lesions which impact the 9th, 10th and 12th CNs - the resulting impediment primarily involves the mechanisms of speech and swallowing

223
Q

Bulbar palsy causes

A
  • MND (Progressive bulbar palsy variant)
  • Myasthenia gravis
  • GBS
  • Brainstem strokes
  • Syringobulbia
224
Q

Bulbar palsy features

A
  • Absent or normal jaw jerk
  • Absent gag reflex
  • Flaccid, fasciculation tongue
  • Nasal speech
  • Dysarthria
  • Dysphagia
225
Q

Define Pseudobulbar palsy

A

A condition caused by bilateral lesions affecting the corticobulbar tracts (which runs from the motor cortex to the motor nuclei of CNs 9, 10 and 12 in the medulla). Bilateral lesions are necessary due to the CNs having bilateral cortical representation - this is an UMN lesion affecting speech and swallowing

226
Q

Pseudobulbar palsy causes

A
  • Vascular = bilateral internal capsule stroke
  • MND
  • Progressive supranuclear palsy
  • Neoplasm of the brainstem
  • MS
  • Trauma
227
Q

Pseudobulbar palsy features

A
  • Spastic tongue
  • Slow, thick (hot-potato) speech
  • Brisk jaw jerk
  • Emotional lability
228
Q

Define Pyramidal pattern of weakness

A

A specific UMN lesion sign where there is motor weakness involving the UL extensors and LL flexors - so arm is held in flexion and leg is held in extension (causes pt to trace a semicircle with their foot instead of bending their knee when the walk)

229
Q

Define Spinal stenosis

A

A condition characterised by narrowing of the spinal canal in the lumbar region - resulting in compression of the spinal nerves

230
Q

Spinal stenosis features

A

Neurogenic claudication (intermittent pain/weakness/numbness in the proximal thigh or buttocks), pain aggravated by physical activity or extended spinal positions (e.g. descending stairs), pain relieved by stooped posture or bending over (e.g. when going uphill) absence of vascular risk factors or signs

231
Q

Spinal stenosis management

A

Non-operative (1st line) = NSAIDs, opioids, nerve blocks, physio, WL, lifestyle changes

Surgical = laminectomy, laminoplasty or spinal fusion

232
Q

Define Subacute combined degeneration of the cord

A

Degeneration and demyelination of both the dorsal columns and the corticospinal tracts, whilst preserving pain and temp sensation (spinothalamic tracts intact) - due to vitamin B12 def

233
Q

Subacute combined degeneration of the cord features

A
  • Symmetrical distal sensory symptoms (typically starting and the feet and progressing to the hands)
  • Varying degrees of ataxia
  • Spastic paresis and weakness
  • Loss of vibration sense and proprioception
  • Mixed UMN and LMN signs (e.g. hyper/hypo/areflexia)
  • Autonomic bladder and bowel symptoms
234
Q

Subacute combined degeneration of the cord management

A

Vit B12 replacement w/ hydroxocobalamin 1mg IM on alternating days until no further improvement, followed by maintenance IM injections of 1mg every 2 months

235
Q

Subarachnoid haemorrhage investigations

A
  • CT head
  • LP if CT not definitive (look for xanthochromia) - not reliable w/in 12 hrs of symptom onset
  • CT angiogram is CT suggestive of subarachnoid haemorrhage
236
Q

Subarachnoid haemorrhage management

A

Medical = Nimodipine to prevent vasospasm post-ischaemia

Radiological = endovascular coiling/stenting to stop the bleeding

Surgical = clipping to stop the bleeding

237
Q

Subdural haematoma cause

A

Sheering forces which tear the bridging veins between the cortex and dura mater

238
Q

Subdural haematoma features

A

Headache, N&V, confusion, reduced GCS, focal neuro signs

Presentation is typically subacute (w/in 3 days - 3 wks of trauma) or chronic (>3 wks after trauma)

239
Q

Subdural haematoma investigations

A

CT head - clot appears differently based on its age:
- Hyperacute (<1 hr) = isodense, w/ underlying cerebral oedema
- Acute (<3 days) = crescent-shaped hyperdense extra-axial collection
- Sub-acute (3 days - 3 wks) = isodense, possible midline shift and sulcal effacement - can use enhanced contrast CT or MRI to aid diagnosis
- Chronic (>3 wks) = hypodense

240
Q

Subdural haematoma management

A

Acute = craniotomy
Chronic = Burr holes

241
Q

Causes of a surgical 3rd nerve palsy

A

Most common = posterior communicating artery aneurysm
Other = cavernous sinus lesions (infections, thrombosis, tumour)

242
Q

Define Syringomyelia

A

The formation of a fluid-filled cavity of cyst, known as a syrinx, w/in the spinal cord - it often expands and elongates over time, exerting pressure on the spinal cord and damaging nerve fibres

243
Q

Syringomyelia causes

A
  • CSF blockage or disruption - often secondary to conditions such as arachnoiditis or SOL
  • Spina Bifida
  • Post-trauma
  • Idiopathic
  • Familial predisposition
244
Q

Syringomyelia features

A
  • Pain and temp loss due to dmg to the spinothalamic tract- classically in a ‘shawl-like’ distribution over the arms, shoulders and upper back
  • Dorsal column involvement as syrinx enlarges
  • Muscle weakness as syrinx extends and dmgs anterior horn cells
  • Autonomic dysfunction
245
Q

Syringomyelia management

A

Physio and rehab, surgical

246
Q

TIA management

A

Clopidogrel, lifestyle modifications, control of vascular risk factors, carotid endarterectomy if > 50% stenosis

247
Q

TIA investigations

A

Immediate CT head followed up w/ an MRI to assess ischaemia/haemorrhage, carotid USS, echo, 24 hr Halter

248
Q

Trigeminal neuralgia causes

A

Primary = idiopathic

Secondary = compression (malignancy, AV malformations), MS, sarcoidosis, Lyme disease

249
Q

Trigeminal neuralgia management

A

Medical:
- Carbamazepine (1st line)
- Phenytoin
- Lamotrogine
- Gabapentin

Surgical:
- Microvascular decompression (if vessels are compressing the nerve)
- Treat underlying cause (e.g. remove tumour)
- Alcohol or glycerol injections (dmg the trigeminal nerve and reduce pain signals)

250
Q

Define Vertigo

A

The sensory misperception or illusion of motion

251
Q

Causes of vertigo

A

Peripheral = BPPV, acute labyrinthitis, Meniere’s disease, vestibular neuritis, Ramsey Hunt syndrome

Central = Migraine, MS, cerebrovascular disease

Systemic = orthostatic hypotension, arrhythmias, medication (aminoglycosides, loop diuretics)

252
Q

Which optic pathway is involved in monocular vision loss?

A

Optic nerve

253
Q

Which optic pathway is involved in bitemporal hemianopia?

A

Optic chiasm

254
Q

Which optic pathway is involved in contralateral homonymous hemianopia?

A

Optic radiations

255
Q

Which optic pathway is involved in quadrantanopias?

A

Optic radiation

256
Q

Macular sparing homonymous hemianopia?

A

Occipital lobe

257
Q

What causes a contralateral homonymous superior quadrantanopia?

A

A temporal lobe lesion (PITS - P - parietal I - inferior; T - temporal S - superior)

258
Q

What causes a contralateral homonymous inferior quadrantanopia?

A

A parietal lobe lesion (PITS - P - parietal I - inferior; T - temporal S - superior)

259
Q

Wernicke’s encephalopathy features

A

Triad of:
- Ataxia
- Confusion
- Ocular abnormalities

260
Q

Neurological features of Wilson’s disease

A

Akinetic-rigid syndrome similar to Parkinson’s
- Tremor
- Ataxia
- Dystonia
- Drooling
- spasticity
- Chorea
- Myoclonus

261
Q

Define Thoracic outlet syndrome

A

A disorder involving compression of the brachial plexus, subclavian artery or vein at the thoracic outlet - occurs when neck trauma occurs in a pt w/ a genetic predisposition (such as a cervical rib)

262
Q

Thoracic outlet syndrome features

A

Neurogenic:
- painless muscle wasting of hand muscles, with patients complaining of hand weakness e.g. grasping
- sensory symptoms such as numbness and tingling may be present
- if autonomic nerves are involved, the patient may experience cold hands, blanching or swelling

Vascular:
- subclavian vein compression leads to painful diffuse arm swelling with distended veins
- subclavian artery compression leads to painful arm claudication and in severe cases, ulceration and gangrene

Year 6 (12 decks)

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