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Medicine and Surgery Mushkies > Neurology Mushkies > Flashcards

Neurology Mushkies Flashcards

1
Q

What are 3 signs on inspection of Parkinson’s?

A
  1. Asymmetrical resting tremor (5Hz) exacerbated by reading backwards
  2. Hypomimia
  3. Extrapyramidal posture
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2
Q

Parkinson’s + Nystagmus?

A

MSA

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3
Q

Parkinson’s + Vertical gaze palsy?

A

PSP

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4
Q

What are 4 features of a Parkinsonian gait?

A
  1. Slow initiation
  2. Shuffling
  3. Festination (hurrying)
  4. Absent arm swing
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5
Q

What do you do to complete an examination in a pt with Parkinson’s?

A
  1. MMSE
  2. Drug chart
  3. Abdo exam (hepatomegaly + signs of CLD)
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6
Q

What are causes of Parkinson’s disease?

A
  1. Idiopathic
  2. Parkinson’s plus syndromes = PSP, MSA, CBD, LBD
  3. Vascular = infarcts in the substantia nigra
  4. Wilson’s disease
  5. Drugs = neuroleptics and metoclopramide
  6. Post-encephalitis
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7
Q

What are the 3 cardinal signs of parkinsonism?

A
  1. Rigidity
  2. Brady/akinesia
  3. Tremor
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8
Q

What are 4 autonomic features of parkinsonism?

A
  1. Postural hypotension
  2. Urinary problems (frequency, urgency, nocturia)
  3. Erectile dysfunction
  4. Constipation
  5. Hypersalivation and hyperhidrosis
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9
Q

What are 5 sleep related problems of parkinsonism?

A
  1. Insomnia and
  2. Turning in bed leads to
  3. Excessive Daytime Sleepiness (EDS)
  4. REM behavioural sleep disorder = loss of muscle atonia during sleep leading to violent enactment of dreams
  5. Da SEs = insomnia, drowsiness, EDS
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10
Q

How can you investigate Parkinson’s?

A
  1. Bloods = caeruloplasmin (low in Wilsons)

2. Imaging = CT/MRI (exclude vascular cause), DaTSCAN

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11
Q

What is a DaTSCAN?

A

An Ioflupane I123 injection that binds to dopaminergic neurones and allows visualisation of the substantia nigra

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12
Q

How can you classify the management of Parkinsons?

A
  1. General
  2. Specific
  3. Adjuncts
  4. Other
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13
Q

What is the ‘general’ management of Parkinson’s?

A
  1. MDT = neurologist, PD nurse, physio, OT, social worker, GP and carers
  2. Assess disability = UDPRS
  3. Physio = postural exercises
  4. Depression screening
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14
Q

What is the UDPRS?

A

Unified Parkinson’s Disease Rating Scale

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15
Q

What is the specific management of Parkinson’s? (7 drugs)

A

LDAMCAA

  1. L-DOPA + Carbidopa/benserazide
  2. DA agonists = ropinerole, pramipexole
  3. Apomorphine = SC rescue drug, also a DA agonist
  4. MAO-B inhibitors = rasagiline
  5. COMT inhibitors = tolcapone
  6. Amantadine
  7. Anti-muscarinics = procyclidine
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16
Q

What are 3 adjuncts for treatment of Parkinsons?

A
  1. Domperidone = nausea
  2. Quetiapine = psychosis
  3. Citalopram = depression
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17
Q

What are 2 ‘other’ managements for Parkinsons?

A
  1. Deep brain stimulation

2. Basal ganglia disruption

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18
Q

What is the epidemiology of idiopathic PD?

A

Mean onset 65 y/o

2% prevalence

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19
Q

What is the pathophysiology of PD?

A
  1. Destruction of dopaminergic neurones in the pars compacta of the substantia nigra
  2. Alongside formation of beta amyloid plaques and
  3. Neurofibrillary tangles composed of hyperphosphorylated tau
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20
Q

What are the features of Parkinsonism?

A

TRAPPS PD

  1. Tremor = increased by stress, decreased by sleep
  2. Rigidity = lead-pipe, cog-wheel
  3. Akinesia = 5
  4. Postural instability = stooped gait with festination
  5. Postural hypotension + other autonomic dysfunction
  6. Sleep disorders = insomnia, ED, OSA, RBD
  7. Psychosis = esp. visual hallucinations
  8. Depression/Dementia/Drug SEs
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21
Q

What are the 5 akinetic features of Parkinson’s?

A
  1. Slow initiation
  2. Difficulty with repetitive movement
  3. Micrographia
  4. Monotonous voice
  5. Mask-like face
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22
Q

What are the side effects of L-DOPA?

A 
DOPAMINE
Dyskinesia 
On-off phenomena = motor fluctuations
Psychosis
ABP reduced 
Mouth dryness
Insomnia 
N&V
EDS
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23
Q

What are two type of motor fluctuations you can get in PD?

A
  1. End-of-dose

2. On-Off effect

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24
Q

What is the end-of-dose effect?

A

Deterioration as dose wears off with progressively shorter benefit

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25
Q

What is the on-off effect?

A

Unpredictable fluctuations in motor performance unrelated to timing of dose

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26
Q

What are 4 other causes of parkinsonism?

A
  1. MSA
  2. PSP
  3. CBD
  4. LBD
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27
Q

What is the pathology of MSA?

A

Papp-Lantos bodies = alpha synuclein inclusions in glial cells

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28
Q

What are 3 features of MSA?

A
  1. Autonomic dysfunction = postural hypotension
  2. Parkinsonism
  3. Cerebellar ataxia
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29
Q

What might you call MSA if autonomic features predominate?

A

Shy Drager syndrome

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30
Q

What are 4 features of PSP?

A
  1. Postural instability –> falls
  2. Vertical gaze palsy
  3. Pseudobulbar palsy = speech and swallowing problems
  4. Parkinsonism = symmetrical onset, tremor is unusual
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31
Q

What are 3 features of CBD?

A
  1. Unilateral parkinsonism esp. rigidity
  2. Aphasia
  3. Asterogenesis = cortical sensory loss (–> alien limb phenomenon with autonomous arm movements)
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32
Q

What is the pathology of LBD?

A

Alpha synuclein and ubiquitin Lewy bodies in brainstem and neocortex

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33
Q

What are 3 features of LBD?

A
  1. Fluctuating cognition
  2. Visual hallucinations
  3. Parkinsonism
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34
Q

What are 4 features of vascular Parkinsonism?

A
  1. Sudden onset
  2. Worse in legs than arms
  3. Pyramidal signs
  4. Prominent gait abnormality
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35
Q

How can you classify the causes of tremor?

A
  1. Resting = parkinsonism
  2. Intention = cerebellar
  3. Postural = worse with arms outstretched
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36
Q

What are 5 causes of a postural tremor?

A

BHATS

  1. Benign Essential Tremor
  2. Hyperthyroidism
  3. Alcohol withdrawal
  4. Toxins = beta agonists
  5. Sympathetic = anxiety
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37
Q

What is benign essential tremor (BET)?

A

An predominantly autosomal dominant condition that occurs with movement and is worse with anxiety and caffeine. It does not occur with sleep and is improved by alcohol.

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38
Q

What are the features of cerebellar syndrome?

A 
DANISH
Dysdiadochokinesia 
Ataxia 
Nystagmus + rapid saccades
Intention tremor + dysmetria 
Slurred speech
Hypotonia
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39
Q

What are the causes of cerebellar syndrome?

A

DAISIES PT

  1. Demyelination (MS)
  2. Alcohol/Abscess/Atrophy
  3. Infarct/Infection
  4. SOL = Schwanomma + other CPA tumours
  5. Inherited = Wilsons, Friedrichs, Ataxia Telangiectasia, VHL
  6. Epilepsy medications = Phenytoin
  7. System atrophy, multiple/Spinocerebellar ataxia
  8. Paraneoplastic syndrome
  9. Trauma
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40
Q

Are cerebellar signs usually ipsilateral or bilateral?

A

Ipsilateral

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41
Q

What are bilateral cerebellar signs more likely to represent?

A

Global pathology x 3 (PAM)

  1. Phenytoin
  2. Alcohol
  3. MS
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42
Q

How does a nystagmus due to a cerebellar cause present?

A

Fast phase towards lesion, maximal looking towards lesion

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43
Q

How does a nystagmus due to a vestibular present?

A

Fast phase away from lesion, maximal looking away from lesion

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44
Q

What causes Lateral Medullary syndrome?

A

Occlusion of vertebral artery or PICA

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45
Q

What is the eponymous name for lateral medullary syndrome?

A

Wallenberg’s syndrome

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46
Q

Where do you find signs in lateral medullary syndrome?

A

Signs are ipsilateral apart from body anaesthesia to pain

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47
Q

What are the features of lateral medullary syndrome?

A

DANVAH

  1. Dysphagia = nucleus ambiguus
  2. Ataxia = inferior cerebellar peduncle
  3. Nystagmus = inferior cerebellar peduncle
  4. Vertigo = vestibular nucleus
  5. Anaesthesia = spinothalamic tract (contralateral) or spinal trigeminal nucleus (ipsilateral)
  6. Horner’s syndrome = sympathethic fibres
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48
Q

What is a vestibular schwannoma?

A

A benign, slow growing tumour of the superior vestibular nerve, that is the cause of 80% of CPA tumours, and is associated with NF2

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49
Q

How do vestibular schwannomas present?

A
  1. Unilateral SNHL + tinnitus + vertigo
  2. Headache (raised ICP)
  3. Ipsilateral CN 5,6,7,8 palsies
  4. Cerebellar signs = DANISH
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50
Q

How can you investigate vestibular schwannomas?

A

MRI of CPA (cerebellopontine angle)

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51
Q

What are the differentials for CPA tumours? x4

A
  1. Vestibular Schwannoma
  2. Meningioma
  3. Cerebellar astrocytoma
  4. Metastases
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52
Q

What are 5 features of vHL syndrome?

A
  1. Renal cysts
  2. Bilateral renal cell carcinoma
  3. Phaeochromocytoma
  4. Islet cell tumours
  5. Haemangioblastomas (often in cerebellum)
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53
Q

What is Friedrich’s Ataxia?

A

An autosomal recessive mitochondrial disorder which leads to progressive degeneration of the dorsal column, spinocerebellar tracts and corticospinal tracts

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54
Q

When is the typical onset of Friedrich’s Ataxia and what are two of its associations?

A
  1. Onset in teenage years

2. Associated with HOCM and mild dementia

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55
Q

What is Ataxia telangiectasia?

A

An autosomal recessive disorder leading to defects in DNA repair, leading to progressive ataxia, telangectasia, lymphoproliferative disease and defective cell-mediated immunity and Ab production

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56
Q

What causes Wilson’s disease?

A

AR mutation of ATP7B gene on Chromosome 13

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57
Q

What are the features of Wilson’s disease?

A

CLANK

  1. Cornea = Keiser-Fleischer rings
  2. Liver = CLD
  3. Arthritis
  4. Neuro = Parkinsonism, ataxia, psych problems
  5. Kidney = Fanconi’s syndrome
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58
Q

What causes excessive daytime sleepiness in Parkinsons?

A
  1. Inability to turn
  2. Restless legs
  3. Early morning dystonia (drugs wearing off)
  4. Nocturia
  5. OSA
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59
Q

2 features of REM behavioural sleep disorder in Parkinsons?

A
  1. Loss of muscle atonia during REM sleep

2. Violent enactment of dreams

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60
Q

What causes autonomic dysfunction in Parkinsons?

A

Combination effects of drugs and neurodegeneration

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61
Q

Cerebellar vermis lesion features?

A

Ataxis trunk and gait, with normal arms

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62
Q

Vestibular Schwannoma mx?

A
  1. Gamma knife

2. Surgery

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63
Q

4 features of Friedrich’s Ataxia?

A

PBLL

  1. Pes cavus
  2. Bilateral cerebellar ataxia
  3. Leg wasting + arreflexia but extensor plantars
  4. Loss of vibration and proprioception
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64
Q

UMN inspection?

A
  1. Walking aids
  2. Disuse atrophy and contractures
  3. Leg = extended, internally rotated with foot plantar flexed
  4. Arm = flexed, internally rotated, supinated
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65
Q

Contracture defn?

A

A permanent tightening of tissue

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66
Q

Unilateral UMN gait?

A

Circumducting

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67
Q

Bilateral UMN gait?

A

Scissoring

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68
Q

Pyramidal distribution of UMN leg weakness?

A

Extensors stronger than flexors

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69
Q

Pyramidal distribution of LMN leg weakness?

A

Flexors stronger than extensors

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70
Q

Causes of bilateral lower limb UMN signs (spastic paraparesis)?

A
  1. Common = MS, cord compression, cord trauma, CP

2. Other = familial, vascular (Becks), infection (HTLV1), tumour (ependymoma), syringomyelia

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71
Q

Beck’s syndrome AKA?

A

Anterior spinal artery syndrome

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72
Q

Causes of spastic paraparesis with mixed UMN and LMN signs?

A

MAST

  1. MND
  2. Ataxia, Friedrichs
  3. SCDC
  4. Taboparesis
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73
Q

What is taboparesis?

A

Tabo-paresis is a form of tertiary syphilis which contains features of both tabes dorsalis and general paralysis of the insane

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74
Q

Causes of a unilateral, spastic hemiparesis?

A
  1. Hemisphere = stroke, MS, SOL, CP

2. Hemicord = MS, cord compression

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75
Q

Mx of contractures?

A
  1. Baclofen
  2. Botulinum injection
  3. Physio
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76
Q

Features of cord compression?

A
  1. Pain = local, deep, radicular
  2. Weakness = LMN @ level, UMN below level
  3. Sensory level
  4. Sphincter disturbance
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77
Q

Causes of cord compression?

A
  1. Trauma = vertebral fracture
  2. Disc prolapse
  3. Infection = epidural abscess, TB
  4. Malignancy = primary or secondary
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78
Q

Ix of cord compression?

A

MRI

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79
Q

Mx of cord compression?

A

A neurosurgical emergency

  1. Malignancy = dexamethasone IV, consider chemo/radio/decompressive laminectomy
  2. Abscess = Abx and surgical decompression
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80
Q

Features of cauda equina lesions?

A
  1. Pain = back pain, radicular pain down legs
  2. Weakness = bilateral flaccid, areflexic lower limb weakness
  3. Sensation = saddle anaesthesia
  4. Sphincters = incontinence, poor anal tone
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81
Q

Beck’s syndrome (anterior spinal artery syndrome)?

A

Infarction of the spinal cord in the distribution of the anterior spinal artery, resulting in loss of function of the anterior two-thirds of the spinal cord

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82
Q

Causes of Beck’s syndrome?

A

Aortic aneurysm dissection or repair

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83
Q

Features of Beck’s syndrome?

A
  1. Para/quadriparesis
  2. Impaired pain and temperature sensation
  3. Preserved touch and proprioception
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84
Q

Syringomyelia defn?

A

Disorder in which a cyst or cavity forms within the spinal cord (syrinx = tubal cavity in central canal of the cord)

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85
Q

Where is a syrinx commonly located?

A

Cervical cord

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86
Q

In which direction does a syrinx expand, and thus what does it affect?

A

Expands ventrally, affecting:

  1. Decussating spinothalamic neurones
  2. Anterior horn cells
  3. Corticospinal tracts
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87
Q

Causes of syringomyelia?

A
  1. Blocked CSF circulation with reduced flow from posterior fossa = Arnold-Chiari malformation, masses
  2. Spina bifida
  3. Trauma
  4. Myelitis
  5. Cord tumours
  6. AVMs
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88
Q

What is an Arnold-Chiari malformation?

A

When the cerebellum herniates through the foramen magnum

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89
Q

4 cardinal signs of Syringomyelia?

A
  1. Dissociated sensory loss
  2. Wasting/weakness of hands +/- claw hand
  3. Loss of reflexes in upper limb
  4. Charcot joints (elbow and shoulder)
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90
Q

Dissociated sensory loss in syringomyelia?

A
  1. Loss of pain and temperature –> scars from burns
  2. Preserved touch, proprioception and vibration
  3. Root distribution reflects syrinx location (usually affects upper limbs and chest: ‘cape’)
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91
Q

‘Other’ Syringomyelia signs?

A
  1. UMN weakness in lower limbs with extensor plantars
  2. Horners
  3. Syringobulbia
  4. Kyphoscoliosis
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92
Q

Infectious cause of cord disease?

A

HTLV1 myelopathy (Tropical Spastic Paraplegia)

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93
Q

Stroke pathogenesis?

A
  1. Ischaemic (80%) = atheroma or embolus

2. Haemorrhagic (20%)

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94
Q

Bamford stroke classification?

A
  1. TACS
  2. PACS
  3. POCS
  4. LACS
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95
Q

TACS?

A

Carotid/MCA and ACA territory

  1. Hemiparesis and/or sensory deficit
  2. Homonymous hemianopia
  3. Higher cortical dysfunction
    a. Dominant = aphasia
    b. Non-dominant = neglect, apraxia
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96
Q

PACS?

A

2/3 of:

  1. Hemiparesis and/or sensory deficit
  2. Homonymous hemianopia
  3. Higher cortical dysfunction
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97
Q

POCS?

A 
Vertebrobasilar territory
1 of:
1. Brainstem or cerebellar syndrome
2. LOC
3. Isolated homonymous hemianopia
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98
Q

LACS?

A

Infarct around basal ganglia, internal capsule, thalamus and pons

  1. Pure sensory stroke
  2. Pure motor stroke
  3. Sensorimotor stroke
  4. Ataxic hemiparesis
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99
Q

Mx of Stroke?

A
  1. Resus
  2. Monitor
  3. bloods
  4. Imaging
  5. Medical
  6. Surgery
  7. Stroke unit
  8. Secondary prevention
  9. Rehabilitation
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100
Q

Stroke resus?

A
  1. Airway patent, consider NGT
  2. NBM until swallow assessment by SALT
  3. Dont overhydrate, risk of cerebral oedema
  4. BM: exclude hypogylcaemia
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101
Q

Stroke monitoring?

A
  1. Glucose = 4-11mM, sliding scale if DM
  2. BP = Rx of HTN can reduce cerebral perfusion
  3. Neuro obs
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102
Q

Stroke bloods?

A
  1. FBC = sepsis may –> stroke
  2. U&E = e- disturbance may mimic stroke
  3. Glucose = exclude hypoglycaemia
  4. Clotting = high or low INR may indicate cause
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103
Q

Stroke imaging?

A
  1. CT head

2. Diffusion weighted MRI

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104
Q

Medical stroke Mx?

A
  1. Consider alteplase if <4.5hrs since onset of Sx

2. Aspirin 300mg PO/PR once haemorrhagic stroke excluded +/- PPI

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105
Q

Stroke surgical Mx?

A
  1. Neurosurgical opinion if intracranial haemorrhage
  2. May coil bleeding aneurysms
  3. Decompressive hemicraniectomy for some forms of MCA infarction
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106
Q

Stroke unit?

A
  1. Specialist nursing and physio
  2. Early mobilisation
  3. DVT prophylaxis
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107
Q

Stroke work-up?

A
  1. ECG +/- 24hr tape
  2. Bloods = FBC, U&E, Glucose, Lipids, clotting and thrombophilia screen, vasculitis (ESR, ANA)
  3. Imaging = CXR, Carotid doppler, echo
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108
Q

Thrombophilia screen?

A
  1. FBC, clotting, fibrinogen conc.
  2. APC resistance/FV Leiden
  3. Lupus anticoagulant
  4. Anti-cardiolipin Abs
  5. Protein C and S and AT3 activity assays
  6. PCR for prothrombin gene mutation
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109
Q

Stroke secondary prevention/

A
  1. Statin after 48hrs
  2. Aspirin/clopi for 2 weeks after stroke and then
    a. Clopidogrel 75mg OD OR
    b. Aspirin 75mg OD + Dipyramidole MR 200mg BD
  3. Warfarin instead of asp/clopi if cardioembolic stroke/chronic AF, start from 2 weeks post-stroke
  4. Carotid endarterectomy if good recovery + ipsilateral stenosis >=70%
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110
Q

Stroke rehab?

A

MENDS

  1. MDT = physio, SALT, dietician, OT, specialist nurses, neurologist, family
  2. Eating = swallow screen, malnutrition screen (MUST)
  3. Neurorehab = physio and SALT
  4. DVT prophylaxis
  5. Sores = avoided
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111
Q

MS defn?

A

A chronic inflammatory demyelinating disorder of the CNS characterised by two or more lesions disseminated in time and space

112
Q

MS epidemiology?

A
  1. Lifetime risk = 1/1000
  2. Age = mean of 30 y/o
  3. Sex = 3F:1M
  4. Rarer in blacks
113
Q

MS Aetiology?

A
  1. Genetic = HLA-DRB1, HLA DR2, Il2, IL7

2. Environmental = Latitude, EBV

114
Q

MS Pathophysiology?

A
  1. CD4 cell mediated destruction of oligodendrocytes –> demyelination and eventual neuronal death
  2. Initial viral inflammation primes humoral Ab response vs. MBP
  3. Plaques of demyelination are hallmark
115
Q

Classification of MS?

A
  1. Relapsing Remitting (80%)
  2. Primary Progressive
  3. Secondary Progressive
  4. Progressive Relapsing
116
Q

MS presentation?

A

TEAM

  1. Tingling
  2. Eye = optic neuritis (decreased central vision and eye movement pain)
  3. Ataxia + other cerebellar signs
  4. Motor = usually spastic paraparesis
117
Q

Clinical features of MS?

A
  1. Eye = Optic neuritis, INO, RAPD
  2. Sensory = paraesthesia, reduced vibration sense, trigeminal neuralgia
  3. Motor = spastic weakness, transverse myelitis
  4. Cerebellum = cerebellar features
  5. GI = swallowing disorders, constipation
  6. Sexual = ED + anorgasmia, retention, incontinence
118
Q

Lhermitte’s sign?

A

Neck flexion –> electric shocks in trunk/limbs

119
Q

Optic neuritis clinical features?

A
  1. Pain on movement, rapid decrease in central vision
  2. Uhthoff’s = vision decreases with heat
  3. O/E = reduced acuity, reduced colour vision, white disc, central scotoma, RAPD
120
Q

Internuclear ophthalmoplegia?

A

A disorder of conjugate lateral gaze in which the affected eye shows impairment of adduction, and nystagmus in the unaffected eye

121
Q

INO cause?

A

Lesion to the MLF connecting CN6 to CN3

122
Q

MS Ix?

A
  1. CSF = oligoclonal bands
  2. MRI = periventricular white matter plaques
  3. VEPs = delayed velocity but normal amplitude
  4. Abs = anti-MBP, NMO-IgG
123
Q

NMO-IgG AKA and for what condition?

A

Anti-AQP4, for Devic’s disease

124
Q

Devic’s disease aka?

A

Neuromyelitis optica

125
Q

Neuromyelitis optica?

A

A heterogeneous condition consisting of the inflammation and demyelination of the optic nerve (optic neuritis) and the spinal cord (myelitis). It can be monophasic or recurrent. Currently at least three different kinds are proposed based on the presence of autoantibodies thought to produce the disease: anti-AQP4, anti-MOG and anti-NF.

126
Q

3 inflammatory conditions that may mimic MS plaques?

A
  1. CNS sarcoidosis
  2. SLE
  3. NMO
127
Q

MS acute attack Mx?

A
  1. Methylprednisolone 1g IV/24hr for 3 days

2. Doesnt influence long term outcome, decreases duration and severity of attacks

128
Q

MS relapse preventers?

A
  1. IFNB
  2. Natalizumab = anti-VLA4 Ab
  3. Alemtuzumab = anti-CD52
129
Q

MS symptomatic tx?

A
  1. Acute = methylprednisolone
  2. Antispasmodics = baclofen, botulinum
  3. Neuropathic pain = carbamazepine
  4. Depression = SSRI
  5. ED = sildafenil
  6. Tremor = clonazepam
  7. Laxatives and intermittent catheterisation
130
Q

MND Examination?

A
  1. Inspection = wasting and fasciculation
  2. Tone = spastic
  3. Power = weak
  4. Reflexes = absent and/or brisk (e.g. absent knee jerks with extensor plantars)
  5. Sensation = normal
  6. Completion = speech, jaw-jerk, eye movements
131
Q

MND eyes?

A

MND does not involve the eyes

132
Q

MND speech?

A
  1. Bulbar = nasal

2. Pseudobulbar = hot potato

133
Q

MND jaw-jerk?

A
  1. Bulbar = absent

2. Pseudo-bulbar = brisk

134
Q

MND DDx?

A
  1. Cervical cord compression –> myelopathy
  2. Brainstem lesions
  3. Polio = asymmetrical LMN paralysis
  4. Mixed UMN and LMN signs
135
Q

Mixed UMN and LMN signs?

A

MAST

  1. MND
  2. Ataxia, Friedrichs
  3. SCDC: b12
  4. Taboparesis
136
Q

MND Ix?

A
  1. LP = exclude inflammatory cause
  2. Brain/cord MRI = exclude structural cause
  3. EMG = fasciculation
137
Q

MND diagnostic criteria?

A

Revised El Escorial criteria

138
Q

MND Mx?

A
  1. General
  2. Specific
  3. Supportive
139
Q

MND General Mx?

A
  1. MDT

2. Discussion of end-of-life decisions = Advanced directive, DNAR

140
Q

MND Specific Mx?

A

Riluzole = antiglutaminergic that prolongs life by approx. 3m

141
Q

MND Supportive Mx?

A

DR DPS

  1. Drooling = amitryptiline
  2. Resp. failure = NIV
  3. Dysphagia = NG/PEG feeding
  4. Pain = analgesic ladder
  5. Spasticity = baclofen, botulinum
142
Q

MND prognosis?

A

Most die within 3 years due to bronchopneumonia and respiratory failure

143
Q

MND classification?

A
  1. Amyotrophic Lateral Sclerosis (50%)
  2. Primary Lateral Sclerosis (30%)
  3. Progressive Muscular Atrophy (10%)
  4. Progressive Bulbar Palsy (10%)
144
Q

Amyotrophic lateral sclerosis?

A

Disorder of corticospinal tracts –> UMN and LMN signs and fasciculation

145
Q

Primary lateral sclerosis?

A
  1. Loss of Betz cells in motor cortex –> mainly UMN signs
  2. Marked spastic leg weakness and pseudobulbar palsy
  3. No cognitive decline
146
Q

Progressive muscular atrophy?

A
  1. Anterior horn cell lesion –> LMN signs only
  2. Distal to proximal
  3. Better prognosis cf. ALS
147
Q

Progressive bulbar palsy?

A

Only affects CN 9-12 –> bulbar palsy

148
Q

LMN pathology?

A

Anywhere from anterior horn cell to muscle itself

149
Q

LMN signs?

A
  1. Inspection = wasting, fasciculations
  2. Tone = reduced
  3. Power = weak
  4. Reflexes = hyporeflexia
150
Q

Bilateral, symmetrical, distal LMN signs name?

A

Motor peripheral polyneuropathy

151
Q

Motor peripheral polyneuropathy DDx?

A
  1. HSMN
  2. Paraneoplastic
  3. Lead poisoning
  4. Acute = GBS, Botulism
152
Q

Bilateral, symmetrical, proximal LMN signs name?

A

Proximal myopathy

153
Q

Proximal myopathy DDx?

A
  1. Inherited = muscular dystrophy
  2. Inflammation = polymyositis, dermatomyositis
  3. Endocrine = Cushings, Acromegaly, Thyrotoxicosis, Osteomalacia, Diabetic Amyotrophy
  4. Drugs = alcohol, statins, steroids
  5. Malignancy = paraneoplastic
154
Q

Unilateral LMN signs isolated to single limb with no sensory signs?

155
Q

Unilateral LMN signs localised to group of muscles with same supply?

A
  1. Segmental = nerve roots, plexus

2. Peripheral = mononeuropathy

156
Q

Hand wasting DDx?

A
  1. Anterior horn = syringomyelia, MND, polio
  2. Roots (C8-T1) = spondylosis
  3. Brachial plexus = compression (cervical rib), avulsion (Klumpke’s palsy)
  4. Neuropathy = Generalised (HSMN), mononeuritis multiplex (DM), compressive mononeuropathy
  5. Muscle = disuse (RA), distal myopathy (myotonic dystrophy)
157
Q

Proximal myopathy Ix?

A
  1. Bloods = DM, muscle damage (CK, ESR, LDH), Endo (TSH, Ca, 9am cotrisol, IGF1), Abs (anti-Jo1)
  2. CXR = paraneoplastic
  3. EMG
  4. Genetic analysis
  5. Muscle biopsy
158
Q

Mononeuropathy Ix?

A
  1. Bloods = DM, B12, Folate, vasculitis (ESR, ANA, ANCA)

2. EMG + Nerve conduction

159
Q

Radiculopathy Ix?

160
Q

Peripheral polyneuropathy causes?

A
  1. Mainly sensory

2. Mainly motor

161
Q

Mainly sensory peripheral polyneuropathy cause?

A
  1. DM
  2. Alcohol
  3. B12
  4. CKD
  5. Ca (paraneoplastic)
  6. Vasculitis
  7. Drugs = isoniazid, vincristine
162
Q

Mainly motor peripheral polyneuropathy?

A
  1. HMSN (CMT)
  2. Paraneoplastic
  3. Lead poisoning
  4. Acute = GBS and botulism
163
Q

Peripheral polyneuropathy Ix?

A
  1. Bedside = dipstisk, glucose
  2. Bloods = DM, B12, FBC, U&E, LFT, TFTs, vasculitis
  3. CXR = paraneoplastic
  4. Nerve conduction studies
  5. EMG
  6. Genetic = PMP22 in CMT
  7. Nerve biopsy
164
Q

Nerve conduction study findings and interpretations?

A
  1. Demyelination –> reduced conduction speed

2. Axonal degeneration –> decreased conduction amplitude

165
Q

DM examination of LL findings?

A
  1. Bilateral loss of ankle jerks secondary to sensory neuropathy
  2. Mononeuritis multiplex –> foot drop
166
Q

Femoral neuropathy due to DM?

A

Painful asymmetric weakness and wasting of the quads with loss of knee jerks

167
Q

5 features of diabetic autonomic neuropathy?

A
  1. Postural hypotension
  2. Gastroparesis
  3. Diarrhoea
  4. Urinary retention
  5. ED
168
Q

Charcot-Marie-Tooth syndrome aka?

A
  1. Hereditary Motor and Sensory Neuropathy

2. Peroneal Muscular Atrophy

169
Q

CMT syndrome examination?

A
  1. Inspection = pes cavus, symmetrical distal muscle wasting, thickened nerve (esp. common peroneal around fibula)
  2. Motor = high stepping gait due to foot drop, weak foot and toe dorsiflexion, absent ankle jerks
  3. Sensory = variable loss of sensation in a stocking distribution
170
Q

What is CMT?

A

A group of inherited motor and sensory neuropathies

  1. HMSN1 = most common form, demyelinating, AD mutation in PMP22 gene
  2. HMSN2 = second commonest form, axonal degeneration, AD
171
Q

CMT syndrome nerve conduction studies?

A
  1. HMSN1 = demyelinating = reduced conduction velocity

2. HMSN 2 = axonal degeneration = reduced conduction amplitude

172
Q

Mx of CMT syndrome?

A

Supportive

  1. MDT
  2. Foot care and careful shoe choice
  3. Orthoses = e.g. ankle brace
173
Q

Myasthenia Gravis exam?

A
  1. Inspection = thymectomy scar
  2. Eyes = bilateral ptosis worse on sustained upward gaze, complex ophthalmoplegia
  3. Facial movements = myasthenic snarl on smiling
  4. Voice = nasal, fatigue (count backwards)
  5. Limbs = fatiguability (flap arm)
  6. Completion = resp function (spirometry)
174
Q

Myasthenia Gravis Ix?

A
  1. Bloods = Anti-AChR, Anti-MuSK, TFTs
  2. Tensilon test (improvement with edrophonium, an anticholinesterase) –> can cause heart block and even asystole
  3. EMG = decremented response to a titanic train of impulses
  4. CT mediastinum
175
Q

Myasthenia associations?

A
  1. <50 y/o, female = AI –> DM, SLE, RA, Graves

2. >50 y/o, male = Thymoma

176
Q

Myasthenia Mx?

A
  1. Acute = Plasmapharesis/IVIG, consider ventilation

2. Chronic = Pyridostigmine, Immunosuppression (steroids and azathioprine), thymectomy (benefit even if no thymoma)

177
Q

LEMS?

A
  1. Abs vs. VGCC
  2. Often paraneoplastic e.g. SCLC
  3. Lower limb girdle weakness
  4. Weakness improves upon repetitive testing
178
Q

DDx for bilateral ptosis?

A
  1. MG
  2. Myotonic dystrophy
  3. Congenital
  4. Senile
  5. Bilateral Horner’s
179
Q

GBS classification?

A
  1. AIDP = acute inflammatory demyelinating polyneuropathy

2. Miller fisher = ophthalmolplegia + ataxia + areflexia

180
Q

Pathophysiology of GBS?

A
  1. Molecular mimicry: Abs cross react with ganglioside
  2. Bacteria = C.jejuni, mycoplasma
  3. Viruses = CMV, EBV
181
Q

Features of GBS?

A
  1. Symmetrical ascending flaccid paralysis
  2. Sensory disturbance = paraesthesia
  3. Autoimmune neuropathy = labile BP
182
Q

GBS Ix?

A
  1. Bedside = stool MC + S
  2. Bloods = Infection, anti-ganglioside Abs
  3. LP = raised CSF protein
  4. Nerve conduction studies = demyelination
183
Q

GBS Mx?

A
  1. Supportive = 4As
  2. Immunosuppression = IVIG, Plasma exchange
  3. Physio = prevent flexion contractures
184
Q

GBS supportive Mx?

A

4As

  1. Airway/ventilation = ITU if FVC <1.5L
  2. Analgesia = NSAIDs, gabapentin
  3. Autonomic = inotropes, catheter
  4. Antithrombotic = TEDS, LMWH
185
Q

GBS prognosis?

A
  1. 85% complete recovery
  2. 10% unable to walk alone at 1 year
  3. 5% mortality
186
Q

Facial nerve palsy examination?

A
  1. Inspection

2. Weakness

187
Q

Facial nerve palsy examination on inspection?

A
  1. Unilateral facial droop
  2. Absent nasolabial fold
  3. Absent forehead creases
  4. Scar or parotid mass
  5. Ear rash
188
Q

Facial nerve palsy weakness examination?

A
  1. Raising eyebrows = frontalis
  2. Screwing up eyes = orbicularis oculi (Bell’s sign = eyeball rolls back on closure)
  3. Smiling = orbicularis oris
189
Q

UMN or LMN facial palsy?

A

UMN –> sparing of frontalis and orbicularis oculi due to bilateral cortical representation

190
Q

Millard-Gubler syndrome?

A

Due to unilateral lesion in ventral pons

  1. CN6 nucleus –> ipsilateral lateral rectus palsy
  2. CN7 nucleus –> ipsilateral LMN facial palsy
  3. Corticospinal tracts –> contralateral hemiparesis
191
Q

CPA lesions?

A

Ipsilateral CN 5,6,7,8 palsies and cerebellar signs
5. Facial anaesthesia and absent corneal reflex
6. Lateral rectus palsy
7. LMN facial nerve palsy
8. SNHL
Cerebellar. DANISH

192
Q

Causes of facial nerve palsy?

A
  1. Idiopathic Bell’s Palsy
  2. Supranuclear = vascular, SOL, MS
  3. Pontine = vascular, SOL, MS
  4. CPA = vestibular schwannoma, meningioma, mets
  5. Intra-temporal = Ramsay-Hunt, cholesteatoma, trauma
  6. Infra-temporal = Parotid tumour, trauma
  7. Systemic
    a. Neuropathy = DM, Lyme, Sarcoidosis
    b. Pseudopalsy = MG
193
Q

5 causes of bilateral facial nerve palsy?

A
  1. Infection = Lyme
  2. Inflammation = GBS, Sarcoidosis
  3. Bilateral Bell’s
  4. Pseudopalsy = MG, myotonic dystrophy
194
Q

Hyperacusis path in facial nerve palsy?

A
  1. Chorda tympani and nerve to stapedius arise just distal to geniculate ganglion w/in the temporal bone
  2. Hyperacusis thus indicates a proximal lesion
  3. Common in Ramsay Hunt due to VZV at geniculate ganglion
195
Q

Facial Nerve Palsy Ix?

A
  1. Bedside = urine dip for glucose
  2. Bloods = DM, VZV serology, Lyme serology, anti-AChR
  3. Imaging = MRI posterior cranial fossa
  4. Pure tone audiometry
  5. LP = exclude infection
  6. Nerve conduction studies = may predict delayed recovery when performed @ 2 weeks
196
Q

Facial nerve palsy Mx?

A
  1. Prednisolone w/in 72hrs
  2. Valaciclovir if VZV suspected
  3. Protect eye = dark glasses, artificial tears, tape closed @ night
197
Q

Facial nerve palsy prognosis?

A
  1. Incomplete paralysis = recovers completely w/in weeks
  2. Complete paralysis = 80% have full recovery, remained have delayed recovery/permanent neurological/cosmetic abnormalities
198
Q

Complications of facial nerve palsy?

A
  1. Synkinesis = blinking causes upturning of mouth

2. Crocodile tears syndrome = eating stimulates unilateral lacrimation, not salivation

199
Q

4 key causes of facial nerve palsy?

A
  1. Bell’s Palsy
  2. Ramsay Hunt Syndrome
  3. Cholesteatoma
  4. Lyme disease
200
Q

Bell’s palsy quick facts?

A
  1. Idiopathic facial nerve palsy responsible for 75%
  2. Is a Diagnosis of exclusion
  3. Inflammatory oedema –> compression of CN7 in narrow facial canal
  4. Probably of vial origin (HSV1)
201
Q

Features of Bell’s palsy?

A
  1. Sudden onset
  2. Complete LMN facial palsy
  3. Ageusia = corda tympani
  4. Hyperacusis = stapedius
  5. Associated with other CN involvement in 8%
202
Q

Ramsay Hunt syndrome defn?

A

Facial nerve palsy caused by reactivation of VZV in the geniculate ganglion of CNVII

203
Q

Ramsay Hunt syndrome features?

A
  1. Preceding ear pain or stiff neck
  2. Vesicular rash in auditory canal +/- TM, pinna, tongue, hard palate
  3. Ipsilateral facial nerve weakness, ageusia, and hyperacusis
  4. May affect CN8 –> vertigo, tinnitus, deafness
204
Q

Ramsay Hunt mx?

A

Prednisolone and valaciclovir w/in 72hrs

205
Q

Ramsay Hunt prognosis?

A
  1. Rxed w/in 72hrs = 75% full recovery

2. Otherwise: 1/3rd recover, 1/3rd partial, 1/3rd poor

206
Q

Cholesteatoma defn?

A
  1. Locally destructive expansion of stratified squamous epithelium within the middle ear
  2. Usually secondary to attic perforation in chronic suppurative otitis media
207
Q

Cholesteatoma presentation?

A
  1. Foul smelling white discharge
  2. Vertigo, deafness, headache, pain, facial paralysis
  3. Appears pearly white with surrounding inflammation
208
Q

3 complications of cholesteatoma?

A
  1. Deafness (ossicle destruction)
  2. Meningitis
  3. Cerebral abscess
209
Q

Early features of lyme disease?

A
  1. Erythema chronicum migrans

2. Systemic malaise

210
Q

Late features of lyme disease?

A
  1. Neuro = facial palsy, polyneuropathy, meningoencephalitis
  2. Heart = myocarditis, heart block
  3. Joints = Arthritis
211
Q

Causes of facial anaesthesia?

A
  1. Supranuclear = Infarct, MS, SOL
  2. Nuclear = CPA lesion, lateral medullay syndrome
  3. Peripheral mononeuropathy (DM, sarcoid, vasculitis, cavernous sinus)
212
Q

Horners examination?

A
  1. Face = miosis, ptosis, anhydrosis, enophthalmos
  2. Neck = central lines/carotid endarterectomy
  3. Hands = complete claw hand + intrinsic hand weakness, decreased/absent sensation in T1
  4. Completion = cerebellum, CNs, PNS
213
Q

Horners defn?

A

AKA oculosympathetic paresis, is a combination of symptoms that arises when the sympathetic trunk is damaged

214
Q

Horners DDx?

A
  1. Central = MS, Wallenberg’s
  2. Preganglionic (neck) = Pancoast’s tumour (T1 nerve root lesion), Trauma (CVA insertion or carotid endarterectomy)
  3. Post-ganglionic = Cavernous sinus thrombosis (usually 2ary to spreading facial infection via the ophthalmic veins –> CN 3,4,5,6 palsies)
215
Q

3rd nerve palsy features?

A
  1. Ptosis
  2. Down and out
  3. Fixed, dilated pupil
  4. Ophthalmoplegia and diplopia
216
Q

Medical 3rd nerve palsy?

A
  1. MS
  2. Mononeuritis multiplex (Mellitus)
  3. Midbrain infarct
  4. Migraine
217
Q

Surgical 3rd nerve palsy?

A
  1. Cavernous sinus thrombosis
  2. Posterior communicating artery aneurysm
  3. Cerebral uncal herniation
  4. Cancer
218
Q

Holmes-Adie (Myotonic) Pupil?

A
  1. Dilated pupil that has no response to light and sluggish response to accomodation
  2. Reduced or absent ankle and knee jerks
  3. Benign condition, more common in young females
219
Q

Argyll-Robertson Pupil features?

A
  1. Small, irregular pupils
  2. Accommodate but doesnt reaction to light
  3. Atrophied and depigmented iris
220
Q

Causes of Argyll-Robertson pupil?

A
  1. Quaternary syphilis

2. DM

221
Q

Marcus Gunn pupil aka?

222
Q

RAPD features?

A
  1. Minor constriction to direct light

2. Dilatation on moving light from normal to abnormal eye

223
Q

Features of optic atrophy?

A
  1. Decreased visual acuity
  2. Decreased colour vision
  3. Central scotoma
  4. Pale optic disc
  5. RAPD
224
Q

Causes of RAPD?

A

CAC VISION

  1. Congenital = Leber’s hereditary optic neuropathy, CMT, Friedrich’s, DIDMOAD
  2. Alcohol and Toxins = ethambutol, lead, B12 def.
  3. Compression = neoplasia, glaucoma, Paget’s
  4. Vascular = DM, GCA, thromboembolic
  5. Inflammatory = Optic neuritis = MS, Devic’s, DM
  6. Sarcoid = or other inflammatory
  7. Infection = HZV, TB, syphilis
  8. Oedema = papilloedema
  9. Neoplastic infiltration = lymphoma, leukaemia
225
Q

DIDMOAD?

A

Diabetes Insipidus, Diabetes Mellitus, Optic Atrophy and Deafness

226
Q

Visual pathway?

A
  1. Retina
  2. Optic nerve
  3. Optic chiasm
  4. Optic tract
  5. LGN of thalamus
  6. Optic radiation
    a. superior field = temporal
    b. inferior field = parietal
  7. Visual cortex
227
Q

Visual pathway Ix?

A
  1. Perimetry

2. CT/MRI brain

228
Q

Homonymous hemianopia quick facts?

A
  1. Retrochiasmatic
  2. Greater defect = larger lesion or closer to chiasm
  3. Contralateral
229
Q

Homonymous hemianopia extra examination?

A
  1. Examine for ipsilateral hemiparesis
  2. Examine for cerebellar signs
  3. Right = test for neglect
  4. Left = test for aphase
230
Q

How does MCA stroke affect vision?

A

MCA supplies optic radiation in the temporal and parietal lobes

231
Q

How does PCA stroke affect vision?

A

PCA supplies occipital love and visual cortex –> homonymous hemianopia with macula sparing

232
Q

Causes of homonymous hemianopia?

A
  1. Vascular = ischaemia or haemorrhage
  2. SOL = tumour, abscess
  3. MS
233
Q

Bitemporal hemianopia lesion?

A

Chiasmatic lesion

234
Q

3 conditions to look for with bitemporal hemianopia?

A
  1. Prolactinoma
  2. Acromegaly
  3. Cushings
235
Q

Causes of bitemporal hemianopia?

A
  1. Pituitary tumour = from below = descending visual loss

2. Craniopharyngioma = from above = ascending visual loss

236
Q

What is a craniopharyngioma?

A

A benign suprasellar tumour originating from Rathke’s pouch, that calcifies as it arises from the odontogenic epithelium

237
Q

How to check for monocular blindness?

A

Check counting fingers, movement and light perception

238
Q

Cause of monocular blindness?

A

Lesion proximal to optic chiasm

  1. Eye itself = cornea, vitreous, retina
  2. Optic nerve = e.g. optic neuropathy
239
Q

Ophthalmoplegia defn?

A

Weakness or paralysis of one of the extraocular muscles

240
Q

Ophthalmoplegia exam?

A
  1. Inspection = ptosis, alignment, pupil sizes
  2. Ask pt to tell you if they get double vision
  3. H test = ophthalmoplegia, nystagmus, diplopia (do cover test)
  4. Saccades = vertical and horizontal
241
Q

Diplopia key facts?

A
  1. Maximal in direction of pull of affected muscle

2. Cover test = outer image disappears with affected eye

242
Q

3rd nerve palsy?

A
  1. Ptosis
  2. Down and out at rest
  3. Fixed, dilated pupil
  4. Diplopia maximal = up and in
243
Q

4th nerve palsy?

A
  1. Slight head tilt = ocular torticollis
  2. Normal at rest
  3. Failure to depress eye during adduction
  4. Diplopia maximal = down and in
244
Q

6th nerve palsy?

A
  1. Normal in resting position
  2. Failure to abduct
  3. Diplopia maximal in abduction
  4. Commonly a false localising sign of raised intracranial pressure (contralateral lesion)
245
Q

Causes of simple eye nerve palsies?

A
  1. CNS = Vascular, MS, SOL

2. Peripheral = DM, compression, trauma

246
Q

Ophthalmoplegia Ix?

A
  1. Bedside = urine dip for glucose
  2. Bloods = glucose and HbA1c
  3. Imaging = MRI brain
247
Q

4 causes of Internuclear ophthalmoplegia?

A
  1. MS
  2. Infarct = ischaemic or haemorrhagic
  3. Syringomyelia
  4. Phenytoin toxicity
248
Q

Complex ophthalmoplegia?

A

Diagnosis of exclusion when ophthalmoplegia doesnt fit a single pattern

249
Q

Causes of Complex ophthalmoplegia?

A
  1. DM
  2. MS
  3. MG
  4. Thyrotoxicosis
250
Q

Complex ophthalmoplegia Ix?

A
  1. Bedside = urine dip for glucose
  2. Bloods = BMs, TFTs, anti-AChR
  3. MRI brain = plaques in periventricular white matter
251
Q

Hearing loss tuning fork?

252
Q

Rinne’s test positive?

A

AC > BC (Normal)

253
Q

Rinne’s test negative?

A

BC > AC

  1. true = conductive deafness
  2. false = complete SNHL
254
Q

Weber’s test normal?

255
Q

Weber’s test SNHL?

A

Lateralises to normal ear

256
Q

Weber’s test CHL?

A

Lateralises to abnormal ear

257
Q

Causes of conductive hearing loss?

A

Impaired conduction anywhere b/w auricle and round window

  1. Canal obstruction = wax, FB
  2. TM perforation = trauma, infection
  3. Ossicle defects = otosclerosis, infection
  4. Fluid in middle ear
258
Q

Causes of sensory hearing loss?

A

Defects of cochlea, cochlear nerve, or brain

  1. Congenital
  2. Acquired
259
Q

Congenital SNHL?

A
  1. Alports = SNHL + haematuria

2. Jervell Lange-Nielsen = SNHL + LQT

260
Q

Acquired SNHL?

A
  1. Presbyacusis
  2. Drugs = gentamicin, vancomycin
  3. Infection = meningitis, measles
  4. Tumour = vestibular schwannoma
261
Q

Speech test components?

A
  1. Quick screen
  2. Dysphonia
  3. Dysarthria
  4. Dysphasia
262
Q

Dysphonia?

A

Impaired production of voice sounds

263
Q

Dysarthria?

A

Impaired articulation of sound into words

264
Q

Dysphasia?

A

Impairment of language

265
Q

Quick screen for speech exam?

A

How did you get here today?

  1. Listen to volume, rhythm, clarity and content
  2. Any striking abnormality?
266
Q

Dysarthria?

A
  1. Repetition
    a. Yellow lorry = lingual sounds
    b. Baby hippopotamus = labial sounds
    c. The Leith police dismisseth us = multiple processes
  2. Count to 30 = muscle fatigue in MG
267
Q

Dysphonia?

A
  1. Say ahh = vocal cord tension
  2. Cough = bovine
  3. Voice = quiet or hoarse
268
Q

Dysphasia?

A
  1. Name 3 animals = nominal dysphasia
  2. 3 step command = receptive dysphasia
  3. Repeat sentence = conductive dysphasia
269
Q

Dominant parietal lobe speech lesion additional exams?

A
  1. Dyslexia = read a paragraph

2. Dysgraphia = write a sentence

270
Q

Causes of dysphonia?

A
  1. Vocal cord pathology = laryngitis, tumour, nodule

2. Recurrent laryngeal nerve palsy

271
Q

Dysarthria pathophysiology?

A

Lesion in tongue, lips, mouth or disruption of NM pathway

  1. Bulbar = unilateral UMN weakness, palatal weakness –> donald duck speech
  2. Pseudobulbar = bilateral UMN lesions –> spastic dysarthria, difficult lingual sounds –> hot potato speech, brisk jaw jerk
272
Q

Bulbar dysarthria causes?

A
  1. Brainstem infarct
  2. MND
  3. GBS
273
Q

Pseudobulbar dysarthria causes?

A
  1. CVA e.g. bilateral internal capsule infarcts
  2. MND
  3. MS
274
Q

Dysphasia causes?

A
  1. Expressive = Broca’s, frontal lobe, non-fluent speech, comprehension intact
  2. Receptive = Wernicke’s, temporal lobe, fluent but meaningless speech, comprehension impaired
  3. Conductive = Arcuate fasiculus, comprehension intact, unable to repeat words or phrases
275
Q

Parkinsons deep brain stimulation happens to structures?

A

Subthalamic nucleus or globus pallidus

Medicine and Surgery Mushkies (52 decks)

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