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Selected Notes neuro 1 Flashcards

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1
Q

What is a subarachnoid haemorrhage?

A

<ul><li>Blood within the subarachnoid space(under arachnoid mater)</li><li><img></img><br></br></li></ul>

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2
Q

Describe the epidemiology of SAH

A

<ul><li>F&gt;M</li><li>Peak incidence: 40-50 years</li><li>80% without trauma due to a ruptured berry aneurysm</li></ul>

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3
Q

What is the most common cause of a SAH

A

<ul><li>Head injury</li></ul>

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4
Q

Name some risk factors for developing a Berry aneurysm?

A

<ul><li>Hypertension</li><li>Adult polycystic kideny disease</li><li>EDS</li><li>Coarctation of the aorta</li></ul>

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5
Q

Name the symptoms of a SAH

A

<ul><li>Sudden onset 'thunderclap' headache, peaks in intensityin 1-5 minutes</li><li>May have history of previous less severe 'sentinel' headache</li><li>Altered consciousness</li><li>Nausea and&nbsp; vomiting</li><li>Seizures</li><li>Meningism: photophobia and neck stifness</li></ul>

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6
Q

Name the signs of an SAH

A

<ul><li>Fundoscopy: retinal haemorrhage</li><li>Positive Kernig's/Brudzinksi's sign</li><li>Focal neurological deficits</li></ul>

<div>CN3/4/6-diplopia</div>

<div>Hemiparesis/hemiplegia</div>

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7
Q

What investigations should be done in a patient with a SAH

A

<ul><li>Non contrast CT head-&gt;hyperdense blood in basal cistern</li><li>If normal &gt;6 hours post onset:</li><li>LP if &gt;12 hours post onset: xanthochromia&nbsp;</li><li>CT angiogram to check for aneurysms or vascular abnormalitis</li></ul>

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8
Q

Describe the treatment for an SAH

A

<ul><li>Oral nimodipine to prevent vasospasm-&gt; ischaemic damage</li><li>Coiling, stenting or clipping of aneurysms: neurosrugery</li></ul>

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9
Q

Name some complications of an SAH

A

<ul><li>Re-bleeding</li><li>Hydrocephalus</li><li>Vasospasm</li><li>Hyponatraemia-&gt;SIADH</li><li>Seizures</li></ul>

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10
Q

Describe the prognosis of a patient with an SAH

A

<ul><li>If untreated: 50% mortality</li><li>Of those who survive the 1st month: 50% will beocme dependent, 85% recovery in those admitted to neurosurgical unit</li></ul>

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11
Q

Name some predictive factors for the outcome of a patient with an SAH

A

<ul><li>Age</li><li>Consciousness level on admission</li><li>Amount of blood visible on CT head</li></ul>

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12
Q

Describe the pathophysiology of a patient with a TIA

A

<ul><li>Transient disruption of blood flow to a specific region of the CNS resulting in ischaemia</li></ul>

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13
Q

Describe the presentaiton of a patient with a TIA

A

<ul><li>Completely resolves within 24 hours</li><li>Stroke symptoms</li></ul>

<div>Aphasia/dysarthria</div>

<div>Unilateral weakness/sensory loss</div>

<div>Ataxia, vertigo, balance issues</div>

<div>Visual: amaurosis fugax, diplopia, HH</div>

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14
Q

What investigations should be done in a patient with a suspected TIA?

A

<ul><li>Neuroimaging: MRI(ischaemia, haemorrhage, other pathologies)</li><li>Carotid dopple USS-&gt; atherosclerosis</li><li>Echo: cardiac thrombus</li><li>24hr ECG: AF</li><li>Bloods: glucose, lipid profile, clotting</li></ul>

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15
Q

What is the immediate treatment for a patient with a TIA?

A

<ul><li>Immediate antithrombotic therapy: aspirin 300mg unless CI</li></ul>

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16
Q

Name some contraindications for aspirin therpay in a patient with a TIA

A

<ul><li>Bleeding disorder</li><li>Already on aspirin</li></ul>

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17
Q

For a patient with a TIA in the last 7 days, how urgently should they be reviewed by a specialist?

A

<ul><li>&lt;7 days: urgent assessment within 24 hours</li></ul>

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18
Q

For a patient with a TIA over 7 days ago, how urgently should they be reviewed by a specialist

A

<ul><li>Within 7 days</li></ul>

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19
Q

For a patient with a crescendo TIA or multiple TIAs, how urgently should they be reviewed by a specialist?

A

<ul><li>Admitted immediately</li><li>Liekly cardioembolic source</li></ul>

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20
Q

Describe the secondary management of TIA

A

<ul><li>Antiplatelet therapy: clopidogrel</li><li>Lipid moidification: atorvastatin 20-80mg daily</li><li>Carotid endartectomy if severe carotid stenosis</li></ul>

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21
Q

What is an extradural haemorrhage?

A

<ul><li>Blood collects between the dura mater(outermost meningeal layer) and inner surface of the skull</li></ul>

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22
Q

What is the most common blood vessel implicated in an extradural haemorrhage?

A

<ul><li>Middle meningeal artery-&gt; thin skull at pterion</li></ul>

<div>Usually arterial</div>

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23
Q

Describe the typical presentaiton of a patient with an extradural haemorrhage

A

<ol><li>Initial brief los sof consciousness post initial trauma</li><li>Lucid interval(regianed consciousness and apparent recovery)</li><li>Subsequent deterioration of consciousness and headache onset</li></ol>

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24
Q

Describe the pathophysiology of an extradural haemorrhage

A

<ul><li>Haematoma expands-&gt; uncus of temporal lobe herniates around the tentorium cerebelli-&gt; parasympathetic fibres of CN3 compressed-&gt; fixed and dilated pupil</li></ul>

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25
Name some differentials for a extradural haematoma
  • Subdural haemorrhage
  • SAH
  • Intracerebral haemorrhage
  • Cerebral contusion
26
What investigations should be done in a patient with an extradural haematoma?
  • CT scan: biconvex/lentiform hyperdense collection limited by the suture lines of the skull
  • Assess for midline shift/uncal herniation

27
Describe the management of an extradural haematoma
  • No neurological deficits-> conservative: supportive therapy and radiological observation
  • Definitive: craniotomy and haematoma evacuation
28
What is a subdural haemorrhage?
  • Accumulation of venous blood in the potential space between the dura mater and arachnoid mater of the brain
29
How can subdural haemorrhages be classified?
  • Acute
  • Subacute
  • Chronic
30
Describe the timeline of an acute subdural haemorrhage
  • Sx develop within 48 hours of injury-> rapid neurological deterioration
31
Describe the timeline of a subacute subdural haemorrhage
  • Sx present days-> weeks post injury-> gradual progression of neurological symptoms
32
Describe the timeline of a chronic subdural haemorrhage
  • Elderly: weeks-> months
  • Might not remember specific head injury
33
Name some risk factors for developing a subdural haemorrhage
  • Increasing age
  • Anticoag use
  • Chronic alcohol use
  • Recent trauma
  • Infants (shaken baby)
34
What kind of vessels are implicated in a subdural haemorrhage?
  • Rupture of bridging veins within subdural space
35
Describe the typical way in which a patient with a subdural haemorrhage would present?
  • History of head trauma-> lucid interval-> decline in consciousness
36
Name some clinical neurological signs you might find in a patient with a subdural haemorrhage
  • Altered/fluctuating mental status
  • Focal neurological deficits
  • Headache
  • Memory loss
  • Cognitive impariment
  • Seizures
  • Personality changes
37
Name some possible exam abnormalities in a patient with a subdural haemorrhage
  • Papilloedema (raised ICP)
  • Pupillary changes: unilateral dilated pupil-> CNS compression
  • Gait abnormalities
  • Hemiparesis/hemiplegia
  • Bradycardia, hypertension, irregular respirations (Cushing's triad)
38
What investigations should be done in a patient with a subdural heamorrhage?
  • CT scan: screscent shaped, not restricted by suture lines
  • Hyperacute(<1hr): isodense
  • Acute (<3 days): hyperdense
  • Subacute(3d-3 weeks): idosense
  • Chronic (>3 weeks): hypodense

39
Describe the management of a patient with a subdural haemorrhage
  • Conservative: monitor ICP etc
  • Acute: decompressive craniotomy
  • Chronic: Burr holes
40
What is an ischaemic stroke?
  • Sudden onset neurological deficit of vascular aetiology with symptoms lasting >24 hours
41
Describe the pathophysiology of an ischaemic stroke
  • Decrease in blood flow-> low O2 and glucose-> energy failure and disruption of cellular ion haemostasis-> exotoxicity, oxidative stress, inflammation and apoptosis-> irreversible neuronal damage
  • Can lead to cerebral oedema-> raised ICP-> secondary neuronal damage
42
Name sone strong risk factors for an ischaemic stroke
  • Increasing age
  • Male
  • Family history
  • Hypertension
  • Smoking
  • Diabetes
  • AF
43
Name some weak risk factors for an ischaemic stroke
  • High cholesterol
  • Obesity
  • Poor diet
  • Oestrogen therapy
  • Migraine
44
How is an ischaemic stroke diagnosed?
  • Non contrast CT head
  • Areas of low density/'hyperdense artery' sign
45
What is alteplase?
  • Thrombolytic: tissue plasminogen activator
46
Describe the secondary prevention of an ischaemic stroke
  • Clopidogrel 75mg 
  • Aspiring if clopidogrel CI or not tolerated
  • Carotid endartectomy  within 7 days if severe carotid stenosis
  • Atorvastatin 20-80mg OD
  • Smoking cessation and lifestyle advice
  • Hypertension treatment and diabetes check
47
What artery supplies the lateral cerebral cortex?
  • Middle cerebral artery
48
What artery supplies the anterior cerebral cortex?
  • Middle cerebral artery
49
Describe the symptoms of lateral pontine syndrome and name the implicated artery
  • Ipsilateral:
    -CN3 palsy
    -Vertigo/nystagmus/deafness
    -Poor coordination/tone/balance
  • Anterior inferior cerebellar artery
50
Describe the symptoms of Weber's syndrome
  • Ipsilateral CN3 palsy
  • Contralateral hemiparesis
51
Name some cerebellar signs
  • Nystagmus
  • Vertigo
52
Name some signs of bulbar muscle weakness
  • Dysphagia 
  • Dysarthria
53
What is Horner's syndrome?
  • Ptosis
  • Miosis
  • Anhidrosis
  • Damage to sympathetic nerve supply to the eye
54
What are the criteria for a total anterior circulation stroke?
3/3 of:
  • Unilateral weakness and/or sensory deficit of face, arm and leg
  • Homonymous hemianopia
  • Higher cerebral dysfunction(dysphasia, visuospatial disorder)
55
What are the criteria for a partial anterior circulation stroke
2/3 of:
  • Unilateral weakness and/or sensory deficit of face, arm and leg
  • Homonymous hemianopia
  • Higher cerebral dysfunction(dysphasia, visuospatial disorder)
56
What are the criteria for a posterior circulation stroke?
1/5 of:
  • Cranial nerve palsy and contralateral motor/sensory deficit
  • Bilateral motor/sensory deficit
  • Conjugate eye movement disorder(horizontal gaze palsy)
  • Cerebellar dysfunction (vertigo, nystagmus, ataxia)
  • Isolated homonymous hemianopia
57
What causes a lacunar stroke and which part of the brain does it affect?
  • Subcortical
  • Occurs secondary to small vessel disease
58
How can a lacunar stroke be differentiated from other strokes?
  • NO loss of higher cerebral function
59
What are the criteria for a lacunar stroke?
1/4 of:
  • Pure sensory stroke
  • Pure motor stroke
  • Sensori-motor stroke
  • Ataxic hemiparesis
60
What can a CN5 palsy result in?
Trigeminal
  • Trigeminal neuralgia
  • Loss of corneal reflex
  • Loss of facial sensation
  • Paralysis of mastication muscles
  • Deviation of jaw to weak side
61
What can a CN6 palsy result in?
Abducens
  • Defective abduction-> hortizontal diplopia
62
What can a CN7 palsy result in?
Facial
  • Flaccid paralysis of upper and lower face
  • Loss of corneal reflex(efferent)
  • Loss of taste
  • Hyperacusis
63
What can a CN8 palsy result in?
Vestibulocochlear
  • Hearing loss
  • Vertigo, nystagmus
  • Acoustic neuromas
64
What can CN9 palsy result in?
Glossopharyngeal
  • Hypersensitive carotid sinus reflux
  • Loss of gag reflex (afferent)
65
What can a CN10 palsy result in?
Vagus
  • Uvula deviates away from site of lesion
  • Loss of gag reflex(efferent)
66
What can a CN11 palsy result in?
Accessory
  • Weakness turning head to contralateral side
67
What can a CN12 palsy result in?
Hypoglossal
  • Tongue deviates towards the side of lesion
68
What is encephalitis?
  • Inflammation of the brain parenchyma
69
Describe the epidemiology of encephalitis
  • Peak: >70 yrs, <1 year
  • M:F 1:1
70
Describe the symptoms of encephalitis
  • Fever
  • Headaches
  • Seizures
  • Psych sympotms
  • Vomiting
  • Focal features
  • Flu-like prodromal illness
71
Name some differentials for encephalitis
  • Hypoglycaemia
  • HE
  • DKA
  • Uremic/drug induced encephalopathy
72
What investigations should be done in a patient with suspected encephalitis?
  • CSF testing: lymohocytosis, hgih protein, viral PCR analysis of CSF
  • MRI
  • EEG
  • CT
73
How is encephalitis treated?
  • 10mg/kg aciclovir TDS for 2 weeks
  • Broad spectrum antibiotics e.g. ceftriaxone
  • Supportive-seizure management
74
Name some side effects of aciclovir
  • GI changes
  • Photosensitivity and rashes
  • Acute renal failure
  • Hepatitis
75
Describe the prognosis of encephalitis
  • 10-20% mortality of treatment started promptly
  • 80% mortality if untreated
76
What is meningitis?
  • Inflammation of the meninges (dura, arachnoid, pia)
  • Can be infective or non infective
77
Describe the epidemiology of meningitis
  • Viral(enteroviruses) most common
  • Bacterial: associated with increased morbidity and mortality
  • Fungal/parasitic: rare except in immunosuppressed
78
Name the most common bacterial causes of meningitis and the groups they are present in
  • S.pneumoniae
  • N.meningitidis
  • H. influenza: infants
  • Listeria monocytogenes: Elderly
79
Name some viral causes of meningitis
  • Enteroviruses
  • Herpes
  • VZV
  • Measles/rubella
80
What is the most common fungal cause of meningitis?
  • Cryptococcus neoformans
81
Name the parasitic causes of meningitis
  • Amoeba
  • Toxoplasma gardii
82
Name some non infective causes of meningitis
  • Malignancies: leukaemia, lymphoma
  • Drugs: NSAIDs, trimethoprim
  • Systemic inflammatory diseases: Sarcoidosis, SLE, Behcets
83
Describe the symptoms of meningitis
  • Headahce
  • Fever
  • Nausea and vomiting
  • Seizures
  • Decreased consciousness
  • Photophobia
  • neck stuffness
  • Non blanching petechial/purpuric rash-> DIC
84
Name some signs in a patient with meningitis
  • Kernig's sign: Pain and resistance to knee extension
  • Brudzinski's sign: passive neck flexion results in involuntary hip and knee flexion
85
Name some differential diagnoses for meningitis
  • Encephalitis
  • SAH
  • Brain abscess
  • Sinusitis
  • Migraine
86
What investigations should be done in a patient with suspected meningitis?
  • Bloods: FBC, CRP, coag screen, cultures, PCR, glucose
  • ABG
  • CT head
  • LP and CSF analysis 
87
Describe the treatment of a patient with suspected meningitis if presenting to a GP
  • IM benzylpenicillin and urgent hospital transfer
88
Describe the treatment of a patient with suspected bacterial meningitis in hospital
  • IV cefotaxima/ceftriaxone and IV dexamethasone
  • Add amoxicillin for listeria cover(age extremes)
89
Describe the treatment of suspected viral meningitis
  • If enteroviruses: nothing
  • If HSV/VZV: aciclovir
90
What are the prophylaxis recommendations for contacts of meningitis
  • If in contact 7 days prior to onseet: One off dose of oral ciprofloxacin
91
Name some complications of meningitis
  • Sepsis
  • DIC
  • SIADH
  • Seizures
  • Waterhouse friedrichsen syndrome
  • Delayed: hearing loss, cranial nerve dysfunction, intellectual deficits, ataxia, blindness
92
What is Waterhouse friedrichsen syndrome?
  • Adrenal insufficiency caused by intra-abdominal haemorrhage from DIC
93
Name the causes of meningitis is neonates(0-3 months)
  • Group B strep
  • E.Coli
  • Gram negative bacilli
  • Listeria
  • S.pneumoniae
94
Name the causes of meningitis in infants(3 months-6 years)
  • S.pneumoniae
  • N.meningitidis
  • H. influenzae
95
Name the causes of meningitis in adults(6-60 years)
  • S.pneumoniae
  • N.meningitidis
96
Name the causes of meningitis in the elderly (>60yrs)
  • S.pneumoniae
  • N.meningitidis
  • Listeria
  • Gram negative bacilli
97
How does S.pneumoniae appear on microbiology?
  • Gram positive diplococcus in chains
98
How does Group B strep appear on microbiology?
  • Gram positive coccus in chains
99
What age groups is most likely to have meningitis cauased by Group B strep and why?
  • Neonates
  • Colonises in maternal vagina
100
What age group is most likely to get meningitis from listeria monocytogenes?
  • Extremes of age, pregnant
  • Found in cheese
101
What does listeria monocytogenes appear like on microbiology?
  • Gram positive bacillus
102
What is neurofibromatosis?
  • Genetic condiiton that causes nerve tumours(neuromas) to develop in the nervous system
  • Benign but can cause neurological/structural problems
103
What are the types of neurofibromatosis and which is more common?
  • Type 1-more common
  • Type 2
104
What is neurofibromatosis type 1 also called?
  • Von Recklinghausen's syndrome
105
Describe the inheritance pattern of neurofibromatosis type 1
  • Autosomal dominant
106
Describe the features of neurofibromatosis type 1
CRABBING
  • C{{c1::afe au lait spots(>15mm)}}
  • R{{c2::elative with F1}}
  • A{{c3::xillary/inguinal freckles}}
  • B{{c4::ony dysplasia-bowing of long bones or sphenoid wing dysplasia}}
  • I{{c5::ris hamartomas(Lisch nodules)-yellow/brown spots on iris}}
  • N{{c6::eurofibromas(over 2 significant unless more than 1 plexiform)}}
  • G{{c7::lioma of optic pathway}}
107
How is neurofibromatosis diagnosed?
  • Diagnostic criteria and genetic testing
108
Describe the treatment of neurofibromatosistype 1
  • Monitor and manage symptoms, treat complications
109
Name some complications of neurofibromatosis type 1
  • Malignant peripheral nerve sheath tumours(MPNST)
  • Gastrointestinal stromal tumours(GIST)
  • Migraines
  • Epilepsy
  • Hypertension from renal artery stenosis
  • Scoliosis
  • Brain.spinal tumours
  • High cancer risk
110
What is the inheritance pattern of neurofibromatosis type 2
  • Autosomal dominant
111
What is the main symptom/complication of neurofibromatosis type 2?
  • Bilateral acoustic neuromas
112
What is giant cell arteritis/temporal arteritis?
  • Vasculitis of unknown cause that affects medium-large sized vessel arteries, especially at the temples
  • Overlap with PMR
113
Describe the epidemiology of giant cell arteritis
  • Most common primary vasculitis
  • >50 years, peaks in 70s
  • M:F 1:3
114
Name some risk factors for giant cell arteritis
  • Genetics
  • Environmental
  • Age-fmales
  • Sex
  • Ethnicity(Mc caucasian-scandinavian)
115
Describe the presentation of a patient with giant cell arteritis
  • Usually rapid onset: <1 month
  • Temporal headache
  • Jaw claudication
  • Amaurosis fugax, diplopia
  • Tender, palpable temporal artery, scalp tenderness, bruits(rare)
  • 50% have PMR features(aching, morning proximal limb weakness, lethargy)
116
What investigations should be done in a patient with giant cell arteritis?
  • High ESR/CRP
  • Normal creatine kinase and EMG
  • Temporal artery biopsy-> granulomatous inflammatin and infiltration of giant cells
  • Doppler USS: 'halo' sign
117
Describe the managmeent of giant cell arteritis
  • Urget high dose steroids: 40-60mg prednisolone OD to prevent blindness
  • Then taper(use bisphosphonates/PPI)
  • Low dose aspiring to reduce risk of stroke/blindness
118
Name some complications of giant cell arteritis
  • Permanent monocular blindness
  • Diplopia
  • Stroke
  • Aortic aneurysms
119
How can giant cell arteritis result in permanent monocular blindness?
  • Anterior ischaemic optic neuropathy-> occlusion of posterior ciliary artery-> ischaemia of optic nerve head
120
How can giant cell arteritis cause diplopia?
  • Involvement of any paart of oculomotor system(e.g. cranial nerves)
121
What is Bell's palsy?
  • Acute, unilateral, idiopathic facial nerve paralysis
122
Describe the presentation of Bell's palsy
  • Acute(not sudden) onset of unilateral LMN facial weakness with NO foreheard sparing
  • Post auriicular otalgia(may precede paralysis)
  • Hyperacusis
  • Nervus intermedius symptoms: altered taste, dry eyes/mouth
123
Name some differential diagnoses for bell's palsy
  • Ramsay Hunt syndrome
  • Stroke-forehead sparing
  • Guillain Barre
124
What investigations might be done in a patient presenting with suspected Bell's palsy?
  • Clinical: rule out other causes/assess extent of damage
  • FBC/ESR/CRP/viral serology/lyme serology/otoscopy/EMG/MRI/CT
125
Describe the management of Bell's palsy
  • 50mg oral pred OD for 10 days then taper
  • Aciclovir in certain patients (e.g. for Ramsay Hunt)
  • Supportive: artificial tears/ocular lubricants/eye tape
126
Describe the prognosis of Bell's palsy
  • Complete recovery: 70-80% in weeks-months
  • If untreated: 15% have permanent moderate/severe weakness
127
Name some poor prognostic factors for Bell's palsy
  • Older age
  • More severe initial facial weakness
128
What is essential tremore?
  • Common movement disorder characterised by a rhythmic postural or kinetic tremor primarily affecting the upper extremities
129
Describe the epidemiology of essential tremor
  • Commmon
  • Increased age: peak 40-50 years
  • F:M:1:1
  • Family history
130
Describe the pathophysiology of essential tremor
  • GABA-ergic dysfunction-> increased activity in cerebellar-thalamic cortical circuit
131
Describe the features of essential tremor
  • Postural/kinetic tremor that predominantly affects the upper limbs distally
  • Usually bilatera: high frequency: 6-12Hz
  • Exacerbated by intentional movements, absent on rest
  • Increasing amplitude over time
  • Relieved by alcohol
  • Exacerbated by anxiety, excitement etc
  • Can affect head, lower limbs, voice, tongue, face and trunk
132
What additional features of essential tremor might prompt further investigation to look for differentials?
  • Difficulty with tandem gait
  • Mild cognitive impairment
  • Slight resting tremor alongside action tremor
133
How is essential tremor diagnosed?
  • CLinical diagnosis
  • bilateral uppper limb action tremor lasting >3 years with no other tremor/neurological signs
134
Name some differential diagnoses for essential tremor
  • Parkinson's
  • Hyperthyroidism
  • Dystonic tremor
  • Spasmodic dysphonia
135
Describe the management of essential tremor
Pharmacological:
  • Propanolol
  • Primidone
  • 2nd line: gabapentin, topirimate, nimodipine
Surgical: 
  • DBS
  • Botulinum toxin type A injections
136
Describe the prognosis of essential tremor
  • Typically worsens with increasing age
  • Can remain isolated or can spread e..g. to head or voice over years
  • Cna cause major disability
137
What is myasthenia gravis?
  • Autoimmune disease-> AChR(nicotinic ACH receptor antibodies)
138
Describe the epidemiology of myasthenia gravis
  • M:F 1:1
  • Bimodal distribution
  • Peak incidence in F<40 years and M>60 years
139
Describe the pathophysiology of myasthenia gravis
85%:
  • AChR antibodies-> lower ability of ACh to trigger muscle contractioons-> weakness
  • Also MuSK(muscle-specific kinase) and LLRP4(low density lipoprotein receptor related protein)-> creation and organisation of AChR-> inadequate AChR
140
Describe the presentation of a patient with myasethnia gravis
  • Muscle weakness that worsens with repetitive activity and weakens with rest(typically ocular/bulbar and limb muscles)
  • Ptosis
  • Diplopia
  • Dysarthria
  • Dysphagia
  • Proximal limb weakness
  • EExacerbated by beta blockers, lithium, phenytoin and certain abx
141
How is myasthenia gravis investigated/diagnosed?
  • Bedside: ice pack test
  • Serology for AChR antibodies, MuSK and LRP4 antibodies
  • CT/MRI chest to look for thymomas/thymic hyperplasia
  • Edrophonium test
142
What is the ice pack test for myasthenia gravis?
  • Measure degree of ptosis
  • Apply ice pack for a few minutes
  • Measure degreee of ptosis again
  • Positive if >2mm improvement
143
What is the edrophonium test for myasthenia gravis?
  • Administer small amount of edrophonium chloride (Tensilon)
  • See effects 
  • If rapid, transient increase in muscle strenght-> indicative of diagnosis
144
Describe the management of myasthenia gravis
  • ACh inhibitors: pyridostigmine, neostigmine
  • Immunosuppression-> steroids, azathioprine
  • Thymectomy
  • Rituximab
  • Plasma exchange and IVIG
145
Name some prognostic factors for myasthenia gravis
  • Age of onset
  • Antibody subtype
  • Thymus histology
  • Response to treatment
146
Name one complication of myasthenia gravis
  • Myasthenic crisis
147
What is a myasthenic crisis?
  • Life threatening acute worsening of symptoms, often triggered by another illness like a URTI-> can result in respiratory muscle failure
148
How is a myasthenic crisis treated?
  • Usual meds
  • IVIG and plasmapharesis
  • If FVC<=15mL/kg: mechanical ventilation
149
What is chronic fatigue syndrome?
  • Chronic disabling condition characterised by profound fatigue and impariment following minimal physical/cognitive effort
150
Describe the symptoms of chronic fatigue syndrome
  • Extreme fatigue
  • Post-exertional malaise
  • Sleep disturbances and unrefreshing sleep
  • Cognitive impairment
  • Orthostatic intolerance
  • Immune/neurological/autonomi/psychiatric manifestations
151
Name some differential diagnoses for chronic fatigue syndrome
  • Fibromyalgia
  • Depression
  • Hypothyroidism
  • AI disorders
152
How is chronic fatigue syndrome diagnosed?
  • Most clinical-rule out other causes
TFT's, bloods: inflammation, infection, blood cell abnormalities

Has to last >3 months and significantly decrease ability to engage in activities
153
Describe the managment of chronic fatigue syndrome
  • Refere to specialist CSF service if >3 months
  • Energy management
  • Graded exercise therapy no longer recommended
  • Symptoms control-treat other conditions, pain and sleep management
  • CBT
154
What is an acoustic neuroma also known as?
  • Vestibular schwannoma
155
What is an acoustic neuroma?
  • Benign subarachnoid tumour that exerts local pressure on cranial nerve 8
156
Describe the epidmiology of acoustic neuromas
  • Rare in UK
  • Adults aged 40-60 years
157
Describe the presentation of acoustic neuroma
  • Asymmetric/unilateral hearing loss
  • Progressive ipsilateral tinnitus
  • Sensorineural deaffness
  • Larger tumours: raised ICP like focal neurology: CN5/67/8
  • Dizziness, headaches, disequilibrium
158
Name some differential diagnoses for acoustic neuroma
  • Meniere's disease
  • Labyrinthitis
  • BPPV
159
What investigations should be done in a patient with a suspected acoustic neuroma?
  • Audiometry
  • MRI scan of cerebellopontine angle
160
Describe the management of an acoustic neuroma
  • Urgetn referral to ENT
  • >40mm: surgery
  • <40mm: 6 monthly annual surveillance scans via MRI
161
What focal neurology might be seen in a patient with an acoustic neuroma?
  • CN8: vertigo, unilateral sensorineural hearing loss, unilateral tinnitus
  • CN5: absent corneal reflex
  • CN7: facial palsy
162
What is Meniere's disease?
  • Inner ear disorder caused by increased fluid pressure in the endolymphatic spaces of the membranous labyrinth
163
Describe the epidemiology of Meniere's disease?
  • 30-60 years
  • Predominantly unilateral
164
Describe the presentation of meniere's disease
  • Sudden attacks of paroxysmal vertigo
  • Attacks last minutes to hours
  • Associated deafness
  • Tinnitus
  • Attacks often occur in clusters with period of remission where funciton is recovered
  • Can cause nystagmus and positive Romberg's test
  • Can be very disabling-> bedbound with nausea, vomiting and fluctuating hearing
165
Name some differential diagnoses for meniere's disease
  • Vestibular neuritis
  • Labyrinthitis
  • BPPV
166
What investigations are used to diagnose meniere's disease?
  • Clinical evaluation
  • Audiometric testing
  • Imaging/other tests may be used ot rule out other potential causes of symptoms
167
Describe the management of meniere's disease
  • ENT assessment
  • Prophylactic use of betahistine to reduce frequenct
  • Acute: prochlorperazine
  • Diuretics-> reduce endolymphatic fluid(only prescribed by specialists)
  • Low salt diets can help rpevent attacks
  • DVLA: no driving until good control of sx
168
Describe the natural history of Meniere's disease
  • Sympotms resolve in most patients after 10-15 years
  • Majority of patients left with a degree of hearing loss
  • Psychological distress common
169
What is trigeminal neuralgia?
  • Chronic pain condition characterised by severe sudden and brief bouts of shooting/stabbing pain that follow the distribution of one or more divisions of the trigeminal nerve, affecting the patients facial region
170
Describe the epidemiology of trigeminal neuralgia
  • >50yrs
  • F>M
171
Describe the presentation of a patient with trigeminal neuralgia
  • Unilateral facial pain that is sudden, severe and brief
  • Pain is shooting/stabbing
  • Triggered by lightly touching affected side of face, eating, or wind blowing
  • Neuro exam is typically normal
172
Name some differential diagnoses for trigeminal neuralgia
  • Post herpetic neuralgia
  • Temperomandibular joint disorders
  • Giant cell arteritis
  • Cluster headache
173
How is trigeminal neuralgia diagnosed?
  • Mostly clinical
  • MRI or other neuroimaging to rule out secondary causes
174
Describe the management of trigeminal neuralgia
Medical:
  1. Carbamazepine
  2. Phenytoin
  3. Lamotrigine
  4. Gabapentin
Surgical:
  • Microvascular decompression-remove/relocate vessels
  • Treat underlying cause like AVM/tumour
  • Alcohol/glycerol injections

Failure to respond to treatment/atypical: refer to neuro
175
Name some red flag symptoms for trigeminal neuralgia
  • Sensory changes
  • Deafness
  • Pain only in ophthalmic division(eye socket, forehead and nose) or bilaterally
  • Optic neuritis
  • FHx of MS
  • <40 yrs
176
What is bulbar palsy?
  • Subtype of LMN lesion impacting the 9/10/12th cranial nerves
177
Name the major causes of bulbar palsy
  • Motor neurone disease-mc
  • Myasthenia gravis
  • Guillain-barre
  • Brainstem stroke-Wallenberg's/lateral medullary syndrome
  • Syringobulbia
178
Describe the signs and symptoms of bulbar palsy
  • Dysarthria and dysphagia
  • Absent/normal jaw jerk reflex
  • Absent gag reflex
  • Flaccid, fasciculating tongue
  • Nasal speech, often described as 'quiet'
  • Additional signs suggestive of underlying cause(e.g. limb fasciculations: MND)
179
Name some differentials for bulbar palsy
  • Pseudobulbar palsy
  • Brainstem tumour
  • MS
  • Polymyositis and dermatomyositis
180
What investigations should be done in a patient with bulbar palsy?
  • Neuro exam
  • EMG and nerve conduction studies:MND/mysthenia gravis
  • Bloods: FBC, electrolytes, CK, autoantibody screening
  • MRI-lesions in brainstem
  • LP: rule out infections/AI causes
181
How is bulbar palsy managed?
  • Speech and swallowing therapy-manage dysarthria and dysphagia
  • Nutritional support
  • Treat underlying cause
182
How can Horner's syndrome be characterised?
  • Pre-ganglionic
  • Post-ganglionic
  • Central
Dependent on locatoin of sympathetic nerve interruption
183
Name some causes of Horner's syndrome
  • Pancoast tumour: pre-ganglionic
  • Stroke-central
  • Carotid artery dissection: post-ganglionic
  • Trauma, tumours, surgery-central
184
What is a pancoast tumour and how can it case Horner's syndrome?
  • Non-small cell lung carcinoma
  • Located at superior sulcus of lung affects lower roots of brachial plexus anf sympathetic chain
185
How do patients with Horner's syndrome typically present?
  • Ptosis-dropping of upper eyelid
  • Miosis-constriction of pupil
  • Anhidrosis
  • Enophthlamos-eye may appear sunken
  • Heterochromia-eye colour may change, more common in congenital Horner's syndrome

186
Name some differential diagnoses for Horner's syndrome
  • Oculomotor nerve palsy-will also have ophthalmoplegia
  • Myasthenia gravis
  • Bell's palsy
187
What investigations might be done in a patient presenting with Horner's syndrome?
  • Imaging: MRI/CT head neck and chest to ID structural causes
  • Bloods: assess for diabetes or AI disorders
Pharmacological pupil testing to confirm diagnosis and differentiate between pre- and post-ganglionic lesions
188
Describe the management of Horner's syndrome
  • Treat underlying cause
  • If no casue identified, observatoin and regular follow up
  • Cosemtic interventions for ptosis or miosis may be considered
189
What is Guillain Barre syndrome?
  • Ascending inflammatory demyelinating polyneuropathy-> acute onset of bilateral and roughly symmetric limb weakness
190
How do patients with Guillan Barre present?
  • Progressive ascending symmetrical limb weakness-> lower limbs first
  • Low back pain from radiculopathy
  • Paraesthesia
  • LMN signs in lower limbs: hypotonia, flaccid paralysis, areflexia
  • Cranial nerve signs: opthlamoplegia, facial nerve palsy, bulbar palsy
  • Potential autonomic dysfunction
  • Potential respiratory muscle involvement
191
Name some variants of Guillaim Barre syndrome
  • Parapetic
  • Miller-Fischer
  • Pure motor
  • Bilateral facial palsy with paraesthesias
  • Pharyngeal brachial cervical weakness
  • Bickerstaff's brainstem encephalitis
192
Name some differential diagnoses for Guillain Barre
  • Vascular: strokes
  • Infective/inflammatory: polio, lyme, CMV, TB, HIV, CIDP, myastehnia gravis
  • Spinal cord compression
  • Metabolic-porphyria, electrolyte abnormalitis
193
What investigations might be done in a patient with suspected Guillain Barre?
  • Monitoring of FVC for respiratory muscle involvement
  • Serological: anti ganglioside antibodies
  • LP: albuminocytological dissociation
  • Nerve conduction studies: prolongation or loss of the F wave
  • ID underlying cuase: stool cultures, serology, CSF virology
194
What might be seen on an LP of a patient with Guillain barre?
  • albuminocytological dissociation
  • Increased albumin without corresponding increase in white blood cells
195
How is Guillain Barre managed?
  • Regular FVC monitoring-can rapidly deteriorate
  • VTW prophylaxis: TEDS and LMWH
  • Analgesia if needed
  • Manage complications: arrhythmias, autonomic dysfunction
  • Enteral feeding if unsafe swallow
If significant disability:
  • IVIG for 5 days
  • Plasmapharesis(more side effects that IVIG)
196
What is the prognosis of Guillain Barre syndrome
  • Mostly full recovery
  • Can have residual weakness or fatigue
197
Give some prognostic factors for Guillain Barre
  • Speed of onset
  • Severity
  • Age
  • Presence of preceding diarrhoeal illness
198
What is Miller Fisher syndrome?
  • Variant of GBS
  • Ophthalmoplegia, areflexia and atacis(eye muscles affected first-descending paralysis)
  • Anti GQ1b antibodies in 90%
199
Describe the pathophysiology of Guillain Barre syndrome
  • Cross reaction of antibodies with gangliosides in the peripheral nervous system
  • Correlation between anti-ganglioside antibody and clinical features
  • Anti-GM1 antibodies 
200
What is Huntington's disease?
  • Genetic disorder that causes progressive breakdown of nerve cells in brain leading to motor, cognitive and psychiatric abnormalitis
201
Describe the epidemiology of Huntington's disease
  • Most common neurodegenerative disorder
202
What is meant by 'anticipation' with regards to genetics in Huntington's disease
  • Number of CAG repeats directly correlated with disease severity and age of onset
  • Symptoms present earlier in excessive generations due to increase in number of repeats
203
Describe the presentation of a patient with Huntington's disease
  • Choreoathetosis: unpredictable flowing and writhing movements
  • Cognitive impairment: dementia
  • Psychiatric abnormalitis: depression, irritability apathya nd sometimes psychosis

Usually over age 35YRS
Dystonia
Saccadic eye movements
204
Give some differential diagnoses for Huntington's disease
  • Parkinson's
  • Wilson's disease
  • Huntington's disease like disorders
  • Neuroacathocytosis syndromes
205
How is Huntington's Disease diagnosed?
  • MRI/CT: loss of striatal volume and enlarged frontal horn of lateral ventricles
  • Genetics: including for at risk family members
206
How is Huntington's disease managed?
  • Chorea management; tetrabenazine
  • Depression: SSRI
  • Psychosis: atypical antipsychotics
  • Supportive: physical and emotional support from MDT
207
What is the prognosis for Huntington's Disease?
  • Decline in physical and cognitive abilitys
  • Detah usually due to complications related to physical decline like pneumonia
  • Suicide second mc cause of death
208
Describe the pathophysiology of Huntington's disease
  • Autosomal dominant mutaiton results in degeneration of cholinergic and GABAergic neurons in striatum of basal ganglia
209
What is  a seizure?
  • Transient occurences of signs and symptoms due to abnormal excessive or synchronous neuronal activity in the brain
210
Name some differential diagnoses for epilepsy
  • Syncope
  • TIA
  • Migraines
  • Panic disorder
  • Non epileptic attack disorder
211
What investigations might be done in a patient with a seizure?
  • History including collateral and neuro exam
  • Imaging like CT/MRI
  • EEG
  • Might consider LP, bloods, advanced imaging depending on background
212
Name some localising features of temporal lobe seizures
  • Can occur with/without impairment of consciousness or awareness
  • Usually has an aura: rising epigastric sensation, psychic phenomena
  • Automatisms: lip smacking, grabbing, plucking
213
Name some localising features of frontal lobe seizures
Frontal lobe-motor
  • Head/leg movements
  • Posturing
  • Post-ictal weakness
  • Jacksonian march
214
Name some localising features of parietal lobe seizures
Parietal lobe-sensory
  • Paraesthesia
215
Name some localising features of occipital lobe seizures
Occipital-visual
  • Floaters/flashers
216
What is the new seizure classification based on?
  1. Where seizure started in the brain
  2. Level of awareness during seizure
  3. Other features
217
What are focal seizures?
  • Previously: partial seizures
  • Start in a specific area on one side of the brain
  • Level of awareness can vary
218
How can focal seizures be further classified?
Based on awareness:
  • Focal aware(simple partial)
  • Focal impaired awareness(complex partial)
219
Describe the features of a generalised seizure
  • Involve both sides of the brain at onset
  • Consciousness lost immediately
  • Can be further divided into tonic-clonic and absence etc
220
What is Jacksonian March?
  • Type of focal motor seizure that progressively 'marches' through adjacent areas of brain
  • Typically starts in hands and face then speards to other muscle group(hands, arm, shoulder, face)
  • Seizure may progress into generalised tonic clonic seizure
  • Often associated with structural brain lesions
221
What is Todd's paresis?
  • Temporary postictal weakness or paralysis following a seizure
  • Usually lasts minutes to hours but can last up to 48 hours
  • Usually unilateral but can be bilateral
  • Transient so patient will recover following resolution of postictal state
222
Describe the treatment of generalised tonic-clonic seizures
  • Males: sodium valproate
  • Females: lamotrigine or levetiracetam
223
Describe the management of focal seizures
  1. Lamotrigine/levetiracetam
  2. Carbamazepine
foCaL = Carbamazepine + lamotrigine/levetiracetam
generaLiSed = lamotrigine/levetiracetam + sodium valproate
abSEnce= sodium valproate + ethosuximide
224
Describe the management of absence seizures
  1. Ethosuximide
  2. Lamotrigine/levetiracetam(sodium valproate in males)
foCaL = Carbamazepine + lamotrigine/levetiracetam
generaLiSed = lamotrigine/levetiracetam + sodium valproate
abSEnce= sodium valproate + ethosuximide
225
Describe the management of myoclonic seizures
  • Males: sodium valproate
  • Females: levetiracetam
foCaL = Carbamazepine + lamotrigine/levetiracetam
generaLiSed = lamotrigine/levetiracetam + sodium valproate
abSEnce= sodium valproate + ethosuximide
226
Describe the management of tonic/atonic seizures
  • Males: sodium valproate
  • Females: lamotrigine
foCaL = Carbamazepine + lamotrigine/levetiracetam
generaLiSed = lamotrigine/levetiracetam + sodium valproate
abSEnce= sodium valproate + ethosuximide
227
What is sodium valproate associated with when used in pregnancy?
  • Neural tube defects
228
What is phenytoin associated with when used in pregnancy?
  • Cleft palate
229
Name some complications of epilepsy
  • Status epilepticus
  • Psychiatric complications-> increased risk of depression adn epilepsy
  • Sudden unexpected death in epilepsy(SUDEP)
230
Name some side effects of topirimate
  • Abdo pain
  • Cognitive impairment
  • Confusion
  • Muscle spams
  • mood changes
  • n+v
  • trmor
  • weight loss
231
Name some side effects of lamotrigine
  • blurred vision
  • arthralgia
  • ataxia
  • diarrhoea
  • dizziness
  • headache
  • insomnia
  • rash
  • tremor
232
Name some side effects of carbamazepine
  • ataxia
  • blood disorders
  • blurred vision
  • fatigue
  • hyponatraemia
233
name some side effects of sodium valproate
  • ataxia
  • anaemia
  • confusion
  • gastric irritation
  • haemorrhage
  • hyponatraemia
  • tremor
  • weight gain
234
name some side effects of phenytoin
  • acne
  • anorexia
  • constipation
  • hirsutism
  • insomnia
  • rash]tremor
235
What are the DVLA rules with regards to epilepsy?
  • Car/motorbike: 1 seizure: 6 months, >1: 1 year
  • If following change to medication have to wait 6 months
  • bus/coach lorry: 5 years after 1 off seizure. If >1 seizure: 10 seizure freee years
236
What is status epilepticus?
  • Seizure lasting >5 minutes OR
  • Multiple seizures over 5 minutes without fully regaining consciousness between 
237
Describe the management of status epilepticus
  • Buccal midazolam or rectal diazepam-can repeat 
  • If IV access: IV lorazepam repeated after 10-20 minutes
  • MAX 2 dose benxos
  • 2nd line: levitiracetam, phenytoin, sodium valproate
Refractory status(20-90 minutes)-general anaesthesia
  • Propofol
  • midazolam infusion
  • thiopental sodium
238
What investigations might be done in a patient with status epilepticus?
  • ABG
  • Bloods: FBC, U&E, LFT, CRP, clotting, bone profile
  • Toxicologyc screen
  • Anti epileptic drug
  • Imagine to determien cause: CT/MRI, LP
239
Describe the epidemiology of MS
  • Females: 2.3:1
  • Average onset 30yrs
240
Describe the symptoms of MS
Visual:
  • Optic neuritis
  • Optic atrophy
  • Uhtoff's phenomenon: worsening of vision following rise in body temperature
  • Internuclear ophthalmoplegia
Sensory:
  • Paraesthesia
  • Lhermittes phenomenon: paraesthesia in limbs on neck flexion
Motor:
  • Spastic weakness
Cerebellar:
  • Ataxia
  • Tremor
Others:
  • Urinary incontinence
  • Sexual dysfunction
241
How can MS be classified?
  • Relapsing remitting-> may become secondary progressive
  • Primary progressive
242
Name some differentials for MS
  • SLE
  • Lyme disease
  • Neurosarcoidosis
  • Vitamin B12 deficiency
243
How is MS diagnosed?
  • MRI showing >2 periventricular white matter lesions disseminated in time and space
  • Oligoclonal bands in CSF electrophoresis
244
What criteria is used to diagnose MS?
  • McDonald criteria
245
Describe the long term management of MS
  • Natalizumab-biologics
  • Ocrelizumab
  • Beta-interferon-injectable
Symptomatice therapies:
  • Physio
  • Baclofen and botox for spasticity
  • Anticholinergics for bladder dysfunction
  • Sildenafil for ED
246
Name some risk factors that might suggest a worse prognosis for a patient with MS
  • Older age at onset
  • Make
  • Primary progressive
  • High relapse rate
  • Rapid accumulation of disability
  • Comorbid conditions
  • Smoking
247
What is normal pressure hydrocephalus?
  • Neurological disorder where CSF accumulates in the ventricles causing them to enlarge
248
Describe the epidemiology of normal pressure hydrocephalus
  • More common in older adults
  • Considered a significant cause of reversible dementia 
249
How can diabetic peripheral neuropathy be categorised?
  • Distal symmetrical sensory neuropathy
  • Small fibre predominant neuropathy
  • Diabetic amyotrophy
  • Mononeuritis multiples
  • Autonomic neruopathy
250
What is the most common subtype of diabetic peripheral neuropathy
  • Distal symmetrical sensory neuropathy
251
Describe the features of distal symmetrical sensory neuropathy
  • Most common form of diabetic peripheral neuropathy
  • Results from loss of large sensory fibres
  • 'glove and stocking' distribution affecting touch, vibration and proprioception
252
Describe the features of small fibre predominant neuropathy
  • Loss of small sensory fibres
  • Loss of pain and temperature sensation in 'glove and stocking' distribution accompanied by epsiodes of burning pain
253
Describe the features of diabetic amyotrophy
  • Originates from inflammation of the lumbrosacral plexus or cervical plexus
  • Characterised by severe pain around thighs and hips and proximal weakness
254
Describe the features of mononeuritis multiplex
  • Painful
  • Neuropathies involving >=2 distinct peripheral nerves
255
Describe the features of autonomic neuropathy
  • Postural hypotension
  • Gatroparesis
  • Constipation
  • Urinary retention
  • Arrhythmias
  • Erectile dysfunction
256
Name some differentials for diabetic peripheral neuropathy
  • Vitamin B12 deficiency
  • Alcohol induced peripheral neuropathy
  • CIDP
  • Hypothyroidism
257
What investigations might be done in a patient with diabetic peripheral neuropathy?
  • Neuro exam
  • Nerve conduction tests
  • Bloods-HbA1c, B12, TFTs, LFTs
258
Name some complicaitons of diabetic peripheral neuropathy
  • Foot ulcers due to loss of sensation
  • Autonomic neuropathy-> cardiac, GI and GU disturbances
259
Describe the management of diabetic peripheral neuropathy
  • Control of blood glucose levels and treat complications(foot ulcers etc)
  • 1)amitriptyline, duloxetine, gabapentin, pregabalin
  • 2)Try other drugs from first line if one fails
  • 3)Tramadol as 'rescue therapy' for exacerbations
  • Topical capsaicin if localised
260
What is Charcot neuropathy?
  • Chronic progressive condition characterised by painful or painless bone and joint destruction in limbs that have lost sensory innervation
261
What are the signs and symptoms of Charcot arthropathy?
6D's
  • Destruciton of bone and joint
  • Deformity
  • Degeneration
  • Dense bones
  • Debris of bone fragments
  • Dislocation
262
Name some differentials for charcot arthropathy
  • Osteomyelitis-> important to rule out
263
What investigations are used to diagnose charcot arthropathy
  • Clinical dx mostly
  • X-rays 1st line imaging: bone destruction, debris, sclerosis and dislocation
  • MRI if ostemyelitis suspected
264
How is charcot arthropathy managed?
  • Conservative: lifestyle, footwear, orthotics
  • Medications: bisphosphonates, gabapentin
  • Surgical: resection of bony prominences, amputation if severe
265
Describe the symptoms of cerebellar dysfunction
DANISH
  • Dysdiadochokinesia
  • Ataxia
  • Nystagmus
  • Intention tremor
  • Slurred speech
  • Hypotonia
266
Name the causes of cerebellar syndrome
PASTRIES
  • Paraneoplastic syndrome
  • Alcohol
  • Sclerosis-MS
  • Tumours
  • Rare-Friedreich's ataxia
  • Iatrogenic-phenytoin, carbamazepine
  • Endocrine/metabolic: hypothyroidism/Wilson's
  • Stroke
267
How is cerebellar dysfunction investigated/diagnosed?
  • CT/MRI: ID stroke, tumours, trauma
  • Serologu: infectious/inflammatory causes
  • LP: infection, inflammation, malignancy
  • Genetics-hereditary
268
How is cerebellar dysfunction managed?
  • Treat underlying cause
  • Surgery/meds as required
  • Lifestyle-alcohol etc
  • Rehab: OT, physio etc
269
What is Parkinson's disease?
  • Chronic progressive neurological condition
270
Describe the epidemiology of parkinson's disease
  • 2nd mc neurodegenerative disorder after Alzheimer's
  • >65yrs
  • M>F
271
Describe the pathophysiology of Parkinson's disease
  • Accumulation of Lewy bodies in the substantia nigra of the basal ganglia-> neuronal cell death of dopaminergic cells
272
What are lewy bodies?
  • intracellular inclusions composed mostly of misfolded alpha synuclein
273
What are the components of the basal ganglia?
  • Striatum-> dorsal and ventral
  • Globus pallidus
  • Thalamus
  • Substantia nigra
  • Subthalamic nucleus
274
How does parkinson's affect the direct movement pathway?
  • Decreased levels of dopamine
  • Decreases direct pathway
  • Can't initiate increased movement-> decreased movement
275
Describe the indirect motor pathway in the substantia nigra
  • Inhibitory
  • Decreases thalamus activity
  • Decreases movement
276
How does parkinson's affect the indirect movement pathway?
  • Less dopamine
  • Increases indirect pathway
  • Can't prevent excessive movement pathway
  • Decreases movement
277
Name some risk factors for Parkinson's disease
  • Family hx-especially when onset <50yrs
  • Previous head injury
278
Name some protective factors for Parkinson's disease
  • Smoking-> including past smoking
  • Caffeine intake
  • Physical activity
279
What is the triad of symptoms associated with Parkinson's disease?
Tremor
Muscle rigidity
Bradykinesia
280
Describe the tremor associated with Parkinson's disease
  • Resting tremor
  • 'pill rolling'
  • Asymmetrical
  • 3-5Hz
281
How does bradykinesia present in a patient with Parkinson's disease
  • Parkinsonian gait-> shuffling, slowness of movement especially on initiation and turning
282
How does muscle rigidity present in Parkinson's disease?
  • 'Cogwheel rigidity'
  • Decreased arm swing
  • Stooped posture
283
Name some motor symptoms of Parkinson's disease
Triad of:
  • Tremor
  • Bradykinesia
  • Muscle rigidity
Also:
  • Postural instability-> increased falls
  • Hypomimic facies
  • Hypokinetic dysarthria, speech impairment, dysphagia
  • Micrographia
284
Name some non motor symptoms of Parkinson's disease
  • Autonomic dysfunction
  • Sleep dysfunction(REM behavioural disorder)
  • Olfactory loss
  • Psychiatric-> depression, anxiety, hallucinations, psychotic episodes, paranoid delusions
285
How is Parkinson's disease diagnosed?
  • Most clinical and positive response to treatment trials(excluded by absolute failure to respond to 1-1.5g levodopa daily)
If doubt:
  • MRI head-absence of swallow tail sign
  • Dopamine transporter scan
286
Name some differentials for Parkinson's disease
  • Essential tremor
  • Multiple system atrophy
  • Lewy body dementia
287
How is essential tremor differentiated from Parkinson's disease tremor?
Essential tremor vs Parkinson's
  • Symmetrical bs asymmetrical
  • 6-12Hz vs 3-6hz
  • Improves at rest vs worse at rest
  • Worse with intentional movements vs improves with movement
  • Improves with alcohol vs no changes with alcohol
Parkinson's: additional parkinson's features
288
Name some complications of Parkinson's disease 
  • Autonomic dysfunction
  • Recurrent falls
  • Cognitive imapirment
289
What is the 1st line treatment for Parkinson's disease
  • Levodopa
290
How does levodopa work for Parkinson's disease
  • Dopaminergic
  • Precursor to dopamine-> converted in CNS and periphery
291
What drug is levodopa often dosed with for treating Parkinson's disease patients and why?
  • Carbidopa
  • Decreases conversion of levodopa in periphery-> increases CNS availability and decreases peripheral side effects
292
Name some peripheral side effects of levodopa
  • Postural hypotension
  • Nausea and vomiting
293
Name some central side effects of levodopa
  • Hallucinations
  • Confusion
  • Dyskinesia
  • Psychosis
294
What are 2 problems with long term levodopa therapy other than side effects?
  • End of dose effect
  • On and off phenomenon
295
What is the end of dose effect in levodopa therapy?
  • AKA wearing off effect
  • Medications effect wears off as next dose is due so symptoms get worse
296
What is the on and off phenomenon in patients with levodopa therapy
  • 'On' periods where medication works well and 'off' periods where medication doesn't work as well
  • As it progresses, duration of 'on' periods can shorten and 'off' periods becomme more frequent
297
Give some examples of MAO-B inhibitors and how they can help in Parkinson's disease
  • Rasagiline and selegilin
  • Decrease dopamine breakdwon peripherally so increase central uptake
298
What is an important potential complication of using MAO-B inhibitors?
  • Can cause serotonin syndrome
299
Give some examples of COMT inhibitors and how they are used in Parkinson's disease treatment
  • Entacapone and tolcapone
  • Extend use of levodopa-> good for wearing off effect of levodopa
300
Give some examples of dopamine agonists and how they are useful for Parkinson's disease
  • ropinirole
  • rotigotine
  • apomorphine-most potent
  • mimic dopamine
301
What is an important side effect of apomorphine?
  • Haemolytic anaemia
302
What is hypoxic-ischaemic encephalopathy?
  • Neurological condition resulting form inadequate cerebral oxygen supply
303
Name some situations in which hypoxic-ischaemic encephalopathy can occur
  • Neonates: pperinatal asphyxia
  • Adults: secondary to cardiac arrest/severe systemic hypoxia
304
Describe the pathophysiology of hypoxic-ischaemic encephalopathy
  • Primary: immediately after event-> anaerobic respiration, lactic acidosis and cytotoxic oedema
  • Latent phase: brain appears to recover
  • Secondary: hours to days later-> renewed accumulation of toxic metabolites and free radicals causing further neuronal death
305
How does hypoxic-ischaemic encephalopathy present clinically?
  • Altered consciousness ranging from lethary to coma
  • Seizures
  • Abnormal tone and reflexes
306
How is hypoxic-ischaemic encephalopathy managed?
  • Supportive: maintain normal body temp and blood glucose levels
  • Seizure control
  • Neonates within 6 hours of birth: therapeutic hypothermia
307
What investigations might be done in hypoxic-ischaemic encephalopathy?
  • ABG
  • CBC
  • Electrolytes and glucose
  • LFTs aand U&Es
  • Neuoimaging: MRI and cranial USS(neonates)
  • EEG monitoring
  • Metabolic screening if atypical

Diagnosis: clinical mostly
308
Name some complications of hypoxic-ischaemic encephalopathy
  • Cerebral palsy
  • Seizure disorders
  • Cognitive impairment
  • Motor deficits
  • Sensory impairments
  • Microcephaly
  • Behavioural disorders
  • Multisystem organ failure of severe: CVR, renal, hepatic, resp
309
What is placenta accreta?
  • Spectrum of abnormalities of placental implantation into the myometrium of the uterine wall due to a defective decidua basalis

310
Name some risk factors for placenta accreta
  • Previous C section
  • Placenta praevia
  • Previous termination of pregnancy
  • Dilatation and curettage
  • Advanced maternal age
  • Uterine struuctural defects
311
What are the different types of placenta accreta?
  1. Placenta accreta
  2. Placenta increta
  3. Placenta percreta
312
What is the placenta accreta type of placenta accreta?
  • Chorionic villi attach into myometrium rather than being restricted within the decidua basalis(does not penetrate through the thickness of the muscle)

313
What is placenta increta?
  • Chorionic villi invade into but not through the myometrium

314
What is placenta percreta?
  • Chorionic villi invade through the perimetrium(through full thickness of myometrium to the serosa)
  • Increased risk of uterine rupture and in severe cases may attach to other abdominal organs like the bladder/rectum

315
How is placental accreta diagnosed?
  • Doppler US
  • MRI
  • Can be difficult to diagnose antenatally
316
Name some complications of placenta accreta
  • Increased risk of severe postpartum bleeding
  • Preterm delivery
  • Uterine rupture
317
How is placenta accreta managed?
  • Elective C-section and hysterectomy
  • If fertility key: attempt placental resection
318
What are Capgras delusions?
  • Misidentification syndrome characterised by belief that the closse person is replaced by an imposter who looks physically the same
319
What is a brain abscess?
  • Collection of pus within the brain parenchyma linkes with significant morbidity and mortality
320
Name some risk factors for developing a brain abscess
  • Immunocompromised states
  • Congenital heart defects and endocarditis
  • Chronic otitis/sinusitis
  • IVDU
  • Dental head and neck procedures
321
Describe the pathogenesis of a brain abscess
4 stages:
  • Early/initial cerebritis: 1-3 days
  • Late cerebritis: 4-9 days
  • Early capsule formation: 10-13 days
  • Late capsule formation: 14 days onwards
322
Describe the signs and symptoms of a brain abscesss
  • Headache
  • Focal neurological deficits
  • Infeciton signs: fever, n+v, meningism
  • Raised ICP: headache, 3rd nerve palsy, papilloedema, seizures
323
Name some differentials for a brain abscess
  • Space occupying lesions-cancer, vascular
  • CNS infections
  • Stroke
324
How is a brain abscess diagnosed?
  • MRI with gadolinium contrast-> better at detecting early cerebritis
  • CT for complications like hydrocephalus
  • Stereotactic needle aspiration
  • LP CONTRAINDICATED
325
Describe the management of a brain abscess
  • A-E and consider sepsis 6
  • Surgery: craniotomy-aspiration/excision
  • IV abx: 3rd gen: cephalosporing + meetronidazole
  • Sx management: dexamethasone for raised ICP 
326
Name some complications of a brain abscess
  • Seizures
  • Meningitis
  • Ventriculitis
  • Hydrocephalus
  • Cerebral oedema
  • Herniation
  • Death
  • Permanent neuro deficits
327
Name some causes of space occupying lesions
  • Neoplasia: metastatic and primary CNS tumours
  • Vasulcar: avms/aneurysms
  • Infective: abscesses, TB etc
  • Granulomatouus disease: neurosarcoidosis
328
What is Cushing's reflex?
  • Hypertension
  • Bradycardia
  • Irregular respirations
Sign of raised ICP
329
What investigations might be used for brain metastases
  • CT head-1st line in acute settings e.g. if presenting with seizures
  • MRI brain for details
  • PET scan
  • Biopsy
330
How are brain metastases treated?
  • Often not treatable with surgrical intervention
  • Chemo/radiation may be used
  • If metastases, often indicates stage 4 disease-> palliative care
  • Manage raised ICP-steroids, osmotic agents
331
What is a glioblastoma multiforme?
  • Mc primary brain tumour in adults
  • Malignant and highly aggressive
  • Associated with a poor prognosis-1 yr
332
How does a glioblastoma multiforme appear on imaging?
  • Solid tumours with central necrosis and a rim that enhances with contrast
  • Disruption of blood brain barrier and vasogenic oedema
333
How is a glioblastoma multiforme treated?
  • Surgical with postoperative chemo and/or radiotherapy
  • Dexamethasone for oedema
334
Describe the features of a meningioma
  • 2nd mc primary brain tumour in adults
  • Typically benign, extrinsic tumours of the CNS
  • Aris from dura mater of the meninges and cause sx by compression noot invasion
335
How is a meningioma diagnosed and treated?
  • CT-contrast enhancement and MRI
  • Observation, radiotherapy or surgical resection
336
What is a vestibular schwannoma?
  • Previously acoustic neuroma
  • Benign tumour arising from the 8th cranial nerve
  • Often seen in cerebellopontine angle
337
What might be seen on histology of a vestibular schwannoma?
  • Antoni A or B patterns seen
  • Verocay bodies(acellular areas surrounded by nucelar palisades)
338
What is a pilocytic astrocytoma?
  • Mc primary brain tumour in children
339
What is a medulloblastoma?
  • Aggressive paediatric brain tumour that arises withn the infratentorial compartment
  • Spreads through CSF system
340
What is an oligodendroma?
  • Benign slow growing tumour common in the frontal llobes
341
What might be seen on histology of a patient with an oligodendroma?
  • Calcifications with a 'fried egg' appearrance
342
What is a haemangioblastoma and what is it associated with?
  • Vascular tumour of the cerebellum
  • Associated with von Hippel-Lindau syndrome
343
What is a pituitary adenoma?
  • Benign tumours of the pituitary gland
  • Either secretory or non-secreotry
  • Can be microadenomas(<1cm) or macroadenomas(>1cm)
344
How do patients with pituitary adenomas present?
  • Consequences of hormone excess
  • Cushing's: ACTH
  • Acromegaly: GH
  • Compression of optic chiasm: bitemporal hemianopia due ot crossing nasal fibres
345
How is a pituitary adenoma diagnosed?
  • Pituitary blood profile
  • MRI
346
How can pituitary adenomas be treated?
  • Hormonal
  • Surgical: transphenoidal resection
347
What is a craniopharyngioma?
  • Most common paediatric supratentorial tumour
  • Solid/cystic tumour of the cellar region derived from the remnants of Rathke's pugh
  • Can be in adults too
348
How might patients with craniopharyngioma present?
  • Hormonal distrubance
  • Hydrocephalus
  • Bitemporal hemianopia
349
What might be seen on histology of a patient with craniopharyngioma?
  • Derived from remnants of Rathke's pouch
350
How is a craniopharyngioma diagnosed?
  • Pituitary blood profile
  • MRI
351
How is a craniopharyngioma treated?
  • Typically surgical +/- postoperative radiotherapy
352
What is herpes zoster ophthalmicus?
  • Serious, vision threatening infection caused byt the reactivation of the varicella zoster virus within the ophthalmic division of the trigeminal nerve
353
Describe the epidemiology of herpes zoster ophthalmicus
  • Primarily older adults: 60-70yrs
  • Immunocompromised
354
Name some risk factors for herpes zoster ophthalmicus
  • Age: >60yrs
  • Immunosuppression
  • Past hx of chickenpox
355
Describe the presentation of a patient with herpes zoster ophthalmicus
  • Painful red eye
  • Fevere
  • Malaise
  • headache
  • Erythematous vesicular rash over the trigeminal division of the opthalmic nerve
Hutchinson's sign: skin lesion on tip/side o fnose indicative of nasocilliary nerve involvement-> higher risk of ocular involvement
356
Name some differentials for herpes zoster ophthalmicus
  • Bacterial conjunctivitis
  • Uveitis
  • Keratitis
357
What investigations are used to diagnose herpes zoster ophthalmicus
  • Ophthalmic exam to assess extent of ocular involvement and potnetial complications
  • Viral culture/PCR testing from skin lesions/ocular speciemens to confirm dx
358
How is herpes zoster ophthalmicus mnaged?
  • Ig Hutchinson's sign: urgen ophthalmology review
  • Oral aciclovir
  • Topical steroids-> may be used under guidance of ophthalmology to reduce inflammation and prevent scarring(caution as might exacerbate infection)
359
What is shingles?
  • Reactivation of the varicella zoster virus which can lie dormant in the nerve ganglia following primary infection(chickenpox)
360
In what age groups does shingles commonly occur?
  • Elderly
  • If in young person should prompt investigation for underlying immune condition
361
Describe the presentation of shingles
  • Tingling feeling in a dermatomal distribution
  • Progressess to erythematous papules occuring along one or more dermatomes within a few days-> develop into fluid filled vesicles which then crust over and heal
  • Associated with viral sx: fever, headache, malaise
  • Herpes zoster ophthalmicus
362
Describe the management of shingles
  • Oral antiviral(valaciclovir) within 72hr rash onset if immunocompromised or moderate/severe rash/pain or non-truncal involvemets
  • Hospital and IV antivirals if severe, immunocompromised/ophthalmic sx, suspicion of meningitis/encephalitis
  • Avoid contact with pregnany women, babies and immunocompromised until lesions are fully crusted over
  • Pain management with NSAIDs, back up amitryptyline, duloxetine, gabapentin
363
Name some complications of shingles
  • Secondary bacterial infection of skin lesions
  • Corneal ulcers, scarring and blindness if eye involved
  • Post herpetic neuralgia
364
Describe the features of post herpetic neuralgia
  • Pain occuring at site of healed shingles infection
  • Can cause neuropathic pain(burning, pins and needles)
  • Can cause allodynia(perception of pain from a normally non-painful stimulus like light touch)
365
Name some risk factors for normal pressure hydrocephalus
  • SAH
  • Meningitis
  • Traumatic brain injury
  • Intracranial tumours
  • Ventricular shunting or LP
366
Describe the pathophysiology of normal pressure hydrocephalus
  • Ventricular dilation without an apparent increase in intracranial pressure-> periventricular stress-> disruption of blood brain barrier-> inflammatory response-> cerebral perfusion changes
367
Name some differentials for normal pressure hydropcephalus
  • Alzheimer's
  • Parkinson's
  • Other dementias
368
How is normal pressure hydrocephalus investigated?
  • CT.MR imaging: dilated lateral ventricles-can also be seen in demenita
  • LP: measure walking ability and cognition before and after
369
Describe the management of normal pressure hydrocephalus
  • Therapeutic LP
  • Ventriculoperitoneal shunt-redirect excess CSF to abdomen
370
What is idiopathic intracranial hypertension?
  • AKA psudotumour cerebri/benign intracranial hypertension
  • Increased intracranial pressure without any clear cause evident on neuroimaging and other investigations
371
Describe the epidemiology of idiopathic intracranial hypertension
  • Young and obese women
  • 9:1 women
372
Name some risk factors for idiopathic intracranial hypertension
  • Femal gender
  • Obesity
  • Pregnancy
373
Name some differentials for idiopathic intracranial hypertension
  • Brain tumour
  • Venous sinus thrombosis
  • Sleep apnoea
  • Migraines
374
What investigations might be done in a patient with suspected idiopathic intracranial hypertension
  • Ophthalmoscopy-> bilateral papilloedema
  • CT/MRI: increased ICP, MRI venogram to rulee out venous sinus thrombosis
  • LP: KEY: opening pressure >20cmH20. Rule out other causes: CSF profile should be normal
375
Describe the management of idiopathic intracranial hypertension
  • Weight losss
  • Carbonic anhydrase inhibitors-acetazolamide-poorly tolerated
  • Topirimate and candesartan
  • Invasive: therapeutic LP, surgical CSF shunting, optic nerve sheath fenestration-prevent progressive visual loss
376
Describe the prognosis of idiopathic intracranial hypertension
  • Most patients have benign course-smal proportion develop severe vissual impairment or blindness
Visual morbidity: mostly mainly from delay in diagnosis or inadequate treatment
Even modest weight loss can significantly reduce pressure
377
What is narcolespy?
  • Neurological condiiton that distrubs the sleep wake cycles
  • Excessive sleepiness during daytime and may also suddnely fall asleep during activities-early onset of REM sleep
378
What gene is narcolepsy associated with?
  • HLA-DR2
379
What is narcolepsy associated with low levels of?
  • Orexin(hypocretin)-> protein responsible for controlling appetitie and sleep patterns
380
How is narcolepsy investigated/diagnosed?
  • Multiple sleep latency EEG
381
Describe the management of narcolepsy
  • Daytime stimulants(e.g. modafanil)
  • Nighttime sodium oxybate
382
What is motor neurone disease?
  • Group of progressive neurological disorders that destroy motor neurones: the cells that control voluntary muscle activity
383
Describe the epidemiology of motor neurone disease
  • M>F
  • 50-60yrs
  • 90% sporadic, 10% familial
384
Name some genes associated with familial MND
  • SOD1
  • FUS
  • C9ORF72
385
What condition overlaps with MND?
  • Fontotemporal dementia
  • C90RF72 mutation found in both
386
Name some UMN signs
  • Spasticity
  • Hyperreflexia
  • Upgoing plantars(alhtouth often downgoing n MND)
387
Name some LMN signs
  • Fasciculations
  • Muscle atrophy
388
Describe the general presentation of a patient with MND
  • Combination of lower and upper MN signs
  • Fasciculations
  • Asymmetric limb weakness
  • Wastig of small hands muscles
  • Absence of sensory signs/sx
389
What are the different types of MND?
  • Amyotrophic lateral sclerosis(ALS)-most common
  • Primary lateral sclerosis
  • Progressive muscular atrophy
  • Progressive bulbar palsy
  • Spinal muscular atrophy
390
Describe the features of amyotrophic lateral sclerosis(ALS)
  • Typically LMN signs in arms and UMN in legs
  • If familial: gene is on chromosome 21 and codes for superoxide dismutase
  • Can have bulbar onset in some cases
391
Describe the features of primary lateral sclerosis
  • UMN signs only
392
Describe the features of progressive musclular atrophy
  • LMN signs only
  • Distal muscles before proximal
  • Best prognosis
393
Describe the features of progressive bulbar palsy
  • UMN and LMN signs
  • Palsy of tongue, muscle of masticaiton and facial muscles due to loss of function of brainstem motor nuclei-> dysphagia/dysarthria
  • Carries worst prognosis
394
Name some differentials for MND
  • MS
  • Chronic inflammatory demyelinating neuropathy
  • Myasthenia gravis
  • Brainstem lesions
  • Paraproteinaemias
395
How is MND investigated/diagnosed?
  • Clinical
  • Nerve conduction studies-> normal motor conduction so exclude a neuropathy
  • EMG: reduced number of action potentials with increased amplitude
  • MIR: brasintem lesions/cervical cord compression/myelopathy
396
Describe the management of MND
  • Mostly supportive 
  • Riluzole-> extends life expectancy by about 3 months, used mainly in ALS
  • Respiratory care: BIPAP at night
  • Nutrition: PEG as bulbar disease progresses
  • Discuss advanced care early
  • Anticholinergics for drooling
397
How does riluzole work?
  • Prevents stimulation of glutamate receptors
398
Describe the prognosis of MND
  • Poor: 50% die within 3 years
  • Most <5yrs
  • Most die from respiratory complications
399
What is myopathy?
  • Condition affecting skeletal muscles
400
Describe the features of myopathy
  • Symmetrical muscle weakness(proximal > distal)
  • Problems rising from chair/getting out of bath
  • Normal sensation, normal reflexes, no fasciculation
401
Name some causes of myopathy
  • Inflammatory: polymyositis
  • Inherited: Duchenne/Becker muscular dystrophy, myotonic dystrophy
  • Endocrine: Cushing's, thyrotoxicosis
  • Alcohol
402
What is degenerative cervical myelopathy?
  • Spinal cord dysfunction from compression in the neck
403
Name some risk factors for degenerative cervical myelopathy
  • Smoking
  • Genetics
  • Occupation-> high axial loading
404
Describe the presentation of a patient with degenerative cervical myelopathy
  • Variable-fluctuating but progressive
  • Pain-neck, upper, lower limbs
  • Loss of motor function-hard to do up shirts/use a fork
  • Loss of sensory function-> numbness
  • Loss of autonomic function-> urinary/faecal incontinence and impotence
  • Hoffman's sign
405
What is Hoffman's sign?
  • Used for cervical myelopathy
  • Flick one finger on a patients hand-> positive if reflex twitching of other fingers on same hand
406
How is degenerative cervical myelopathy diagnosed?
  • MRI cervical spine: disc degeneration and ligament hypertrophy with accompanying cord signal change
407
What is degenerative cervical myelopathy sometimes misdiagnosed as?
  • Carpal tunnel
408
Describe the management of degenerative cervical myelopathy
  • Urgent assessment by specialist spinal services-> early treatment to prevent rpogression
  • Surgical decompression
  • Physio-only by specilaist services to avoid further damage
409
What conditions affect the dorsal column?
  • Tabes dorsalis(neurosyphilis)
  • Subacute combined degeneration of spinal cord
410
What is the anal sphincter innervated by?
  • S2,3,4
411
What is a spinal cord compression and how is it different to cauda equina?
  • Form of myelopathy caused by pressure on cord-> causes an UMN lesion
  • Cauda equina: compression below level of L1-> LMN
412
Name some causes of spinal cord compression
  • Trauma: mc-vertebral fracturas/dislocation of facet joints
  • Malignancy
  • Infection: TB and abscess formation
  • Epidural haematoma
  • Intervertebral disco prolapse-rare
413
Describe the symptoms of a patient with spinal cord compression
  • Back pain: severe, progressive and aggravated by straining(couhging etc)
  • Difficulty walking
  • Weakness/numbess bleow level compressed(usually bilateral and symmetrical)
  • Incontinence
  • Urinary retention
  • Constipation
  • Systemi e.g. weight loss, fatigue, fevers if MSCC/TB
414
Name some signs seen in a patient with spinal cord compression
  • Hypertonia
  • Hyperreflexia(may be absent at level compressed)
  • Clonus
  • Upgoing plantars
  • Sensory loss
415
Name some differentials for spinal cord compression
  • Transverse myelitis
  • Cauda equine
  • Peripheral neuropathy
  • Spinal metastases
  • Sciatica
416
How is spinal cord compression investigated/diagnosed?
  • MRI whole spine-urgent if suspected MSCC
  • Bladder scan if suspected urinary retention
  • EEG and baseline bloods
  • If MSCC: ix to find primary cancer
417
Describe the management of spinal cord compression
  • Immobilise and spinal precautions
  • Analgesia for pain
  • VTE prophylaxis
  • Catheteris if retention
  • Treat underlying cause
  • Neurosurgery-> consider surgical decompression
418
Describe the management of metastatic spinal cord compression
  • Hihg dose steroids: 16mg dexamethasone to reduce oedema and compression +PPI + monitor glucose
  • Refer to neuro:  surgical decompression(vertebroplasty/kyphoplasty)
  • Oncology input
419
In patients with metastatic spinal cord compression where do the metastases most commonly come from?
  • Lung
  • Breast
  • Prostate
420
What is cauda equina syndrome?
  • Lumbosacral nerve roots that extend below the spinal cord(L1/L2 level) are compressed
421
Name some causes of cauda equina syndrome
  • Lumbar disc herniation at L4/5 or L5/S1-mc
  • Tumours-primary/metastatic
  • Trauma
  • Infection: abscess, discitis
  • Epidural haematoma
422
Describe the symptoms of cauda equina syndrome
  • Low back pain
  • Radicular pain-often symmetrical
  • Leg weakness
  • Difficulty walking
  • Saddle anaesthesia
  • Bowel incontinence/constipation
  • Urinary incontience/retention
  • Erectile dysfunction or sexual dysfunction
423
Describe the signs of cauda equina syndrome
  • Loss of lower limb power
  • Hypotonia in lower limbs
  • Hyporeflexia in lower limbs
  • Sensory loss/paraesthesias in legs
  • Reduced perianal sensation
  • Loss of anal tone
  • Bladder palpable and dull to percussion in urinary retention
424
Name some differentials for cauda equina syndrome
  • Compression of ocnus medullaris
  • Spinal cord compression
  • Sciatica
425
How is cauda equina syndrome diagnosed?
  • Urgent whole spine MRI
426
Describe the management of cauda equina syndrome
  • Surgical decompression
427
Name some complications of cauda equina syndrome
  • Permanent paralysis of lower limbs
  • Sensory loss
  • Bladder/bowel dysfunction
  • Sexual dysfunction
  • Pressure ulcers
  • VTE due to immobility
428
If damage to the DCML occurs in the spinal cord, what side will the symptoms be?
  • Same side
429
What is sub-acute combined degeneration of the spinal cord?
  • Degeneration of the dorsal columns, lateral corticospinal tracts and spinocerebellar tracts associated with vitamin B12 deficiency
430
Describe the signs and symptoms of a patient with sub-acute combined degeneration of the spinal cord
  • Symmetrical distal sensory sx, usually start at feet and progress to hands
  • Varying degrees of ataxia
  • Mixed UMN and LMN sings: exaggerated/diminished/absent reflexes
  • Autonomic bowel/bladder sx
  • Haematological manifestations may be present/absent
431
How is sub-acute combined degeneration of the spinal cord investigated/diagnosed?
  • Assess B12 and folate
  • Homocysteine: raised level despite normal B12-> functional B12 deficiency
  • MRI of spine-exclude myelopathy
  • Nreve conduction studies: axonal neuropathy
432
Describe the management of sub-acute combined degeneration of the spinal cord
  • Urgent Vitamin B12 repkacement using hydroxocobalamin 1mg IM alternate days until no further imporvement
  • Maintainence tx with hydroxocobalamin 1g IM every 2 months
433
What are muscular dystrophies?
  • Group of inherited genetic disorders characterised by progressive degeneration and weakening of muscles
434
Name some types of muscular dystrophies
  • Duchenne Muscular Dysrophy
  • Becker muscular dystrophy
435
Describe the symptoms of Duchenne muscular dystrophy
  • Progressive proximal muscle weakness from 5 years
  • Calf pseudohypertrophy
  • intellectual impariment
  • Gower's sing: child uses arms to stand from a squatted position
436
Describe the features of Becker's muscular dystrophy
  • Presents later in childhood with muscle wasting and weakness
  • Wheelchair bound in teens and can survive into thirties
437
How is Duchenne muscular dystrophy investigated/diagnosed?
  • Raised creatinine kinase
  • Genetics-replaced muscle biopsy
438
Describe the management of Duchenne muscular dystrophy
  • Supportive: low impact exercise, mobility aids, OT, physio
  • Manage complications: dysphagia, chest infections etc
  • Glucocorticoids: slow muscle regeneration for 6 months-2 years
  • Newer: ataluren and creatinine supplemebts
  • Genetic counselling
439
What is the prognosis like for Duchenne and Becker's muscular dystrophy
  • Most children can't walk by age 12
  • Typicaly survive to age 25-30yrs
  • Better for Becker's: live into 30s
440
Name some complications of Duchenne muscular dystrophy
  • Joint contractures
  • Respiratory muscle failure-hypoventilation, poor cough and recurrent pneumonia(cause of death)
  • Dilated cardiomyopathy
  • Anaesthetic complications(rhabdo and malignant hyperthermia
441
Describe the epidemiology of migraine
  • Common
  • F>M
  • Peak: 30-39yrs
442
Name some triggering factors for migraines
  • Tiredness/stress
  • Alcohol
  • COCP
  • Lack of food/hydraiton
  • Cheese, chocolate, red wines, citrus fruits
  • Menstruation
  • Bright lights
443
How might migraines present in children?
  • May be shorter lasting
  • Bilateral headaches
  • More prominent GI disturbance
444
Describe the symptoms of a migraine
  • Aura: visual/sensory sx preceding headache
  • Unilateral throbbing headache
  • Photophobia/phonophobia
  • Nause ande/or vomiting
445
Name some differentials for a migraine
  • Tension type headache
  • Cluster headache
  • SAH/stroke
  • Giant cell arteritis
446
Describe the features of a hemiplegic migraine
  • Migraine variant in which motor weakness is a manifestation of aura in at least some attacks
  • Strong family history in 50%
  • Very rare, most common in adolescent females
447
What aura symptoms of a migraine might prompt further investigation/referral?
  • Motor weakness
  • Double vision
  • Visual sx in only one eye
  • Poor balance
  • Decreased level of consciousness
448
Describe the prophylactic management of migraines
  • Propanolol-CI in asthma
  • Topirimate-not for women of childbearing age/onc ontraceptive
  • Amitryptaline
  • Candesartan

Injections:
  • Greater occipital nerve block
  • Botulinum toxin injections
  • Acupuncture 
449
Describe the general management if migraines with regards to drug classes
  • 5 HT receptor agonists for acute
  • 5 HT receptor antagonists for prophylaxis
450
What is the problem with regular use of acute migrain medications?
  1. If used >10-15 days/month-> medication overuse headache
451
Describe the treatment of migraines in pregnancy
  • Paracetemol 1g first line
  • NSAIDS second line in 1st and 2nd trimester
  • Avoid aspirin and opioids like codeine
452
How does a PMH of migraines affect COCP and HRT use?
  • COCP: absolute contraindication in patients with aura due to risk of stroke
  • HRT: safe to prescribe but may make migraines worse
453
Name some red flags for headaches
  • <20yrs+ hx of cancer
  • Vomiting wihtout other obvious cause
  • Worsenign headache iwth fever
  • Thunderclap headache
  • New onset neuro deficit/cognitive dysfunction/consciousness/personality changes
  • Recent head trauma
  • Headache triggered by cough, sneeze or exercise or orthostatic headache
  • Sx suggestive of GCA or acute narrow angle gluacoma
454
Name some risk factors for cluster headaches
  • Male
  • >30yrs
  • Alcohol consumption
  • Prior brain surgery/trauma
  • Fhx
455
How are cluster headaches diagnosed/investigated?
  • Generally clinical diagnosis but neuroimaging done in most patients-underlying brain lesion can be found in some patients
  • MRI with gadolinium contrast
456
Describe the prophylactic treatment for cluster headaches
  • Verapamil
  • Topirimate
  • Sometimes tapering dose of prednisolone
457
What is needed to be monitored if treating a patient with verapamil?
  • ECG to check cardiac function
458
Describe the epidemiology of tension headaches
  • Mc cause of chronic recurring head pain
  • Women?men
459
Name some contributing factors to tension headaches
  • Stress
  • Poor posture
  • Eye strain
460
How is a tension headache managed?
  • Stress management
  • PT
  • Analgeisa: paracetemol or NSAIDS then step it up
  • Be careful of mediaction overuse headaches
461
What is a central venous sinus thrombosis?
  • Occlusion of venous vessels in sinuses of the cerebral veins
462
Name some risk factors for central venous sinus thrombosis
  • Hormoanl(pill, pregnancy etc)
  • Prothrombotic haem conditions/malignancy
  • Systemic disease(dehydration/sepsis)
  • Local(skull abnormaliites, trauma, local infection
463
Describe the presentation of central venous sinus thrombosis
  • Very variable
  • Headache
  • Confusion/drowsiness/impaired consciousness
  • IMpaired vision
  • N+V
  • Focal neuro deficits
  • Cranial nerve palsies
  • Papilloedema

464
How is central venous sinus thrombosis investigated/diagnosed?
  • NCCT head: hyperdenstiy in affected sinus
  • CT venogram-filling defect-empty delta sign
465
What is the most common form of dural venous sinus thrombosis
  • Superior sagittal sinus
466
How is central venous sinus thrombosis treated?
  • LMWH
  • Adress undelying risk factors that increase risk of clotting
  • After initial therapy with LMWH can be bridged to warfarin
467
How do patients with central venous sinus thrombosis present?
  • Chemosis
  • Exophthalmos
  • Peri-orbital swelling
468
What is Brown-Sequard syndrome?
  • Lateral hemisection of the spinal cord

469
Name some causes of Brown-Sequard syndrome
  • Cord trauma-penetratin injury mc
  • Neoplasms
  • Disc herniation
  • Demyelination
  • Infective/inflammatory lesions
  • Epidural haematomas
470
Describe the management of Brown-Sequard syndrome
  • Depends on causative pathology
  • Medical management preferred if infective/inflammatory/demyelinating
  • Surgical if pathologies causing extrinsice cord compression
471
What is the spinothalamic tract responsible for?
  • Anterolateral cord
  • Contralateral pain and temperature sensation
472
What is the dorsal column tract responsible for?
  • Posterior cord
  • Ipsilateral vibration and proprioception
473
What is the lateral corticospinal tract responsible for?
  • Ipsilateral movement of limbs
474
What is mononeuropathy?
  • Damage/dysfunction of a single peripheral nerve-> most cause motor and sensory impairment
475
What is the most common mononeuropathy?
  • Carpal tunnel syndrome
476
What are the general symptoms of mononeuropathies
Depends on underlying cause and affected nerve
  • Sensory: numbness, pain, tingling
  • Motor: weakness, atrophy, loss of coordination
477
How are mononeuropathies generally treated?
  • Conservative: rest, heat, avoid/remove causative activity, NSAIDs, bracing
  • Oral/injected corticosteroids
  • Surgical decompression
478
What is carpal tunnel syndrome?
  • Compression of median nerve in the carpal tunnel

479
In what circumstances is carpal tunnel commonly seen in?
  • Repetitive wrist activites
  • Systemic disease: diabetes/RA
  • Pregnancy
  • Anatomical variations
Anything that causes an increase in pressure within the carpal tunnel or decreases the tunnel's size
480
Describe the symptoms of carpal tunnel syndrome
  • Pain and paraesthesia in thumb index and middle finger-impingement of palmar digital branch of median nerve
  • Symptoms worse at night or after activities involving writs flexion
481
What might be seen on examination in a patient with carpal tunnel syndrome?
  • Weakness of thumb abduciton(abductor pollicis brevis)
  • Wasting of thenar eminence NOT hypothenar
  • Tinel's signL tapping causes paraesthesia
  • Phalen's sign: felxion of wrist causes sx
482
Name some differentials for carpal tunnel syndrome
  • Cubital tunnel syndrome
  • Thoracic outlet syndrome
  • Radial tunnel syndrome
  • Ulnar neuropathy
483
How is carpal tunnel diagnosed?
  • EMG and nerve conducton studies: motor+sensory prolongation of action potential
484
Describe the management of carpal tunnel syndrome
  • Conservative: splints at night, NSAIDS, corticosteroid injecitons, adjust activities 
  • Surgeryical decompression: flexor retinaculum division
485
What is radiculopathy?
  • Symptoms cuased by compression off a nerve root in the spinal common

486
How can radiculopathy be classified?
  • Cervical
  • Lumbar
487
Describe the sympotms of cervical radiculopathy
  • Pian in neck, shoulders, upper back or arms
488
What age group is most commonly affected by cervical radiculopathy
  • 30-60yrs
489
Name some causes of cervical radiculopathy
  • Disc degeneration
  • Sponylosis
  • Bone disease
  • Cancer
  • Herniated disc
490
Name 2 examples of lumbar radiculopathy
  • Sciatica-mc
  • Cauda equina syndrome
491
Describe the symptoms of sciatica
  • Pain and numbness from spinal nerve root location to legs or feet
492
Name some causes of lumbar radiculopathy
  • Disc herniation
  • Bone spurs
  • Bone disease
  • Cancer
493
Describe the treatment for radiculopathy
  • OTC anaglesia
  • PT: lower pain, improve posture, strengthen muscles
  • Steroid injecitons
  • Oral steroids
  • Anti-epileptics
  • Surgical spinal decompression

3A med mine (12 decks)

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