Brainscape's Knowledge GenomeTM

Browse over 1 million classes created by top students, professors, publishers, and experts.


See full index

Anki 3a exports > neuro anki 1 > Flashcards

neuro anki 1 Flashcards

1
Q

What is a subarachnoid haemorrhage?

A

Blood within the subarachnoid space(under arachnoid mater)

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
2
Q

Describe the epidemiology of SAH

A

F>M
Peak incidence: 40-50 years
80% without trauma due to a ruptured berry aneurysm

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
3
Q

Describe the aetiology of SAH

A

MC: head injury
LC: spontaenous
Berry aneurysm: 85% of cases
AVM’s
Pituitary apoplexy
Myocitic(infective) aneurysms

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
4
Q

Name some risk factors for developing a Berry aneurysm?

A

Hypertension
Adult polycystic kidney disease
EDS
Coarctation of the aorta

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
5
Q

Name the symptoms of a SAH

A

Sudden onset ‘thunderclap’ headache, peaks in intensity in 1-5 minutes
May have history of previous less severe ‘sentinel’ headache
Altered consciousness
Nausea and vomiting
Seizures
Meningism: photophobia and neck stifness

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
6
Q

Name the signs of an SAH

A

Fundoscopy: retinal haemorrhage
Positive Kernig’s/Brudzinksi’s sign
Focal neurological deficits
CN3/4/6-diplopia
Hemiparesis/hemiplegia

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
7
Q

What investigations should be done in a patient with a SAH

A

Non contrast CT head->hyperdense blood in basal cistern
If CT done >6hrs post sx onset and normal-> LP
if >12 hours post onset: xanthochromia:
CT angiogram to check for aneurysms or vascular abnormalities

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
8
Q

Describe the treatment for an SAH

A

Oral nimodipine to prevent vasospasm->ischaemic damage
Coiling, stenting or clipping of aneurysms: neurosurgery

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
9
Q

Name some complications of an SAH

A

Re-bleeding
Hydrocephalus
Vasospasm
Hyponatraemia->SIADH
Seizures

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
10
Q

Describe the prognosis of a patient with an SAH

A

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

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
11
Q

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

A

Age
Consciousness level on admission
Amount of blood visible on CT head

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
12
Q

Define a TIA

A

Sudden onset focal neurological deficit with a vascular aetiology typically lasting <1hr but always <24 hours
Completely resolves

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
13
Q

Describe the epidemiology of a TIA

A

Peak >70 years
M>F

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
14
Q

Describe the pathophysiology of a patient with a TIA

A

Transient disruption of blood flow to a specific region of the CNS resulting in ischaemia

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
15
Q

Describe the aetiology of a TIA

A

MC: Embolism: often from atherosclerotic plaques in the heart
Lacunar
Haemodynamic compromise(stenosis of major artery)

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
16
Q

Describe the presentaiton of a patient with a TIA

A

Completely resolves within 24 hours
Stroke symptoms
Aphasia/dysarthria
Unilateral weakness/sensory loss
Ataxia, vertigo, balance issues
Visual: amaurosis fugax, diplopia, HH

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
17
Q

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

A

Neuroimaging:
MRI(ischaemia, haemorrhage, other pathologies)
Carotid doppler USS-> atherosclerosis
Echo: cardiac thrombus
24hr ECG: AF
Bloods: glucose, lipid profile, clotting

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
18
Q

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

A

Bleeding disorder
Already on aspirin

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
19
Q

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

A

Urgent assessment within 24 hours

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
20
Q

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

A

Within 7 days

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
21
Q

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

A

Admitted immediately
Likely cardioembolic source

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
22
Q

Describe the secondary management of TIA

A

Antiplatelet therapy: clopidogrel
Lipid moidification: atorvastatin 20-80mg daily
Carotid endartectomy if severe carotid stenosis

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
23
Q

Describe the drivinfg rules for a patient with a TIA

A

Cannot drive until seen by a specialist
If dr happy and no lasting effects: can drive again after 1 month
If lorry/bus: 1 year

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
24
Q

What is an extradural haemorrhage?

A

Blood collects between the dura mater(outermost meningeal layer) and inner surface of the skull

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
25
Q

Describe the typical presentaiton of a patient with an extradural haemorrhage

A

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

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
26
Q

How might an extradural haemorrhage result in afixed and dilated pupil?

A

Haematoma expands->uncus of temporal lobe herniates around the tentorium cerebelli->parasympathetic fibres of CN3 compressed->fixed and dilated pupil

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
27
Q

Name some differentials for a extradural haematoma

A

Subdural haemorrhage
SAH
Intracerebral haemorrhage
Cerebral contusion

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
28
Q

What investigations should be done in a patient with an extradural haematoma?

A

CT scan: biconvex/lentiform hyperdense collection limited by the suture lines of the skull
Assess for midline shift/uncal herniation

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
29
Q

Describe the management of an extradural haematoma

A

No neurological deficits->conservative: supportive therapy and radiological observation
Definitive: craniotomy and haematoma evacuation

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
30
Q

What is a subdural haemorrhage?

A

Accumulation of venous blood in the potential space between the dura mater and arachnoid mater of the brain

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
31
Q

How can subdural haemorrhages be classified?

A

Acute
Subacute
Chronic

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
32
Q

Describe the timeline of an acute subdural haemorrhage

A

Sx develop within 48 hours of injury->rapid neurological deterioration

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
33
Q

Describe the timeline of a subacute subdural haemorrhage

A

Sx present days->weeks post injury-> gradual progression of neurological symptoms

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
34
Q

Describe the timeline of a chronic subdural haemorrhage

A

Elderly: weeks-> months
Might not remember specific head injury

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
35
Q

Describe the epidemiology of a subdural haemorrhage

A

Elderly: >65 years
Infants-shaken baby

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
36
Q

Name some risk factors for developing a subdural haemorrhage

A

Increasing age
Anticoag use
Chronic alcohol use
Recent trauma
Infants (shaken baby)

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
37
Q

Name some symptoms you might find in a patient with a subdural haemorrhage

A

Altered/fluctuating mental status
Focal neurological deficits
Headache
Memory loss
Cognitive impairment
Seizures
Personality changes

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
38
Q

Name some possible exam abnormalities in a patient with a subdural haemorrhage

A

Papilloedema (raised ICP)
Pupillary changes: unilateral dilated pupil- CNS compression
Gait abnormalities
Hemiparesis/hemiplegia
Bradycardia, hypertension, irregular respirations (Cushing’s triad)

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
39
Q

What investigations should be done in a patient with a subdural heamorrhage?

A

CT scan: crescent shaped, not restricted by suture lines
Hyperacute(<1hr): isodense
Acute (<3 days): hyperdense
Subacute(3d-3 weeks): idosense
Chronic (>3 weeks): hypodense

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
40
Q

Describe the management of a patient with a subdural haemorrhage

A

Conservative: monitor ICP etc
Acute: decompressive craniotomy
Chronic: Burr holes

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
41
Q

What is an ischaemic stroke?

A

Sudden onset neurological deficit of vascular aetiology with symptoms lasting >24 hours

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
42
Q

Describe the aetiology of ischaemic strokes

A

Thrombotic: thrombus wihtin artery supplying blood to brain(atherosclerosis)
Embolic: embolus from elsewhere in the body

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
43
Q

Describe the pathophysiology of an ischaemic stroke

A

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

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
44
Q

Name sone strong risk factors for an ischaemic stroke

A

Increasing age
Male
Family history
Hypertension
Smoking
Diabetes
AF

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
45
Q

Name some weak risk factors for an ischaemic stroke

A

High cholesterol
Obesity
Poor diet
Oestrogen therapy
Migraine

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
46
Q

How is an ischaemic stroke diagnosed?

A

Non contrast CT head
Rule out haemorrhagic stroke
Areas of low density/’hyperdense artery’ sign

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
47
Q

Describe the acute management of an ischamic stroke

A

Rule out haemorrhagic:
NCCT head
Aspirin 300mg orally/rectally
<4.5 hours post onset: thrombolysis with IV alteplase
CT/MRI angiography
Mechanical thrombectomy

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
48
Q

What is alteplase?

A

Thrombolytic: tissue plasminogen activator

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
49
Q

Describe the secondary prevention of an ischaemic stroke

A

Clopidogrel 75mg
Aspiringif 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

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
50
Q

What artery supplies the lateral cerebral cortex?

A

Middle cerebral artery

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
51
Q

What artery supplies the anterior cerebral cortex?

A

Middle cerebral artery

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
52
Q

Describe the symptoms of lateral pontine syndrome and name the implicated artery

A

Ipsilateral:
-CN3 palsy
-Vertigo/nystagmus/deafness
-Poor coordination/tone/balance

-Anterior inferior cerebellar artery

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
53
Q

Describe the symptoms of Weber’s syndrome

A

Ipsilateral CN3 palsy
Contralateral hemiparesis

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
54
Q

Descirbe the symptoms of a Wallenberg’s stroke

A

Ipsilateral Horner’s syndrome
Ipsilateral loss of pain and temperature sensation in face
Contralateral loss of pain and temperature sensation in trunks and limbs
Ipsilateral cerebellar signs
Ipsilateral bulbar muscle weakness
Diplopia

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
55
Q

Name some cerebellar signs

A

Nystagmus
Vertigo

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
56
Q

Name some signs of bulbar muscle weakness

A

Dysphagia
Dysarthria

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
57
Q

What are the criteria for a total anterior circulation stroke?

A

3/3 of:
Unilateral weakness and/or sensory deficit of face, arm and leg
Homonymous hemianopia
Higher cerebral dysfunction(dysphasia, visuospatial disorder)

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
58
Q

What are the criteria for a partial anterior circulation stroke

A

2/3 of:
Unilateral weakness and/or sensory deficit of face, arm and leg
Homonymous hemianopia
Higher cerebral dysfunction(dysphasia, visuospatial disorder)

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
59
Q

What are the criteria for a posterior circulation stroke?

A

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

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
60
Q

What causes a lacunar stroke and which part of the brain does it affect?

A

Subcortical
Occurs secondary to small vessel disease

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
61
Q

How can a lacunar stroke be differentiated from other strokes?

A

NO loss of higher cerebral function

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
62
Q

What are the criteria for a lacunar stroke?

A

1/4 of:
Pure sensory stroke
Pure motor stroke
Sensori-motor stroke
Ataxic hemiparesis

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
63
Q

What can a CN5 palsy result in?

A

Trigeminal neuralgia
Loss of corneal reflex
Loss of facial sensation
Paralysis of mastication muscles
Deviation of jaw to weak side

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
64
Q

What can a CN6 palsy result in?

A

Abducens
Defective abduction-> hortizontal diplopia

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
65
Q

What can a CN7 palsy result in?

A

Facial
Flaccid paralysis of upper and lower face
Loss of corneal reflex(efferent)
Loss of taste
Hyperacusis

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
66
Q

What can a CN8 palsy result in?

A

Vestibulocochlear
Hearing loss
Vertigo, nystagmus
Acoustic neuromas

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
67
Q

What can CN9 palsy result in?

A

Glossopharyngeal
Hypersensitive carotid sinus reflux
Loss of gag reflex (afferent)

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
68
Q

What can a CN10 palsy result in?

A

Vagus
Uvula deviates away from site of lesion
Loss of gag reflex(efferent)

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
69
Q

What can a CN11 palsy result in?

A

Accessory
Weakness turning head to contralateral side

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
70
Q

What can a CN12 palsy result in?

A

Hypoglossal
Tongue deviates towards the side of lesion

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
71
Q

Describe the epidemiology of encephalitis

A

Peak: >70 yrs, <1yr
M:F 1:1

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
72
Q

Describe the aetiology of encephalitis

A

HSV1 responsible for 95% of cases in adults
Also: HSV2, CMV, EBV, VZV, HIV
Autoimmune encephalitis: NMDA receptor antibody associated encephalitis

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
73
Q

Describe the symptoms of encephalitis

A

Fever
Headaches
Seizures
Psych symptoms
Vomiting
Focal features
Flu-like prodromal illness

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
74
Q

Name some differentials for encephalitis

A

Hypoglycaemia
HE
DKA
Uremic/drug induced encephalopathy

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
75
Q

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

A

CSF testing: lymohocytosis, hgih protein, viral PCR analysis of CSF
MRI
EEG
CT

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
76
Q

How is encephalitis treated?

A

10mg/kg aciclovir TDS for 2 weeks
Broad spectrum antibiotics e.g. ceftriaxone
Supportive-seizure management

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
77
Q

Name some side effects of aciclovir

A

GI changes
Photosensitivity and rashes
Acute renal failure
Hepatitis

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
78
Q

Describe the prognosis of encephalitis

A

10-20% mortality of treatment started promptly
80% mortality if untreated

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
79
Q

Describe the epidemiology of meningitis

A

Viral(enteroviruses) most common
Bacterial: associated with increased morbidity and mortality
Fungal/parasitic: rare except in immunosuppressed

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
80
Q

Name the most common bacterial causes of meningitis and the groups they are present in

A

S.pneumoniae
N.meningitidis
H. influenza: infants
Listeria monocytogenes: Elderly

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
81
Q

Name some viral causes of meningitis

A

Enteroviruses
Herpes
VZV
Measles/rubella

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
82
Q

Name the parasitic causes of meningitis

A

Amoeba
Toxoplasma gardii

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
83
Q

Name some non infective causes of meningitis

A

Malignancies: leukaemia, lymphoma
Drugs: NSAIDs, trimethoprim
Systemic inflammatory diseases: Sarcoidosis, SLE, Behcets

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
84
Q

Describe the symptoms of meningitis

A

Headache
Fever
Nausea and vomiting
Seizures
Decreased consciousness
Photophobia
neck stiffness N
on blanching petechial/purpuric rash-> DIC

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
85
Q

Name some signs in a patient with meningitis

A

Kernig’s sign: Pain and resistance to knee extension
Brudzinski’s sign: passive neck flexion results in involuntary hip and knee flexion

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
86
Q

Name some differential diagnoses for meningitis

A

Encephalitis
SAH
Brain abscess
Sinusitis
Migraine

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
87
Q

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

A

Bloods: FBC, CRP, coag screen, cultures, PCR, glucose
ABG
CT head
LP
CSF analysis

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
88
Q

At what vertebral level is an LP taken?

A

L3/L4

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
89
Q

Describe the results of an LP in a patient with bacterial meningitis

A

Opening pressure: High
Appearance: cloudy/yellow
Glucose vs serum: Low <50%
Protein: High >1g/L
WCC: High, neutrophilia

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
90
Q

Describe the results of an LP in a patient with viral meningitis

A

Opening pressure: Normal
Appearance: cloudy/clear
Glucose vs serum: High >60%
Protein: Normal
WCC: High, lymphocytosis

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
91
Q

Describe the results of an LP in a patient with fungal/TB meningitis

A

Opening pressure: High
Appearance: cloudy/fibrous
Glucose vs serum: Low <50%
Protein: High
WCC: High, lymphocytosis

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
92
Q

Describe the treatment of a patient with suspected meningitis if presenting to a GP

A

IM benzylpenicillin and urgent hospital transfer

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
93
Q

Describe the treatment of a patient with suspected bacterial meningitis in hospital

A

IV cefotaxima/ceftriaxone and IV dexamethasone
Add amoxicillin for listeria cover(age extremes)

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
94
Q

Describe the treatment of suspected viral meningitis

A

If enteroviruses: nothing
If HSV/VZV: aciclovir

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
95
Q

What are the prophylaxis recommendations for contacts of meningitis

A

If in contact 7 days prior to onseet: One off dose of oral ciprofloxacin

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
96
Q

Name some complications of meningitis

A

Sepsis
DIC
SIADH
Seizures
Waterhouse friedrichsen syndrome
Delayed: hearing loss, cranial nerve dysfunction, intellectual deficits, ataxia, blindness

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
97
Q

Name the causes of meningitis is neonates(0-3 months)

A

Group B strep
E.Coli
Gram negative bacilli
Listeria
S.pneumoniae

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
98
Q

Name the causes of meningitis in infants(3 months-6 years)

A

S.pneumoniae
N.meningitidis
H. influenzae

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
99
Q

Name the causes of meningitis in adults(6-60 years)

A

S.pneumoniae
N.meningitidis

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
100
Q

Name the causes of meningitis in the elderly (>60yrs)

A

S.pneumoniae
N.meningitidis
Listeria
Gram negative bacilli

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
101
Q

How does S.pneumoniae appear on microbiology?

A

Gram positive diplococcus in chains

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
102
Q

How does Group B strep appear on microbiology?

A

Gram positive coccus in chains

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
103
Q

What age groups is most likely to have meningitis cauased by Group B strep and why?

A

Neonates
Colonises in maternal vagina

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
104
Q

What age group is most likely to get meningitis from listeria monocytogenes?

A

Extremes of age, pregnant
Found in cheese

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
105
Q

What does listeria monocytogenes appear like on microbiology?

A

Gram positive bacillus

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
106
Q

What are the types of neurofibromatosis and which is more common?

A

Type 1-more commonType 2

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
107
Q

Describe the aetiology of neurofibromatosis type 1

A

Mutation on chromosome 17 which codes for neurofibromin(tumour suppressor protein)

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
108
Q

Describe the inheritance pattern of neurofibromatosis type 1

A

Autosomal dominant

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
109
Q

Describe the features of neurofibromatosis type 1

A

CRABBING
Cafe au lait spots >15mm
Relative with NF1
Bony dysplasia-bowing of long bones or sphenoid wing dysplasia
Iris hamartomas(lisch nodules)-yellow/brown spots on iris
Neurofibromas > 2 significant or 1> if plexiform
Glioma of optic pathway

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
110
Q

How is neurofibromatosis diagnosed?

A

Diagnostic criteria and genetic testing

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
111
Q

Describe the treatment of neurofibromatosistype 1

A

Monitor and manage symptoms, treat complications

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
112
Q

Name some complications of neurofibromatosis type 1

A

Malignant peripheral nerve sheath tumours(MPNST)
Gastrointestinal stromal tumours(GIST)
Migraines
Epilepsy
Hypertension from renal artery stenosis
Scoliosis
Brain/spinal tumours
High cancer risk

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
113
Q

Describe the aetiology of neurofibromatosis type 2

A

Mutation on chromosome 22->merlin->tumour suppressor protein important in schwann cells resulting in schwannomas

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
114
Q

Describe the epidemiology of giant cell arteritis

A

Most common primary vasculitis->50 years, peaks in 70s
M:F 1:3

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
115
Q

Name some risk factors for giant cell arteritis

A

Genetics
Environmental
Age-
females
Sex
Ethnicity(Mc caucasian-scandinavian)

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
116
Q

Describe the presentation of a patient with giant cell arteritis

A

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)

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
117
Q

What investigations should be done in a patient with giant cell arteritis?

A

High ESR/CRP
Normal creatine kinase and EMG
Temporal artery biopsy-> granulomatous inflammation and infiltration of giant cells
Doppler USS: ‘halo’ sign

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
118
Q

Describe the managmeent of giant cell arteritis

A

Urgent high dose steroids: 40-60mg prednisolone OD to prevent blindness
Then taper(use bisphosphonates/PPI)
Low dose aspirin to reduce risk of stroke/blindness

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
119
Q

Name some complications of giant cell arteritis

A

Permanent monocular blindness
Diplopia
Stroke
Aortic aneurysms

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
120
Q

How can giant cell arteritis result in permanent monocular blindness?

A

Anterior ischaemic optic neuropathy-> occlusion of posterior ciliary artery-> ischaemia of optic nerve head

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
121
Q

How can giant cell arteritis cause diplopia?

A

Involvement of any paart of oculomotor system(e.g. cranial nerves)

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
122
Q

What is Bell’s palsy?

A

Acute, unilateral, idiopathic facial nerve paralysis

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
123
Q

Describe the epidemiology of bell’s palsy

A

Peak incidence: 15-45 years
Higher prevalence in pregnant women

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
124
Q

Describe the aetiology of Bell’s palsy

A

Unknown
Linked to HSV1
EBV
VZV

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
125
Q

Describe the presentation of Bell’s palsy

A

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

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
126
Q

Name some differential diagnoses for bell’s palsy

A

Ramsay Hunt syndrome
Stroke-forehead sparing
Guillain Barre

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
127
Q

What investigations might be done in a patient presenting with suspected Bell’s palsy?

A

Clinical: rule out other causes/assess extent of damage
FBC/ESR/CRP/viral serology/lyme serology/otoscopy/EMG/MRI/CT

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
128
Q

Describe the management of Bell’s palsy

A

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

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
129
Q

Describe the prognosis of Bell’s palsy

A

Complete recovery: 70-80% in weeks-months
If untreated: 15% have permanent moderate/severe weakness

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
130
Q

Name some poor prognostic factors for Bell’s palsy

A

Older age
More severe initial facial weakness

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
131
Q

Describe the epidemiology of essential tremor

A

Commmon
Increased age: peak 40-50 years
F:M:1:1
Family history

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
132
Q

Describe the aetiology of essential tremor

A

Not fully understood
50% of cases have an autosomal dominant trait

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
133
Q

Describe the pathophysiology of essential tremor

A

GABA-ergic dysfunction-> increased activity in cerebellar-thalamic cortical circuit

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
134
Q

Describe the features of essential tremor

A

Postural/kinetic tremor that predominantly affects the upper limbs distally
Usually bilateraL: high frequency: 6-12Hz
Exacerbated by intentional movements, absent on restIncreasing amplitude over time
Relieved by alcohol
Exacerbated by anxiety, excitement etc
Can affect head, lower limbs, voice, tongue, face and trunk

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
135
Q

What additional features of essential tremor might prompt further investigation to look for differentials?

A

Difficulty with tandem gait
Mild cognitive impairment
Slight resting tremor alongside action tremor

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
136
Q

How is essential tremor diagnosed?

A

CLinical diagnosis
bilateral uppper limb action tremor lasting >3 years with no other tremor/neurological signs

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
137
Q

Name some differential diagnoses for essential tremor

A

Parkinson’s
Hyperthyroidism
Dystonic tremor
Spasmodic dysphonia

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
138
Q

Describe the management of essential tremor

A

Pharmacological:
Propanolol
Primidone

2nd line:
gabapentin,
topirimate,
nimodipine

Surgical
DBS
Botulinum toxin type A injections

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
139
Q

Describe the prognosis of essential tremor

A

Typically worsens with increasing age
Can remain isolated or can spread e..g. to head or voice over years
Can cause major disability

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
140
Q

Describe the epidemiology of myasthenia gravis

A

M:F 1:1
Bimodal distribution
Peak incidence in F<40 years and M>60 years

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
141
Q

Describe the pathophysiology of myasthenia gravis

A

85%:AChR antibodies->lower ability of ACh to trigger muscle contractions->; weakness
Also MuSK(muscle-specific kinase) and LLRP4(low density lipoprotein receptor related protein)->creation and organisation of AChR-> inadequate AChR

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
142
Q

Describe the presentation of a patient with myasethnia gravis

A

Muscle weakness that worsens with repetitive activity and weakens with rest(typically ocular/bulbar and limb muscles)
Ptosis
Diplopia
Dysarthria
Dysphagia
Proximal limb weakness
Exacerbated by beta blockers, lithium, phenytoin and certain abx

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
143
Q

How is myasthenia gravis investigated/diagnosed?

A

Bedside: ice pack test
Serology for AChR antibodies, MuSK and LRP4 antibodies
CT/MRI chest to look for thymomas/thymic hyperplasia
Edrophonium test

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
144
Q

Describe the management of myasthenia gravis

A

ACh inhibitors: pyridostigmine, neostigmineImmunosuppression->steroids, azathioprine
Thymectomy
Rituximab
Plasma exchange and IVIG

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
145
Q

Name some prognostic factors for myasthenia gravis

A

Age of onset
Antibody subtype
Thymus histology
Response to treatment

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
146
Q

Name one complication of myasthenia gravis

A

Myasthenic crisis

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
147
Q

What is a myasthenic crisis?

A

Life threatening acute worsening of symptoms, often triggered by another illness like a URTI-> can result in respiratory muscle failure

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
148
Q

How is a myasthenic crisis treated?

A

Usual meds
IVIG and plasmapharesis
If FVC<15mL/kg: mechanical ventilation

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
149
Q

What is chronic fatigue syndrome?

A

Chronic disabling condition characterised by profound fatigue and impariment following minimal physical/cognitive effort

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
150
Q

Describe the epidemiology of chronic fatigue syndrome

A

Peak: 30-40 years
F:M:2:1

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
151
Q

Describe the aetiology of chronic fatigue syndrome

A

UnknownTriggers like EBV
Psychological stress

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
152
Q

Describe the symptoms of chronic fatigue syndrome

A

Extreme fatigue
Post-exertional malaise
Sleep disturbances and unrefreshing sleep
Cognitive impairment
Orthostatic intolerance
Immune/neurological/autonomic/psychiatric manifestations

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
153
Q

Name some differential diagnoses for chronic fatigue syndrome

A

Fibromyalgia
Depression
Hypothyroidism
AI disorders

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
154
Q

How is chronic fatigue syndrome diagnosed?

A

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

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
155
Q

Describe the managment of chronic fatigue syndrome

A

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

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
156
Q

What is an acoustic neuroma also known as?

A

Vestibular schwannoma

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
157
Q

What is an acoustic neuroma?

A

Benign subarachnoid tumour that exerts local pressure on cranial nerve 8

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
158
Q

Describe the epidmiology of acoustic neuromas

A

Rare in UK
Adults aged 40-60 years

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
159
Q

Describe the aetiology of acoustic neuroma

A

Develop from Schwann cells of vestibulocochlear nerve
Majority are sporadic cases
Can be associated with NF2

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
160
Q

Describe the presentation of acoustic neuroma

A

Asymmetric/unilateral hearing loss
Progressive ipsilateral tinnitus
Sensorineural deaffness
Larger tumours: raised ICP like focal neurology:
CN5/67/8
Dizziness, headaches, disequilibrium

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
161
Q

Name some differential diagnoses for acoustic neuroma

A

Meniere’s disease
Labyrinthitis
BPPV

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
162
Q

What investigations should be done in a patient with a suspected acoustic neuroma?

A

Audiometry
MRI scan of cerebellopontine angle

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
163
Q

Describe the management of an acoustic neuroma

A

Urgent referral to ENT>40mm: surgery
<40mm: 6 monthly annual surveillance scans via MRI

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
164
Q

What focal neurology might be seen in a patient with an acoustic neuroma?

A

CN8: vertigo, unilateral sensorineural hearing loss, unilateral tinnitus
CN5: absent corneal reflex
CN7: facial palsy

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
165
Q

Describe the epidemiology of Meniere’s disease?

A

30-60 years
Predominantly unilateral

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
166
Q

Describe the aetiology of meniere’s disease

A

Dilatoin of endolymphatic spaces of membranous labyrinth resulting in an increased fluid pressure within the inner ear

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
167
Q

Describe the presentation of meniere’s disease

A

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

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
168
Q

Name some differential diagnoses for meniere’s disease

A

Vestibular neuritis
Labyrinthitis
BPPV

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
169
Q

What investigations are used to diagnose meniere’s disease?

A

Clinical evaluation
Audiometric testing
Imaging/other tests may be used to rule out other potential causes of symptoms

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
170
Q

Describe the management of meniere’s disease

A

ENT assessment
Prophylactic use of betahistine to reduce frequency
Acute: prochlorperazine
Diuretics-> reduce endolymphatic fluid(only prescribed by specialists)
Low salt diets can help prevent attacksDVLA: no driving until good control of sx

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
171
Q

Describe the natural history of Meniere’s disease

A

Sympotms resolve in most patients after 10-15 years
Majority of patients left with a degree of hearing loss
Psychological distress common

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
172
Q

Describe the epidemiology of trigeminal neuralgia

A

> 50yrs
F>M

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
173
Q

Describe the aetiology of trigeminal neuralgia

A

Primary-idiopathic or secondary
Secondary causes include:
Malignancy-
nerve compression
AVM
MS
Sarcoidosis
Lyme disease

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
174
Q

Describe the presentation of a patient with trigeminal neuralgia

A

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

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
175
Q

Name some differential diagnoses for trigeminal neuralgia

A

Post herpetic neuralgia
Temperomandibular joint disorders
Giant cell arteritis
Cluster headache

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
176
Q

How is trigeminal neuralgia diagnosed?

A

Mostly clinical
MRI or other neuroimaging to rule out secondary causes

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
177
Q

Describe the management of trigeminal neuralgia

A

Medical:
Carbamazepine
Phenytoin
Lamotrigine
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

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
178
Q

Name some red flag symptoms for trigeminal neuralgia

A

Sensory changes
Deafness
Pain only in ophthalmic division(eye socket, forehead and nose) or bilaterally
Optic neuritis
FHx of MS
<40 yrs

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
179
Q

What is bulbar palsy?

A

Subtype of LMN lesion impacting the 9/10/12th cranial nerves

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
180
Q

Name the major causes of bulbar palsy

A

Motor neurone disease-mc
Myasthenia gravis
Guillain-barre
Brainstem stroke-Wallenberg’s/lateral medullary syndrome
Syringobulbia

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
181
Q

Describe the signs and symptoms of bulbar palsy

A

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)

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
182
Q

Name some differentials for bulbar palsy

A

Pseudobulbar palsy
Brainstem tumour
MS
Polymyositis and dermatomyositis

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
183
Q

What investigations should be done in a patient with bulbar palsy?

A

Neuro exam
EMG and nerve conduction studies:
MND/myasthenia gravis
Bloods: FBC, electrolytes, CK, autoantibody screening
MRI-lesions in brainstem
LP: rule out infections/AI causes

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
184
Q

How is bulbar palsy managed?

A

Speech and swallowing therapy-manage dysarthria and dysphagia
Nutritional support
Treat underlying cause

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
185
Q

How can Horner’s syndrome be characterised?

A

Pre-ganglionic
Post-ganglionic
Central
Dependent on location of sympathetic nerve interruption

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
186
Q

Name some causes of Horner’s syndrome

A

Pancoast tumour: pre-ganglionic
Stroke-central
Carotid artery dissection: post-ganglionic
Trauma, tumours, surgery-central

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
187
Q

What is a pancoast tumour and how can it case Horner’s syndrome?

A

Non-small cell lung carcinoma
Located at superior sulcus of lung affects lower roots of brachial plexus and sympathetic chain

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
188
Q

How do patients with Horner’s syndrome typically present?

A

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

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
189
Q

Name some differential diagnoses for Horner’s syndrome

A

Oculomotor nerve palsy-will also have ophthalmoplegia
Myasthenia gravis
Bell’s palsy

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
190
Q

What investigations might be done in a patient presenting with Horner’s syndrome?

A

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

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
191
Q

Describe the management of Horner’s syndrome

A

Treat underlying causeIf no casue identified, observation and regular follow up
Cosemtic interventions for ptosis or miosis may be considered

192
Q

Describe the aetiology of Guillain Barre syndrome

A

1-3 weeks post infection-mc Campylobacter
Others: mycoplasma and EBV
40% idiopathic
Others: CMV, HIC, hepatitis A, vaccinations

193
Q

How do patients with Guillan Barre present?

A

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

194
Q

Name some variants of Guillaim Barre syndrome

A

Parapetic
Miller-Fischer
Pure motor
Bilateral facial palsy with paraesthesias
Pharyngeal brachial cervical weakness
Bickerstaff’s brainstem encephalitis

195
Q

Name some differential diagnoses for Guillain Barre

A

Vascular: strokesInfective/inflammatory: polio, lyme, CMV, TB, HIV, CIDP, myasthenia gravis
Spinal cord compression
Metabolic-porphyria, electrolyte abnormalities

196
Q

What investigations might be done in a patient with suspected Guillain Barre?

A

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

197
Q

How is Guillain Barre managed?

A

Regular FVC monitoring-can rapidly deteriorate
VTE prophylaxis: TEDS and LMWH
Analgesia if needed
Manage complications: arrhythmias, autonomic dysfunction
Enteral feeding if unsafe swallow
significant disability:IVIG for 5 days
Plasmapharesis(more side effects that IVIG)

198
Q

Give some prognostic factors for Guillain Barre

A

Speed of onset
Severity
Age
Presence of preceding diarrhoeal illness

199
Q

Describe the pathophysiology of Guillain Barre syndrome

A

Cross reaction of antibodies with gangliosides in the peripheral nervous system
Correlation between anti-ganglioside antibody and clinical features
Anti-GM1 antibodies

200
Q

Describe the epidemiology of Huntington’s disease

A

Most common neurodegenerative disorder

201
Q

Describe the aetiology of Huntington’s disease

A

Autosonomal dominant mutation involving excessive repetition of CAG nucelotide in huntingtin gene
Gradual degeneration of caudate nucleus and putamen

202
Q

Describe the presentation of a patient with Huntington’s disease

A

Choreoathetosis: unpredictable flowing and writhing movements
Cognitive impairment: dementia
Psychiatric abnormalitis: depression, irritability apathy and sometimes psychosis
Usually over age 35YRS
Dystonia
Saccadic eye movements

203
Q

Give some differential diagnoses for Huntington’s disease

A

Parkinson’s
Wilson’s disease
Huntington’s disease like disorders
Neuroacathocytosis syndromes

204
Q

How is Huntington’s Disease diagnosed?

A

MRI/CT: loss of striatal volume and enlarged frontal horn of lateral ventricles
Genetics: including for at risk family members

205
Q

How is Huntington’s disease managed?

A

Chorea management; tetrabenazine
Depression: SSRI
Psychosis: atypical antipsychotics
Supportive: physical and emotional support from MDT

206
Q

Describe the pathophysiology of Huntington’s disease

A

Autosomal dominant mutaiton results in degeneration of cholinergic and GABAergic neurons in striatum of basal ganglia

207
Q

What is  a seizure?

A

Transient occurences of signs and symptoms due to abnormal excessive or synchronous neuronal activity in the brain

208
Q

Describe the aetiology of epilepsy

A

Idiopathic generalised epilepsy
Childhood absence
Juvenile absence
Juvenile myoclonic
generalised tonic clonic

Structural:
Stroke
Trauma
Malformations
Genetic
Infectious
Metabolic
Immune
Unknown

209
Q

Name some differential diagnoses for epilepsy

A

Syncope
TIA
Migraines
Panic disorder
Non epileptic attack disorder

210
Q

What investigations might be done in a patient with a seizure?

A

History including collateral and neuro examImaging like CT/MRI
EEG
Might consider LP, bloods, advanced imaging depending on background

211
Q

Name some localising features of temporal lobe seizures

A

Can occur with/without impairment of consciousness or awareness
Usually has an aura: rising epigastric sensation, psychic phenomena
Automatisms: lip smacking, grabbing, plucking

212
Q

Name some localising features of frontal lobe seizures

A

Frontal lobe-motor
Head/leg movements
Posturing
Post-ictal weakness
Jacksonian march

213
Q

Name some localising features of parietal lobe seizures

A

Parietal lobe-sensory
Paraesthesia

214
Q

Name some localising features of occipital lobe seizures

A

Occipital-visual
Floaters/flashers

215
Q

What are focal seizures?

A

Previously: partial seizures
Start in a specific area on one side of the brain
Level of awareness can vary

216
Q

How can focal seizures be further classified?

A

Based on awareness:Focal aware(simple partial)
Focal impaired awareness(complex partial)

217
Q

Describe a focal seizure with impaired awareness

A

Patients lose consciousness, usually post an aure or at seizure onset
Commonly originate from the temporal lobe

218
Q

Describe a focal saware seizure

A

Patients retain consciousness experiencing only focal symtpoms
Usually no ictal symptoms

219
Q

Describe a secondary generalised seizure

A

Focal seizure that evolves into a bilateral tonic-clonic seizure

220
Q

Describe the features of a generalised seizure

A

Involve both sides of the brain at onset
Consciousness lost immediately
Can be further divided into tonic-clonic and absence etc

221
Q

Describe an absence seizure

A

Brief pauses for <10 seconds

222
Q

Describe a tonic clonic seizure

A

Loss of consciousness
Stiffening(tonic) and jerking(clonic) of limbs
Post-ictal confusion common

223
Q

Describe a myoclonic seizure

A

Sudden jerks of a limb, trunk or face

224
Q

Describe an atonic seizure

A

Sudden loss of muscle tone causing the patient to fall with consciousness retained

225
Q

Describe the treatment of generalised tonic-clonic seizures

A

Males: sodium valproate
Females: lamotrigine or levetiracetam

226
Q

Describe the management of focal seizures

A

Lamotrigine/levetiracetam
Carbamazepine

227
Q

Describe the management of absence seizures

A

Ethosuximide
Lamotrigine/levetiracetam(sodium valproate in males)=
Carbamazepine

228
Q

Describe the management of myoclonic seizures

A

Males: sodium valproate
Females: levetiracetam

229
Q

Describe the management of tonic/atonic seizures

A

Males: sodium valproate
Females: lamotrigine
Carbamazepine

230
Q

Name some complications of epilepsy

A

Status epilepticus
Psychiatric complications-> increased risk of depression and epilepsy
Sudden unexpected death in epilepsy(SUDEP)

231
Q

Name some side effects of topirimate

A

Abdo pain
Cognitive impairment
Confusion
Muscle spams
mood changes
n+v
tremor
weight loss

232
Q

Name some side effects of lamotrigine

A

blurred vision
arthralgia
ataxia
diarrhoea
dizziness
headache
insomnia
rash
tremor

233
Q

Name some side effects of carbamazepine

A

ataxia
blood disorders
blurred vision
fatigue
hyponatraemia

234
Q

name some side effects of sodium valproate

A

ataxia
anaemia
confusion
gastric irritation
haemorrhage
hyponatraemia
tremor
weight gain

235
Q

name some side effects of phenytoin

A

acne
anorexia
constipation
hirsutism
insomnia
rash
tremor

236
Q

What are the DVLA rules with regards to epilepsy?

A

Car/motorbike: 1 seizure: 6 months, >1 seizure: 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 free years

237
Q

Describe the management of status epilepticus

A

Buccal midazolam or rectal diazepam-can repeat
If IV access: IV lorazepam repeated after 10-20 minutes MAX 2 dose benzos 2nd line: levetiracetam, phenytoin, sodium valproate
Refractory status(20-90 minutes)-general anaesthesia
Propofol
midazolam
infusion
thiopental sodium

238
Q

What investigations might be done in a patient with status epilepticus?

A

ABG
Bloods: FBC, U&E, LFT, CRP, clotting, bone profile
Toxicologyc screen
Anti epileptic drug
Imaging to determien cause: CT/MRI, LP

239
Q

Describe the epidemiology of MS

A

Females: 2.3:1
Average onset 30yrs

240
Q

Describe the aetiology of MS

A

Combination of genetic and environmental factors including potential viral pathogens
CD4 mediated destruction oligodendrogial cells and humoral response to myelin binding protein

241
Q

Describe the symptoms of MS

A

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

242
Q

How can MS be classified?

A

Relapsing remitting-> may become secondary progressive
Primary progressive

243
Q

Name some differentials for MS

A

SLE
Lyme disease
Neurosarcoidosis
Vitamin B12 deficiency

244
Q

How is MS diagnosed?

A

MRI showing >2 periventricular white matter lesions disseminated in time and space
Oligoclonal bands in CSF electrophoresis

245
Q

What criteria is used to diagnose MS?

A

McDonald criteria

246
Q

Describe the acute management of an MS flare?

A

High dose IV methylprednisolone for 5 days
Reduce duration or relapse not severity
Rule out infection

247
Q

Describe the long term management of MS

A

Natalizumab-biologics->Ocrelizumab
Beta-interferon-injectable
Symptomatice therapies:PhysioBaclofen and botox for spasticity
Anticholinergics for bladder dysfunction
Sildenafil for ED

248
Q

Name some risk factors that might suggest a worse prognosis for a patient with MS

A

Older age at onset
Primary progressive
High relapse rate
Rapid accumulation of disability
Comorbid conditions
Smoking

249
Q

Describe the epidemiology of normal pressure hydrocephalus

A

More common in older adults
Considered a significant cause of reversible dementia

250
Q

Describe the epidemiology of diabetic peripheral neuropathy

A

Common complication of both types of diabetes
Occurs in 50% of long term diabetic patients
Risk increases with duration of diabetes and poor glycaemic control

251
Q

Describe the aetiology of diabetic peripheral neuropathy

A

Chronic hyperglycaemia-> accumulation of advanced glycation end products, oxidative stress and inflammatory pathways

252
Q

How can diabetic peripheral neuropathy be categorised?

A

Distal symmetrical sensory neuropathy
Small fibre predominant neuropathy
Diabetic amyotrophy
Mononeuritis multiplex
Autonomic neruopathy

253
Q

Describe the features of distal symmetrical sensory neuropathy

A

Most common form of diabetic peripheral neuropathy
Results from loss of large sensory fibres’glove and stocking’ distribution affecting touch, vibration and proprioception

254
Q

Describe the features of small fibre predominant neuropathy

A

Loss of small sensory fibres
Loss of pain and temperature sensation in ‘glove and stocking’ distribution accompanied by epsiodes of burning pain

255
Q

Describe the features of diabetic amyotrophy

A

Originates from inflammation of the lumbrosacral plexus or cervical plexus
Characterised by severe pain around thighs and hips and proximal weakness

256
Q

Describe the features of mononeuritis multiplex

A

Painful
Neuropathies involving >=2 distinct peripheral nerves

257
Q

Describe the features of autonomic neuropathy

A

Postural hypotension
Gatroparesis
Constipation
Urinary retention
Arrhythmias
Erectile dysfunction

258
Q

Name some differentials for diabetic peripheral neuropathy

A

Vitamin B12 deficiency
Alcohol induced peripheral neuropathy
CIDP
Hypothyroidism

259
Q

What investigations might be done in a patient with diabetic peripheral neuropathy?

A

Neuro exam
Nerve conduction tests
Bloods-HbA1c, B12, TFTs, LFTs

260
Q

Name some complicaitons of diabetic peripheral neuropathy

A

Foot ulcers due to loss of sensation
Autonomic neuropathy-> cardiac, GI and GU disturbances

261
Q

Describe the management of diabetic peripheral neuropathy

A

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

262
Q

What is Charcot neuropathy?

A

Chronic progressive condition characterised by painful or painless bone and joint destruction in limbs that have lost sensory innervation

263
Q

Describe the epidemiology of charcot arthropathy

A

MC in pts with long standing DM
Middle aged and elderly population

264
Q

Describe the aetiology of Charcot neuropathy

A

DM(mc)->microvascular disease, autonomic and peropheral neuropathy-> cumulative damage to joints
Also:
Chronic alcohol abuse
Syringomyelia
Syphilis

265
Q

What are the signs and symptoms of Charcot arthropathy?

A

6D’s
Destruction of bone and joint
Deformity
Degeneration
Dense bones
Debris of bone fragments
Dislocation

266
Q

Name some differentials for charcot arthropathy

A

Osteomyelitis-> important to rule out

267
Q

What investigations are used to diagnose charcot arthropathy

A

Clinical dx mostlyX-rays 1st line imaging: bone destruction, debris, sclerosis and dislocation
MRI if ostemyelitis suspected

268
Q

How is charcot arthropathy managed?

A

Conservative: lifestyle, footwear, orthotics
Medications: bisphosphonates, gabapentin
Surgical: resection of bony prominences, amputation if severe

269
Q

Describe the symptoms of cerebellar dysfunction

A

DANISH
Dysdiadochokinesia
Ataxia
Nystagmus
Intention tremor
Slurred speech
Hypotonia

270
Q

Name the causes of cerebellar syndrome

A

PASTRIES
Paraneoplastic syndrome
Alcohol
Sclerosis-MS
Tumours
Rare-Friedreich’s ataxiaIatrogenic-phenytoin, carbamazepine
Endocrine/metabolic: hypothyroidism/Wilson’s
Stroke

271
Q

How is cerebellar dysfunction investigated/diagnosed?

A

CT/MRI: ID stroke, tumours, trauma
Serology: infectious/inflammatory causes
LP: infection, inflammation, malignancy
Genetics-hereditary

272
Q

How is cerebellar dysfunction managed?

A

Treat underlying cause
Surgery/meds as required
Lifestyle-alcohol etc
Rehab: OT, physio etc

273
Q

Describe the epidemiology of parkinson’s disease

A

2nd mc neurodegenerative disorder after Alzheimer’s
65yrsM>F

274
Q

Describe the pathophysiology of Parkinson’s disease

A

Accumulation of Lewy bodies in the substantia nigra of the basal ganglia-> neuronal cell death of dopaminergic cells

275
Q

What are lewy bodies?

A

intracellular inclusions composed mostly of misfolded alpha synuclein

276
Q

What are the components of the basal ganglia?

A

Striatum-> dorsal and ventral
Globus pallidus
Thalamus
Substantia nigra
Subthalamic nucleus

277
Q

Describe the direct movement pathway in the substantia nigra

A

Excitatory
Increases thalamus activity-> increase movement

278
Q

How does parkinson’s affect the direct movement pathway?

A

Decreased levels of dopamine
Decreases direct pathway
Can’t initiate increased movement->decreased movement

279
Q

Describe the indirect motor pathway in the substantia nigra

A

Inhibitory
Decreases thalamus activity
Decreases movement

280
Q

How does parkinson’s affect the indirect movement pathway?

A

Less dopamine
Increases indirect pathway
Can’t prevent excessive movement pathway
Decreases movement

281
Q

Name some risk factors for Parkinson’s disease

A

Family hx-especially when onset <50yrs
Previous head injury

282
Q

Name some protective factors for Parkinson’s disease

A

Smoking> including past smoking
Caffeine intake
Physical activity

283
Q

Describe the tremor associated with Parkinson’s disease

A

Resting tremor’pill rolling’
Asymmetrical
3-5Hz

284
Q

How does bradykinesia present in a patient with Parkinson’s disease

A

Parkinsonian gait->shuffling, slowness of movement especially on initiation and turning

285
Q

How does muscle rigidity present in Parkinson’s disease?

A

‘Cogwheel rigidity’
Decreased arm swing
Stooped posture

286
Q

Name some motor symptoms of Parkinson’s disease

A

Triad of:
Tremor
Bradykinesia
Muscle rigidity

Also:
Postural instability->increased falls
Hypomimic facies
Hypokinetic dysarthria, speech impairment, dysphagia
Micrographia

287
Q

Name some non motor symptoms of Parkinson’s disease

A

Autonomic dysfunction
Sleep dysfunction(REM behavioural disorder)
Olfactory loss
Psychiatric->depression, anxiety, hallucinations, psychotic episodes, paranoid delusions

288
Q

How is Parkinson’s disease diagnosed?

A

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

289
Q

Name some differentials for Parkinson’s disease

A

Essential tremor
Multiple system atrophy
Lewy body dementia

290
Q

How is essential tremor differentiated from Parkinson’s disease tremor?

A

Essential tremor vs Parkinson’s
Symmetrical vs 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

291
Q

Name some complications of Parkinson’s disease

A

Autonomic dysfunction
Recurrent falls
Cognitive imapirment

292
Q

How does levodopa work for Parkinson’s disease

A

Dopaminergic
Precursor to dopamine->converted in CNS and periphery

293
Q

What drug is levodopa often dosed with for treating Parkinson’s disease patients and why?

A

Carbidopa
Decreases conversion of levodopa in periphery-> increases CNS availability and decreases peripheral side effects

294
Q

Name some peripheral side effects of levodopa

A

Postural hypotension
Nausea and vomiting

295
Q

Name some central side effects of levodopa

A

Hallucinations
Confusion
Dyskinesia
Psychosis

296
Q

What are 2 problems with long term levodopa therapy other than side effects?

A

End of dose effect
On and off phenomenon

297
Q

Aside from levodopa, what medication groups might be used to treat Parkinson’s disease?

A

Monoamine oxidase B inhibitors(MAO-B inhibitors)
COMT inhibitors
Dopamine agonists
Amantadine
Anticholinergics

298
Q

Give some examples of MAO-B inhibitors and how they can help in Parkinson’s disease

A

Rasagiline and selegilin
Decrease dopamine breakdown peripherally so increase central uptake

299
Q

What is an important potential complication of using MAO-B inhibitors?

A

Can cause serotonin syndrome

300
Q

Give some examples of COMT inhibitors and how they are used in Parkinson’s disease treatment

A

Entacapone and tolcapone
Extend use of levodopa-> good for wearing off effect of levodopa

301
Q

Give some examples of dopamine agonists and how they are useful for Parkinson’s disease

A

ropinirole
rotigotine
apomorphine-most potentmimic dopamine

302
Q

What is an important side effect of apomorphine?

A

Haemolytic anaemia

303
Q

Aside from medications, what treatments are available for Parkinson’s disease?

A

Deep brain stimulation
Physio, SALT, OT

304
Q

Name some situations in which hypoxic-ischaemic encephalopathy can occur

A

Neonates: pperinatal asphyxia
Adults: secondary to cardiac arrest/severe systemic hypoxia

305
Q

Describe the pathophysiology of hypoxic-ischaemic encephalopathy

A

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

306
Q

How does hypoxic-ischaemic encephalopathy present clinically?

A

Altered consciousness ranging from lethary to coma
Seizures
Abnormal tone and reflexes

307
Q

How is hypoxic-ischaemic encephalopathy managed?

A

Supportive: maintain normal body temp and blood glucose levels
Seizure control
Neonates within 6 hours of birth: therapeutic hypothermia

308
Q

What investigations might be done in hypoxic-ischaemic encephalopathy?

A

ABG
CBC
Electrolytes and glucose
LFTs and U&Es
Neuroimaging: MRI and cranial USS(neonates)
EEG monitoring
Metabolic screening if atypical
Diagnosis: clinical mostly

309
Q

Name some complications of hypoxic-ischaemic encephalopathy

A

Cerebral palsy
Seizure disorders
Cognitive impairment
Motor deficits
Sensory impairments
Microcephaly
Behavioural disorders
Multisystem organ failure of severe: CVR, renal, hepatic, resp

310
Q

What is a brain abscess?

A

Collection of pus within the brain parenchyma linkes with significant morbidity and mortality

311
Q

Describe the aetiology of a brain abscess

A

Usually contiguous spread of infection from sinusitis, otitis media or dental infection
Haematogenous spread from distant sources; endocardities etc
Direct inoculation: trauma/neurosurgery

312
Q

Name some risk factors for developing a brain abscess

A

Immunocompromised states
Congenital heart defects and endocarditis
Chronic otitis/sinusitis
IVDU
Dental head and neck procedures

313
Q

Describe the pathogenesis of a brain abscess

A

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

314
Q

Describe the signs and symptoms of a brain abscesss

A

Headache
Focal neurological deficits
Infeciton signs: fever, n+v, meningism
Raised ICP: headache, 3rd nerve palsy, papilloedema, seizures

315
Q

Name some differentials for a brain abscess

A

Space occupying lesions-cancer, vascular
CNS infections
Stroke

316
Q

How is a brain abscess diagnosed?

A

MRI with gadolinium contrast-> better at detecting early cerebritis
CT for complications like hydrocephalus
Stereotactic needle aspiration
LP CONTRAINDICATED

317
Q

Describe the management of a brain abscess

A

A-E and consider sepsis 6
Surgery: craniotomy-aspiration/excision
IV abx: 3rd gen: cephalosporin + metronidazole
Sx management: dexamethasone for raised ICP

318
Q

Name some complications of a brain abscess

A

Seizures
Meningitis
Ventriculitis
Hydrocephalus
Cerebral oedema
Herniation
Death
Permanent neuro deficits

319
Q

Name some causes of space occupying lesions

A

Neoplasia: metastatic and primary CNS tumours
Vasulcar: avms/aneurysms
Infective: abscesses, TB etc
Granulomatouus disease: neurosarcoidosis

320
Q

What is Cushing’s reflex?

A

Hypertension
Bradycardia
Irregular respirations
Sign of raised ICP

321
Q

Describe some potential signs/symptoms of brain metastases

A

Headache: worse on waking, lying down or with coughing/straining
Raised ICP
Neuro deficits
Cushing’s reflex
Systemic: weight loss, night sweats, fevers etc

322
Q

What investigations might be used for brain metastases

A

CT head-1st line in acute settings e.g. if presenting with seizures
MRI brain for details
PET scan
Biopsy

323
Q

How are brain metastases treated?

A

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

324
Q

What is a glioblastoma multiforme?

A

Mc primary brain tumour in adults
Malignant and highly aggressive
Associated with a poor prognosis-1 yr

325
Q

How does a glioblastoma multiforme appear on imaging?

A

Solid tumours with central necrosis and a rim that enhances with contrast
Disruption of blood brain barrier and vasogenic oedema

326
Q

How is a glioblastoma multiforme treated?

A

Surgical with postoperative chemo and/or radiotherapy
Dexamethasone for oedema

327
Q

Describe the features of a meningioma

A

2nd mc primary brain tumour in adults
Typically benign, extrinsic tumours of the CNS
Arise from dura mater of the meninges and cause sx by compression noot invasion

328
Q

How is a meningioma diagnosed and treated?

A

CT-contrast enhancement and MRI
Observation, radiotherapy or surgical resection

329
Q

What is a vestibular schwannoma?

A

Previously acoustic neuroma
Benign tumour arising from the 8th cranial nerve
Often seen in cerebellopontine angle

330
Q

What is a pilocytic astrocytoma?

A

Mc primary brain tumour in children

331
Q

What is a medulloblastoma?

A

Aggressive paediatric brain tumour that arises withn the infratentorial compartment
Spreads through CSF system

332
Q

What is an oligodendroma?

A

Benign slow growing tumour common in the frontal lobes

333
Q

What is a haemangioblastoma and what is it associated with?

A

Vascular tumour of the cerebellum
Associated with von Hippel-Lindau syndrome

334
Q

What is a pituitary adenoma?

A

Benign tumours of the pituitary gland
Either secretory or non-secreotry
Can be microadenomas(<1cm) or macroadenomas(>1cm)

335
Q

How do patients with pituitary adenomas present?

A

Consequences of hormone excess
Cushing’s: ACTH
Acromegaly: GH
Compression of optic chiasm: bitemporal hemianopia due ot crossing nasal fibres

336
Q

How is a pituitary adenoma diagnosed?

A

Pituitary blood profile
MRI

337
Q

How can pituitary adenomas be treated?

A

Hormonal
Surgical: transphenoidal resection

338
Q

What is a craniopharyngioma?

A

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

339
Q

How might patients with craniopharyngioma present?

A

Hormonal distrubance
Hydrocephalus
Bitemporal hemianopia

340
Q

How is a craniopharyngioma diagnosed?

A

Pituitary blood profile
MRI

341
Q

How is a craniopharyngioma treated?

A

Typically surgical +/- postoperative radiotherapy

342
Q

Describe the epidemiology of herpes zoster ophthalmicus

A

Primarily older adults: 60-70yrs
Immunocompromised

343
Q

Name some risk factors for herpes zoster ophthalmicus

A

Age: >60yrs
Immunosuppression
Past hx of chickenpox

344
Q

Describe the aetiology of herpes zoster ophthalmicus

A

Varicella zoster virus which remains dormant in the trigeminal ganglion following chickenpox, reactivates andn spreads along the opthlamic division of the trigeminal nerve

345
Q

Describe the presentation of a patient with herpes zoster ophthalmicus

A

Painful red eye
Fever
Malaise
headache
Erythematous vesicular rash over the trigeminal division of the opthalmic nerve
Hutchinson’s sign: skin lesion on tip/side of nose indicative of nasocilliary nerve involvement->higher risk of ocular involvement

346
Q

Name some differentials for herpes zoster ophthalmicus

A

Bacterial conjunctivitis
Uveitis
Keratitis

347
Q

What investigations are used to diagnose herpes zoster ophthalmicus

A

Ophthalmic exam to assess extent of ocular involvement and potential complications
Viral culture/PCR testing from skin lesions/ocular specimens to confirm dx

348
Q

How is herpes zoster ophthalmicus mnaged?

A

Ig Hutchinson’s sign: urgent ophthalmology review
Oral aciclovir
Topical steroids-> may be used under guidance of ophthalmology to reduce inflammation and prevent scarring(caution as might exacerbate infection)

349
Q

In what age groups does shingles commonly occur?

A

Elderly
If in young person should prompt investigation for underlying immune condition

350
Q

Describe the presentation of shingles

A

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

351
Q

Describe the management of shingles

A

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

352
Q

Name some complications of shingles

A

Secondary bacterial infection of skin lesions
Corneal ulcers, scarring and blindness if eye involved
Post herpetic neuralgia

353
Q

Describe the features of post herpetic neuralgia

A

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)

354
Q

Name some risk factors for normal pressure hydrocephalus

A

SAH
Meningitis
Traumatic brain injury
Intracranial tumours
Ventricular shunting or LP

355
Q

Describe the pathophysiology of normal pressure hydrocephalus

A

Ventricular dilation without an apparent increase in intracranial pressure-> periventricular stress-> disruption of blood brain barrier-> inflammatory response-> cerebral perfusion changes

356
Q

Describe the clinical features of normal pressure hydrocephalus

A

‘Wet, wacky and wobbly’
Incontinence
Dementia
Magnetic gait-often appear as though ‘stuck’ can’t lift feet off floor

357
Q

Name some differentials for normal pressure hydropcephalus

A

Alzheimer’s
Parkinson’s
Other dementias

358
Q

How is normal pressure hydrocephalus investigated?

A

CT/MRI imaging: dilated lateral ventricles-can also be seen in demenita
LP: measure walking ability and cognition before and after

359
Q

Describe the management of normal pressure hydrocephalus

A

Therapeutic LP
Ventriculoperitoneal shunt-redirect excess CSF to abdomen

360
Q

Describe the epidemiology of idiopathic intracranial hypertension

A

Young and obese women
9:1 women

361
Q

Name some risk factors for idiopathic intracranial hypertension

A

Femal gender
Obesity
Pregnancy

362
Q

Describe the clinical features of idiopathic intracranial hypertension

A

Non-pulsatile bilateral headaches, worse in the morning or after bending forwards
Morning vomiting
Visual disturbances: transient visual darkening/loss-> optic nerve ischaemia
Bilateral papilloedema on fundoscopy
6th nerve palsy: horizontal diplopia
Pulsatile tinnitus
Photopsia

363
Q

Name some differentials for idiopathic intracranial hypertension

A

Brain tumour
Venous sinus thrombosis
Sleep apnoea
Migraines

364
Q

What investigations might be done in a patient with suspected idiopathic intracranial hypertension

A

Ophthalmoscopy->bilateral papilloedema
CT/MRI: increased ICP,
MRI venogram to rule out venous sinus thrombosis
LP: KEY: opening pressure >20cmH20.
Rule out other causes: CSF profile should be normal

365
Q

Describe the management of idiopathic intracranial hypertension

A

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

366
Q

Describe the prognosis of idiopathic intracranial hypertension

A

Most patients have benign course-small proportion develop severe visual impairment or blindness
Visual morbidity: mostly mainly from delay in diagnosis or inadequate treatment
Even modest weight loss can significantly reduce pressure

367
Q

What gene is narcolepsy associated with?

A

HLA-DR2

368
Q

Describe the clinical features of narcolepsy

A

Typical onset in teenage years
Hypersomnolence
Cataplexy(sudden loss of muscle tone often triggered by emotion)
Sleep paralysis
Vivid hallucinations on going to sleep/waking up

369
Q

How is narcolepsy investigated/diagnosed?

A

Multiple sleep latency EEG

370
Q

Describe the management of narcolepsy

A

Daytime stimulants(e.g. modafanil)
Nighttime sodium oxybate

371
Q

Describe the epidemiology of motor neurone disease

A

M>F
50-60yrs
90% sporadic, 10% familial

372
Q

Name some genes associated with familial MND

A

SOD1
FUSC9
ORF72

373
Q

What condition overlaps with MND?

A

Fontotemporal dementia
C90RF72 mutation found in both

374
Q

Name some UMN signs

A

Spasticity
Hyperreflexia
Upgoing plantars(although often downgoing in MND)

375
Q

Name some LMN signs

A

Fasciculations
Muscle atrophy

376
Q

Describe the general presentation of a patient with MND

A

Combination of lower and upper MN signs
Fasciculations
Asymmetric limb weakness
Wasting of small hands muscles
Absence of sensory signs/sx

377
Q

What are the different types of MND?

A

Amyotrophic lateral sclerosis(ALS)-most common
Primary lateral sclerosis
Progressive muscular atrophy
Progressive bulbar palsy
Spinal muscular atrophy

378
Q

Describe the features of amyotrophic lateral sclerosis(ALS)

A

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

379
Q

Describe the features of primary lateral sclerosis

A

UMN signs only

380
Q

Describe the features of progressive musclular atrophy

A

LMN signs only
Distal muscles before proximal
Best prognosis

381
Q

Describe the features of progressive bulbar palsy

A

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

382
Q

Name some differentials for MND

A

MS
Chronic inflammatory demyelinating neuropathy
Myasthenia gravis
Brainstem lesions
Paraproteinaemias

383
Q

How is MND investigated/diagnosed?

A

Clinical
Nerve conduction studies-> normal motor conduction so exclude a neuropathy
EMG: reduced number of action potentials with increased amplitude
MRI: brasintem lesions/cervical cord compression/myelopathy

384
Q

Describe the management of MND

A

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

385
Q

How does riluzole work?

A

Prevents stimulation of glutamate receptors

386
Q

Describe the prognosis of MND

A

Poor: 50% die within 3 years
Most <5yrs
Most die from respiratory complications

387
Q

Describe the features of myopathy

A

Symmetrical muscle weakness(proximal >distal)
Problems rising from chair/getting out of bath
Normal sensation, normal reflexes, no fasciculation

388
Q

Name some causes of myopathy

A

Inflammatory: polymyositis
Inherited:
Duchenne/Becker muscular dystrophy,
myotonic dystrophy

Endocrine: Cushing’s,
thyrotoxicosis

Alcohol

389
Q

Name some risk factors for degenerative cervical myelopathy

A

Smoking
Genetics
Occupation->high axial loading

390
Q

Describe the presentation of a patient with degenerative cervical myelopathy

A

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

391
Q

How is degenerative cervical myelopathy diagnosed?

A

MRI cervical spine: disc degeneration and ligament hypertrophy with accompanying cord signal change

392
Q

Describe the management of degenerative cervical myelopathy

A

Urgent assessment by specialist spinal services-> early treatment to prevent progression
Surgical decompression
Physio-only by specialist services to avoid further damage

393
Q

What conditions affect the dorsal column?

A

Tabes dorsalis(neurosyphilis)
Subacute combined degeneration of spinal cord

394
Q

What is a spinal cord compression and how is it different to cauda equina?

A

Form of myelopathy caused by pressure on cord-> causes an UMN lesion
Cauda equina: compression below level of L1-> LMN

395
Q

Name some causes of spinal cord compression

A

Trauma: mc-vertebral fracturas/dislocation of facet joints
Malignancy
Infection: TB and abscess formation
Epidural haematoma
Intervertebral disco prolapse-rare

396
Q

Describe the symptoms of a patient with spinal cord compression

A

Back pain: severe, progressive and aggravated by straining(coughing etc)
Difficulty walking
Weakness/numbness below level compressed(usually bilateral and symmetrical)
Incontinence
Urinary retention
Constipation
Systemic e.g. weight loss, fatigue, fevers if MSCC/TB

397
Q

Name some signs seen in a patient with spinal cord compression

A

Hypertonia
Hyperreflexia(may be absent at level compressed)
Clonus
Upgoing plantars
Sensory loss

398
Q

Name some differentials for spinal cord compression

A

Transverse myelitis
Cauda equina
Peripheral neuropathy
Spinal metastases
Sciatica

399
Q

How is spinal cord compression investigated/diagnosed?

A

MRI whole spine-urgent if suspected MSCC
Bladder scan if suspected urinary retention
EEG and baseline bloods
If MSCC: ix to find primary cancer

400
Q

Describe the management of spinal cord compression

A

Immobilise and spinal precautions
Analgesia for pain
VTE prophylaxis
Catheterise if retention
Treat underlying cause
Neurosurgery-> consider surgical decompression

401
Q

Describe the management of metastatic spinal cord compression

A

Hihg dose steroids: 16mg dexamethasone to reduce oedema and compression +PPI + monitor glucose
Refer to neuro: surgical decompression(vertebroplasty/kyphoplasty)
Oncology input

402
Q

In patients with metastatic spinal cord compression where do the metastases most commonly come from?

A

Lung
Breast
Prostate

403
Q

What is cauda equina syndrome?

A

Lumbosacral nerve roots that extend below the spinal cord(L1/L2 level) are compressed

404
Q

Name some causes of cauda equina syndrome

A

Lumbar disc herniation at L4/5 or L5/S1-mc
Tumours-primary/metastatic
Trauma
Infection: abscess, discitis
Epidural haematoma

405
Q

Describe the symptoms of cauda equina syndrome

A

Low back pain
Radicular pain-often symmetrical
Leg weakness
Difficulty walking
Saddle anaesthesia
Bowel incontinence/constipation
Urinary incontience/retention
Erectile dysfunction or sexual dysfunction

406
Q

Describe the signs of cauda equina syndrome

A

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

407
Q

Name some differentials for cauda equina syndrome

A

Compression of conus medullaris
Spinal cord compression
Sciatica

408
Q

How is cauda equina syndrome diagnosed?

A

Urgent whole spine MRI

409
Q

Describe the management of cauda equina syndrome

A

Surgical decompression

410
Q

Name some complications of cauda equina syndrome

A

Permanent paralysis of lower limbs
Sensory loss
Bladder/bowel dysfunction
Sexual dysfunction
Pressure ulcers
VTE due to immobility

411
Q

If damage to the DCML occurs in the spinal cord, what side will the symptoms be?

A

Same side

412
Q

Describe the aetiology of sub-acute combined degeneration of the spinal cord

A

Anything that can cause B12 deficiency:
Pernicious anaemia
Malabsorption syndromes
Dietary deficiencies
Recreational nitrous oxide inhalation

413
Q

Describe the signs and symptoms of a patient with sub-acute combined degeneration of the spinal cord

A

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

414
Q

How is sub-acute combined degeneration of the spinal cord investigated/diagnosed?

A

Assess B12 and folate
Homocysteine: raised level despite normal B12-> functional B12 deficiency
MRI of spine-exclude myelopathy
Nerve conduction studies: axonal neuropathy

415
Q

Describe the management of sub-acute combined degeneration of the spinal cord

A

Urgent Vitamin B12 replacement using hydroxocobalamin 1mg IM alternate days until no further improvement
Maintainence tx with hydroxocobalamin 1g IM every 2 months

416
Q

What are muscular dystrophies?

A

Group of inherited genetic disorders characterised by progressive degeneration and weakening of muscles

417
Q

Name some types of muscular dystrophies

A

Duchenne Muscular Dysrophy
Becker muscular dystrophy

418
Q

Describe the aetiology of Duchenne muscular dystrophy

A

X linked recessive-> mutation in dystrophin genes

419
Q

Describe the epidemiology of Duchenne muscular dystrophy

A

Males predominnalty affected with females are carreirs(X linked)

420
Q

Describe the symptoms of Duchenne muscular dystrophy

A

Progressive proximal muscle weakness from 5 years
Calf pseudohypertrophy
intellectual impairment
Gower’s sing: child uses arms to stand from a squatted position

421
Q

Describe the features of Becker’s muscular dystrophy

A

Presents later in childhood with muscle wasting and weakness
Wheelchair bound in teens and can survive into thirties

422
Q

How is Duchenne muscular dystrophy investigated/diagnosed?

A

Raised creatinine kinase
Genetics-replaced muscle biopsy

423
Q

Describe the management of Duchenne muscular dystrophy

A

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 supplements
Genetic counselling

424
Q

Name some complications of Duchenne muscular dystrophy

A

Joint contractures
Respiratory muscle failure-hypoventilation, poor cough and recurrent pneumonia(cause of death)
Dilated cardiomyopathy
Anaesthetic complications(rhabdo and malignant hyperthermia

425
Q

Describe the epidemiology of migraine

A

CommonF>M
Peak: 30-39yrs

426
Q

Name some triggering factors for migraines

A

Tiredness/stress
Alcohol
COCP
Lack of food/hydraiton
Cheese, chocolate, red wines, citrus fruits
Menstruation
Bright lights

427
Q

How might migraines present in children?

A

May be shorter lasting
Bilateral headaches
More prominent GI disturbance

428
Q

Describe the symptoms of a migraine

A

Aura: visual/sensory sx preceding headache
Unilateral throbbing headache
Photophobia/phonophobia
Nausea and/or vomiting

429
Q

Name some differentials for a migraine

A

Tension type headache
Cluster headache
SAH/stroke
Giant cell arteritis

430
Q

Describe the features of a hemiplegic migraine

A

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

431
Q

What aura symptoms of a migraine might prompt further investigation/referral?

A

Motor weakness
Double vision
Visual sx in only one eye
Poor balance
Decreased level of consciousness

432
Q

Describe the acute management of a migraine

A

Avoid triggers
Oral triptan +NSAID OR oral triptan+ paracetemol(may use nasal triptan especially in younger people
Non-oral metoclopramide or prochlorperazine and add non-oral NSAID/triptan

433
Q

Describe the prophylactic management of migraines

A

Propanolol-CI in asthma
Topirimate-not for women of childbearing age/onc ontraceptive
Amitryptaline
Candesartan
Injections:Greater occipital nerve block
Botulinum toxin injections
Acupuncture

434
Q

Describe the general management if migraines with regards to drug classes

A

5 HT receptor agonists for acute5 HT receptor antagonists for prophylaxis

435
Q

Describe the treatment of migraines in pregnancy

A

Paracetemol 1g first line NSAIDS
second line in 1st and 2nd trimester
Avoid aspirin and opioids like codeine

436
Q

How does a PMH of migraines affect COCP and HRT use?

A

COCP: absolute contraindication in patients with aura due to risk of stroke
HRT: safe to prescribe but may make migraines worse

437
Q

Name some red flags for headaches

A

<20yrs+ hx of cancer
Vomiting without other obvious cause
Worsening headache with 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

438
Q

Describe the epidemiology of a cluster headache

A

Middle aged men
Smokers
Related to nocturnal sleep
Can be triggered by alcohol

439
Q

Name some risk factors for cluster headaches

A

Male
>30yrs
Alcohol consumption
Prior brain surgery/trauma
Fhx

440
Q

Describe the clinical features of a cluster headache

A

Severe intense stabbing sharp pain arund one eye
Conjunctival lacrimation, redness, lid swelling
Mitosis/ptosis
Attacks last 15 minutes-2 hours
Generally attacks in clusters for 4-12 weeks then remission for months/years

441
Q

How are cluster headaches diagnosed/investigated?

A

Generally clinical diagnosis but neuroimaging done in most patients-underlying brain lesion can be found in some patients
MRI with gadolinium contrast

442
Q

Describe the acute management of a cluster headache

A

100% oxygen-usually effective in <10 minutes
SC triptan

443
Q

Describe the prophylactic treatment for cluster headaches

A

Verapamil
Topirimate
Sometimes tapering dose of prednisolone

444
Q

Describe the epidemiology of tension headaches

A

Mc cause of chronic recurring head pain
Women?men

445
Q

Name some contributing factors to tension headaches

A

Stress
Poor posture
Eye strain

446
Q

Describe the clinical features of a tension headache

A

Episodic primary headache’tight band’ or pressure sensation, usually bilateral
Lower intensity than migraine
No aura, n+v
Related to stress
May co-exist with migraine

447
Q

How is a tension headache managed?

A

Stress management
PT
Analgeisa: paracetemol or NSAIDS then step it up
Be careful of mediaction overuse headaches

448
Q

What is a central venous sinus thrombosis?

A

Occlusion of venous vessels in sinuses of the cerebral veins

449
Q

Describe the epidemiology of central venous sinus thrombosis

A

F>M20-35yrs

450
Q

Name some risk factors for central venous sinus thrombosis

A

Hormonal(pill, pregnancy etc)
Prothrombotic haem conditions/malignancy
Systemic disease(dehydration/sepsis)
Local(skull abnormalities, trauma, local infection

451
Q

Describe the presentation of central venous sinus thrombosis

A

Very variable
Headache
Confusion/drowsiness/impaired consciousness
IMpaired vision
N+V
Focal neuro deficits
Cranial nerve palsies
Papilloedema

452
Q

How is central venous sinus thrombosis investigated/diagnosed?

A

NCCT head: hyperdenstiy in affected sinus
CT venogram-filling defect-empty delta sign

453
Q

How is central venous sinus thrombosis treated?

A

LMWH
Adress underlying risk factors that increase risk of clotting
After initial therapy with LMWH can be bridged to warfarin

454
Q

How do patients with central venous sinus thrombosis present?

A

Chemosis
Exophthalmos
Peri-orbital swelling

455
Q

What is Brown-Sequard syndrome?

A

Lateral hemisection of the spinal cord

456
Q

Descirbe the clinical features of Brown-Sequard syndrome

A

Ipsilateral weakness below lesion
Ipsilateral loss of proprioception and vibration sensation
Contralateral loss of pain and temperature sensation

457
Q

Name some causes of Brown-Sequard syndrome

A

Cord trauma-penetration injury mc
Neoplasms
Disc herniation
Demyelination
Infective/inflammatory lesions
Epidural haematomas

458
Q

Describe the management of Brown-Sequard syndrome

A

Depends on causative pathology
Medical management preferred if infective/inflammatory/demyelinating
Surgical if pathologies causing extrinsic cord compression

459
Q

Describe the causes of mononeuropathies

A

Fixed:Nerve compression against hard surface
Entrapment of nerves in narrow anatomical spaces
Transient:Repetitive actions that cause trauma to neuron
Non-compression related:Infections, Radiation, Cold

460
Q

What are the general symptoms of mononeuropathies

A

Depends on underlying cause and affected nerve
Sensory: numbness, pain, tingling
Motor: weakness, atrophy, loss of coordination

461
Q

How are mononeuropathies generally treated?

A

Conservative: rest, heat, avoid/remove causative activity, NSAIDs, bracing
Oral/injected corticosteroids
Surgical decompression

462
Q

What is carpal tunnel syndrome?

A

Compression of median nerve in the carpal tunnel

463
Q

In what circumstances is carpal tunnel commonly seen in?

A

Repetitive wrist activites
Systemic disease: diabetes/RA/PregnancyAnatomical variations
Anything that causes an increase in pressure within the carpal tunnel or decreases the tunnel’s size

464
Q

Describe the symptoms of carpal tunnel syndrome

A

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 wrist flexion

465
Q

Name some differentials for carpal tunnel syndrome

A

Cubital tunnel syndrome
Thoracic outlet syndrome
Radial tunnel syndrome
Ulnar neuropathy

466
Q

How is carpal tunnel diagnosed?

A

EMG and nerve conducton studies: motor+sensory prolongation of action potential

467
Q

Describe the management of carpal tunnel syndrome

A

Conservative: splints at night, NSAIDS, corticosteroid injecitons, adjust activities
Surgical decompression: flexor retinaculum division

468
Q

How can radiculopathy be classified?

A

Cervical
Lumbar

469
Q

Describe the sympotms of cervical radiculopathy

A

Pian in neck, shoulders, upper back or arms

470
Q

What age group is most commonly affected by cervical radiculopathy

A

30-60yrs

471
Q

Name some causes of cervical radiculopathy

A

Disc degeneration
Sponylosis
Bone disease
Cancer
Herniated disc

472
Q

Name 2 examples of lumbar radiculopathy

A

Sciatica-mc
Cauda equina syndrome

473
Q

Describe the symptoms of sciatica

A

Pain and numbness from spinal nerve root location to legs or feet

474
Q

Name some causes of lumbar radiculopathy

A

Disc herniation
Bone spurs
Bone disease
Cancer

475
Q

Describe the treatment for radiculopathy

A

OTC anaglesia
PT: lower pain, improve posture, strengthen muscles
Steroid injections
Oral steroids
Anti-epileptics
Surgical spinal decompression

476
Q
A

Anki 3a exports (11 decks)

Brainscape helps you reach your goals faster, through stronger study habits.
© 2024 Bold Learning Solutions. Terms and Conditions