neuro anki 1 Flashcards
1
Q
What is a subarachnoid haemorrhage?
A
Blood within the subarachnoid space(under arachnoid mater)
2
Q
Describe the epidemiology of SAH
A
F>M
Peak incidence: 40-50 years
80% without trauma due to a ruptured berry aneurysm
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
4
Q
Name some risk factors for developing a Berry aneurysm?
A
Hypertension
Adult polycystic kidney disease
EDS
Coarctation of the aorta
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
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
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
8
Q
Describe the treatment for an SAH
A
Oral nimodipine to prevent vasospasm->ischaemic damage
Coiling, stenting or clipping of aneurysms: neurosurgery
9
Q
Name some complications of an SAH
A
Re-bleeding
Hydrocephalus
Vasospasm
Hyponatraemia->SIADH
Seizures
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
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
12
Q
Define a TIA
A
Sudden onset focal neurological deficit with a vascular aetiology typically lasting <1hr but always <24 hours
Completely resolves
13
Q
Describe the epidemiology of a TIA
A
Peak >70 years
M>F
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
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)
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
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
18
Q
Name some contraindications for aspirin therpay in a patient with a TIA
A
Bleeding disorder
Already on aspirin
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
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
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
22
Q
Describe the secondary management of TIA
A
Antiplatelet therapy: clopidogrel
Lipid moidification: atorvastatin 20-80mg daily
Carotid endartectomy if severe carotid stenosis
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
24
Q
What is an extradural haemorrhage?
A
Blood collects between the dura mater(outermost meningeal layer) and inner surface of the skull
25
Describe the typical presentaiton of a patient with an extradural haemorrhage
Initial brief los sof consciousness post initial trauma
Lucid interval(regianed consciousness and apparent recovery)
Subsequent deterioration of consciousness and headache onset
26
How might an extradural haemorrhage result in afixed and dilated pupil?
Haematoma expands->uncus of temporal lobe herniates around the tentorium cerebelli->parasympathetic fibres of CN3 compressed->fixed and dilated pupil
27
Name some differentials for a extradural haematoma
Subdural haemorrhage
SAH
Intracerebral haemorrhage
Cerebral contusion
28
What investigations should be done in a patient with an extradural haematoma?
CT scan: biconvex/lentiform hyperdense collection limited by the suture lines of the skull
Assess for midline shift/uncal herniation
29
Describe the management of an extradural haematoma
No neurological deficits->conservative: supportive therapy and radiological observation
Definitive: craniotomy and haematoma evacuation
30
What is a subdural haemorrhage?
Accumulation of venous blood in the potential space between the dura mater and arachnoid mater of the brain
31
How can subdural haemorrhages be classified?
Acute
Subacute
Chronic
32
Describe the timeline of an acute subdural haemorrhage
Sx develop within 48 hours of injury->rapid neurological deterioration
33
Describe the timeline of a subacute subdural haemorrhage
Sx present days->weeks post injury-> gradual progression of neurological symptoms
34
Describe the timeline of a chronic subdural haemorrhage
Elderly: weeks-> months
Might not remember specific head injury
35
Describe the epidemiology of a subdural haemorrhage
Elderly: >65 years
Infants-shaken baby
36
Name some risk factors for developing a subdural haemorrhage
Increasing age
Anticoag use
Chronic alcohol use
Recent trauma
Infants (shaken baby)
37
Name some symptoms you might find in a patient with a subdural haemorrhage
Altered/fluctuating mental status
Focal neurological deficits
Headache
Memory loss
Cognitive impairment
Seizures
Personality changes
38
Name some possible exam abnormalities in a patient with a subdural haemorrhage
Papilloedema (raised ICP)
Pupillary changes: unilateral dilated pupil- CNS compression
Gait abnormalities
Hemiparesis/hemiplegia
Bradycardia, hypertension, irregular respirations (Cushing's triad)
39
What investigations should be done in a patient with a subdural heamorrhage?
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
40
Describe the management of a patient with a subdural haemorrhage
Conservative: monitor ICP etc
Acute: decompressive craniotomy
Chronic: Burr holes
41
What is an ischaemic stroke?
Sudden onset neurological deficit of vascular aetiology with symptoms lasting >24 hours
42
Describe the aetiology of ischaemic strokes
Thrombotic: thrombus wihtin artery supplying blood to brain(atherosclerosis)
Embolic: embolus from elsewhere in the body
43
Describe the pathophysiology of an ischaemic stroke
Decrease in blood flow-> low O2 and glucose->energy failure and disruption of cellular ion haemostasis->exotoxicity, oxidative stress, inflammation and apoptosis-> irreversible neuronal damage
Can lead to cerebral oedema->raised ICP-> secondary neuronal damage
44
Name sone strong risk factors for an ischaemic stroke
Increasing age
Male
Family history
Hypertension
Smoking
Diabetes
AF
45
Name some weak risk factors for an ischaemic stroke
High cholesterol
Obesity
Poor diet
Oestrogen therapy
Migraine
46
How is an ischaemic stroke diagnosed?
Non contrast CT head
Rule out haemorrhagic stroke
Areas of low density/'hyperdense artery' sign
47
Describe the acute management of an ischamic stroke
Rule out haemorrhagic:
NCCT head
Aspirin 300mg orally/rectally
<4.5 hours post onset: thrombolysis with IV alteplase
CT/MRI angiography
Mechanical thrombectomy
48
What is alteplase?
Thrombolytic: tissue plasminogen activator
49
Describe the secondary prevention of an ischaemic stroke
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
50
What artery supplies the lateral cerebral cortex?
Middle cerebral artery
51
What artery supplies the anterior cerebral cortex?
Middle cerebral artery
52
Describe the symptoms of lateral pontine syndrome and name the implicated artery
Ipsilateral:
-CN3 palsy
-Vertigo/nystagmus/deafness
-Poor coordination/tone/balance
-Anterior inferior cerebellar artery
53
Describe the symptoms of Weber's syndrome
Ipsilateral CN3 palsy
Contralateral hemiparesis
54
Descirbe the symptoms of a Wallenberg's stroke
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
55
Name some cerebellar signs
Nystagmus
Vertigo
56
Name some signs of bulbar muscle weakness
Dysphagia
Dysarthria
57
What are the criteria for a total anterior circulation stroke?
3/3 of:
Unilateral weakness and/or sensory deficit of face, arm and leg
Homonymous hemianopia
Higher cerebral dysfunction(dysphasia, visuospatial disorder)
58
What are the criteria for a partial anterior circulation stroke
2/3 of:
Unilateral weakness and/or sensory deficit of face, arm and leg
Homonymous hemianopia
Higher cerebral dysfunction(dysphasia, visuospatial disorder)
59
What are the criteria for a posterior circulation stroke?
1/5 of:
Cranial nerve palsy and contralateral motor/sensory deficit
Bilateral motor/sensory deficit
Conjugate eye movement disorder(horizontal gaze palsy)
Cerebellar dysfunction (vertigo, nystagmus, ataxia)
Isolated homonymous hemianopia
60
What causes a lacunar stroke and which part of the brain does it affect?
Internal capsule, thalamus, basal ganglia
61
How can a lacunar stroke be differentiated from other strokes?
NO loss of higher cerebral function
62
What are the criteria for a lacunar stroke?
1/4 of:
Pure sensory stroke
Pure motor stroke
Sensori-motor stroke
Ataxic hemiparesis
63
What can a CN5 palsy result in?
Trigeminal neuralgia
Loss of corneal reflex
Loss of facial sensation
Paralysis of mastication muscles
Deviation of jaw to weak side
64
What can a CN6 palsy result in?
Abducens
Defective abduction-> hortizontal diplopia
65
What can a CN7 palsy result in?
Facial
Flaccid paralysis of upper and lower face
Loss of corneal reflex(efferent)
Loss of taste
Hyperacusis
66
What can a CN8 palsy result in?
Vestibulocochlear
Hearing loss
Vertigo, nystagmus
Acoustic neuromas
67
What can CN9 palsy result in?
Glossopharyngeal
Hypersensitive carotid sinus reflux
Loss of gag reflex (afferent)
68
What can a CN10 palsy result in?
Vagus
Uvula deviates away from site of lesion
Loss of gag reflex(efferent)
69
What can a CN11 palsy result in?
Accessory
Weakness turning head to contralateral side
70
What can a CN12 palsy result in?
Hypoglossal
Tongue deviates towards the side of lesion
71
Describe the epidemiology of encephalitis
Peak: >70 yrs, <1yr
M:F 1:1
72
Describe the aetiology of encephalitis
HSV1 responsible for 95% of cases in adults
Also: HSV2, CMV, EBV, VZV, HIV
Autoimmune encephalitis: NMDA receptor antibody associated encephalitis
73
Describe the symptoms of encephalitis
Fever
Headaches
Seizures
Psych symptoms
Vomiting
Focal features
Flu-like prodromal illness
74
Name some differentials for encephalitis
Hypoglycaemia
HE
DKA
Uremic/drug induced encephalopathy
75
What investigations should be done in a patient with suspected encephalitis?
CSF testing: lymohocytosis, hgih protein, viral PCR analysis of CSF
MRI
EEG
CT
76
How is encephalitis treated?
10mg/kg aciclovir TDS for 2 weeks
Broad spectrum antibiotics e.g. ceftriaxone
Supportive-seizure management
77
Name some side effects of aciclovir
GI changes
Photosensitivity and rashes
Acute renal failure
Hepatitis
78
Describe the prognosis of encephalitis
10-20% mortality of treatment started promptly
80% mortality if untreated
79
Describe the epidemiology of meningitis
Viral(enteroviruses) most common
Bacterial: associated with increased morbidity and mortality
Fungal/parasitic: rare except in immunosuppressed
80
Name the most common bacterial causes of meningitis and the groups they are present in
S.pneumoniae
N.meningitidis
H. influenza: infants
Listeria monocytogenes: Elderly
81
Name some viral causes of meningitis
Enteroviruses
Herpes
VZV
Measles/rubella
82
Name the parasitic causes of meningitis
Amoeba
Toxoplasma gardii
83
Name some non infective causes of meningitis
Malignancies: leukaemia, lymphoma
Drugs: NSAIDs, trimethoprim
Systemic inflammatory diseases: Sarcoidosis, SLE, Behcets
84
Describe the symptoms of meningitis
Headache
Fever
Nausea and vomiting
Seizures
Decreased consciousness
Photophobia
neck stiffness N
on blanching petechial/purpuric rash-> DIC
85
Name some signs in a patient with meningitis
Kernig's sign: Pain and resistance to knee extension
Brudzinski's sign: passive neck flexion results in involuntary hip and knee flexion
86
Name some differential diagnoses for meningitis
Encephalitis
SAH
Brain abscess
Sinusitis
Migraine
87
What investigations should be done in a patient with suspected meningitis?
Bloods: FBC, CRP, coag screen, cultures, PCR, glucose
ABG
CT head
LP
CSF analysis
88
At what vertebral level is an LP taken?
L3/L4
89
Describe the results of an LP in a patient with bacterial meningitis
Opening pressure: High
Appearance: cloudy/yellow
Glucose vs serum: Low <50%
Protein: High >1g/L
WCC: High, neutrophilia
90
Describe the results of an LP in a patient with viral meningitis
Opening pressure: Normal
Appearance: cloudy/clear
Glucose vs serum: High >60%
Protein: Normal
WCC: High, lymphocytosis
91
Describe the results of an LP in a patient with fungal/TB meningitis
Opening pressure: High
Appearance: cloudy/fibrous
Glucose vs serum: Low <50%
Protein: High
WCC: High, lymphocytosis
92
Describe the treatment of a patient with suspected meningitis if presenting to a GP
IM benzylpenicillin and urgent hospital transfer
93
Describe the treatment of a patient with suspected bacterial meningitis in hospital
IV cefotaxima/ceftriaxone and IV dexamethasone
Add amoxicillin for listeria cover(age extremes)
94
Describe the treatment of suspected viral meningitis
If enteroviruses: nothing
If HSV/VZV: aciclovir
95
What are the prophylaxis recommendations for contacts of meningitis
If in contact 7 days prior to onseet: One off dose of oral ciprofloxacin
96
Name some complications of meningitis
Sepsis
DIC
SIADH
Seizures
Waterhouse friedrichsen syndrome
Delayed: hearing loss, cranial nerve dysfunction, intellectual deficits, ataxia, blindness
97
Name the causes of meningitis is neonates(0-3 months)
Group B strep
E.Coli
Gram negative bacilli
Listeria
S.pneumoniae
98
Name the causes of meningitis in infants(3 months-6 years)
S.pneumoniae
N.meningitidis
H. influenzae
99
Name the causes of meningitis in adults(6-60 years)
S.pneumoniae
N.meningitidis
100
Name the causes of meningitis in the elderly (>60yrs)
S.pneumoniae
N.meningitidis
Listeria
Gram negative bacilli
101
How does S.pneumoniae appear on microbiology?
Gram positive diplococcus in chains
102
How does Group B strep appear on microbiology?
Gram positive coccus in chains
103
What age groups is most likely to have meningitis cauased by Group B strep and why?
Neonates
Colonises in maternal vagina
104
What age group is most likely to get meningitis from listeria monocytogenes?
Extremes of age, pregnant
Found in cheese
105
What does listeria monocytogenes appear like on microbiology?
Gram positive bacillus
106
What are the types of neurofibromatosis and which is more common?
Type 1-more commonType 2
107
Describe the aetiology of neurofibromatosis type 1
Mutation on chromosome 17 which codes for neurofibromin(tumour suppressor protein)
108
Describe the inheritance pattern of neurofibromatosis type 1
Autosomal dominant
109
Describe the features of neurofibromatosis type 1
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
110
How is neurofibromatosis diagnosed?
Diagnostic criteria and genetic testing
111
Describe the treatment of neurofibromatosistype 1
Monitor and manage symptoms, treat complications
112
Name some complications of neurofibromatosis type 1
Malignant peripheral nerve sheath tumours(MPNST)
Gastrointestinal stromal tumours(GIST)
Migraines
Epilepsy
Hypertension from renal artery stenosis
Scoliosis
Brain/spinal tumours
High cancer risk
113
Describe the aetiology of neurofibromatosis type 2
Mutation on chromosome 22->merlin->tumour suppressor protein important in schwann cells resulting in schwannomas
114
Describe the epidemiology of giant cell arteritis
Most common primary vasculitis->50 years, peaks in 70s
M:F 1:3
115
Name some risk factors for giant cell arteritis
Genetics
Environmental
Age-
females
Sex
Ethnicity(Mc caucasian-scandinavian)
116
Describe the presentation of a patient with giant cell arteritis
Usually rapid onset: <1 month
Temporal headache
Jaw claudication
Amaurosis fugax, diplopia
Tender, palpable temporal artery, scalp tenderness, bruits(rare)
50% have PMR features(aching, morning proximal limb weakness, lethargy)
117
What investigations should be done in a patient with giant cell arteritis?
High ESR/CRP
Normal creatine kinase and EMG
Temporal artery biopsy-> granulomatous inflammation and infiltration of giant cells
Doppler USS: 'halo' sign
118
Describe the managmeent of giant cell arteritis
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
119
Name some complications of giant cell arteritis
Permanent monocular blindness
Diplopia
Stroke
Aortic aneurysms
120
How can giant cell arteritis result in permanent monocular blindness?
Anterior ischaemic optic neuropathy-> occlusion of posterior ciliary artery-> ischaemia of optic nerve head
121
How can giant cell arteritis cause diplopia?
Involvement of any paart of oculomotor system(e.g. cranial nerves)
122
What is Bell's palsy?
Acute, unilateral, idiopathic facial nerve paralysis
123
Describe the epidemiology of bell's palsy
Peak incidence: 15-45 years
Higher prevalence in pregnant women
124
Describe the aetiology of Bell's palsy
Unknown
Linked to HSV1
EBV
VZV
125
Describe the presentation of Bell's palsy
Acute(not sudden) onset of unilateral LMN facial weakness with NO foreheard sparing
Post-auriicular otalgia(may precede paralysis)
Hyperacusis
Nervus intermedius symptoms: altered taste, dry eyes/mouth
126
Name some differential diagnoses for bell's palsy
Ramsay Hunt syndrome
Stroke-forehead sparing
Guillain Barre
127
What investigations might be done in a patient presenting with suspected Bell's palsy?
Clinical: rule out other causes/assess extent of damage
FBC/ESR/CRP/viral serology/lyme serology/otoscopy/EMG/MRI/CT
128
Describe the management of Bell's palsy
50mg oral pred OD for 10 days then taper
Aciclovir in certain patients (e.g. for Ramsay Hunt)
Supportive: artificial tears/ocular lubricants/eye tape
129
Describe the prognosis of Bell's palsy
Complete recovery: 70-80% in weeks-months
If untreated: 15% have permanent moderate/severe weakness
130
Name some poor prognostic factors for Bell's palsy
Older age
More severe initial facial weakness
131
Describe the epidemiology of essential tremor
Commmon
Increased age: peak 40-50 years
F:M:1:1
Family history
132
Describe the aetiology of essential tremor
Not fully understood
50% of cases have an autosomal dominant trait
133
Describe the pathophysiology of essential tremor
GABA-ergic dysfunction-> increased activity in cerebellar-thalamic cortical circuit
134
Describe the features of essential tremor
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
135
What additional features of essential tremor might prompt further investigation to look for differentials?
Difficulty with tandem gait
Mild cognitive impairment
Slight resting tremor alongside action tremor
136
How is essential tremor diagnosed?
CLinical diagnosis
bilateral uppper limb action tremor lasting >3 years with no other tremor/neurological signs
137
Name some differential diagnoses for essential tremor
Parkinson's
Hyperthyroidism
Dystonic tremor
Spasmodic dysphonia
138
Describe the management of essential tremor
Pharmacological:
Propanolol
Primidone
2nd line:
gabapentin,
topirimate,
nimodipine
Surgical
DBS
Botulinum toxin type A injections
139
Describe the prognosis of essential tremor
Typically worsens with increasing age
Can remain isolated or can spread e..g. to head or voice over years
Can cause major disability
140
Describe the epidemiology of myasthenia gravis
M:F 1:1
Bimodal distribution
Peak incidence in F<40 years and M>60 years
141
Describe the pathophysiology of myasthenia gravis
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
142
Describe the presentation of a patient with myasethnia gravis
Muscle weakness that worsens with repetitive activity and weakens with rest(typically ocular/bulbar and limb muscles)
Ptosis
Diplopia
Dysarthria
Dysphagia
Proximal limb weakness
Exacerbated by beta blockers, lithium, phenytoin and certain abx
143
How is myasthenia gravis investigated/diagnosed?
Bedside: ice pack test
Serology for AChR antibodies, MuSK and LRP4 antibodies
CT/MRI chest to look for thymomas/thymic hyperplasia
Edrophonium test
144
Describe the management of myasthenia gravis
ACh inhibitors: pyridostigmine, neostigmineImmunosuppression->steroids, azathioprine
Thymectomy
Rituximab
Plasma exchange and IVIG
145
Name some prognostic factors for myasthenia gravis
Age of onset
Antibody subtype
Thymus histology
Response to treatment
146
Name one complication of myasthenia gravis
Myasthenic crisis
147
What is a myasthenic crisis?
Life threatening acute worsening of symptoms, often triggered by another illness like a URTI-> can result in respiratory muscle failure
148
How is a myasthenic crisis treated?
Usual meds
IVIG and plasmapharesis
If FVC<15mL/kg: mechanical ventilation
149
What is chronic fatigue syndrome?
Chronic disabling condition characterised by profound fatigue and impariment following minimal physical/cognitive effort
150
Describe the epidemiology of chronic fatigue syndrome
Peak: 30-40 years
F:M:2:1
151
Describe the aetiology of chronic fatigue syndrome
UnknownTriggers like EBV
Psychological stress
152
Describe the symptoms of chronic fatigue syndrome
Extreme fatigue
Post-exertional malaise
Sleep disturbances and unrefreshing sleep
Cognitive impairment
Orthostatic intolerance
Immune/neurological/autonomic/psychiatric manifestations
153
Name some differential diagnoses for chronic fatigue syndrome
Fibromyalgia
Depression
Hypothyroidism
AI disorders
154
How is chronic fatigue syndrome diagnosed?
Most clinical-rule out other causes
TFT's, bloods: inflammation, infection, blood cell abnormalities
Has to last >3 months and significantly decrease ability to engage in activities
155
Describe the managment of chronic fatigue syndrome
Refere to specialist CSF service if >3 months
Energy management
Graded exercise therapy no longer recommended
Symptoms control-treat other conditions, pain and sleep management
CBT
156
What is an acoustic neuroma also known as?
Vestibular schwannoma
157
What is an acoustic neuroma?
Benign subarachnoid tumour that exerts local pressure on cranial nerve 8
158
Describe the epidmiology of acoustic neuromas
Rare in UK
Adults aged 40-60 years
159
Describe the aetiology of acoustic neuroma
Develop from Schwann cells of vestibulocochlear nerve
Majority are sporadic cases
Can be associated with NF2
160
Describe the presentation of acoustic neuroma
Asymmetric/unilateral hearing loss
Progressive ipsilateral tinnitus
Sensorineural deaffness
Larger tumours: raised ICP like focal neurology:
CN5/67/8
Dizziness, headaches, disequilibrium
161
Name some differential diagnoses for acoustic neuroma
Meniere's disease
Labyrinthitis
BPPV
162
What investigations should be done in a patient with a suspected acoustic neuroma?
Audiometry
MRI scan of cerebellopontine angle
163
Describe the management of an acoustic neuroma
Urgent referral to ENT>40mm: surgery
<40mm: 6 monthly annual surveillance scans via MRI
164
What focal neurology might be seen in a patient with an acoustic neuroma?
CN8: vertigo, unilateral sensorineural hearing loss, unilateral tinnitus
CN5: absent corneal reflex
CN7: facial palsy
165
Describe the epidemiology of Meniere's disease?
30-60 years
Predominantly unilateral
166
Describe the aetiology of meniere's disease
Dilatoin of endolymphatic spaces of membranous labyrinth resulting in an increased fluid pressure within the inner ear
167
Describe the presentation of meniere's disease
Sudden attacks of paroxysmal vertigo
Attacks last minutes to hours
Associated deafness
Tinnitus
Attacks often occur in clusters with period of remission where funciton is recovered
Can cause nystagmus and positive Romberg's test
Can be very disabling-> bedbound with nausea, vomiting and fluctuating hearing
168
Name some differential diagnoses for meniere's disease
Vestibular neuritis
Labyrinthitis
BPPV
169
What investigations are used to diagnose meniere's disease?
Clinical evaluation
Audiometric testing
Imaging/other tests may be used to rule out other potential causes of symptoms
170
Describe the management of meniere's disease
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
171
Describe the natural history of Meniere's disease
Sympotms resolve in most patients after 10-15 years
Majority of patients left with a degree of hearing loss
Psychological distress common
172
Describe the epidemiology of trigeminal neuralgia
>50yrs
F>M
173
Describe the aetiology of trigeminal neuralgia
Primary-idiopathic or secondary
Secondary causes include:
Malignancy-
nerve compression
AVM
MS
Sarcoidosis
Lyme disease
174
Describe the presentation of a patient with trigeminal neuralgia
Unilateral facial pain that is sudden, severe and brief
Pain is shooting/stabbing
Triggered by lightly touching affected side of face, eating, or wind blowing
Neuro exam is typically normal
175
Name some differential diagnoses for trigeminal neuralgia
Post herpetic neuralgia
Temperomandibular joint disorders
Giant cell arteritis
Cluster headache
176
How is trigeminal neuralgia diagnosed?
Mostly clinical
MRI or other neuroimaging to rule out secondary causes
177
Describe the management of trigeminal neuralgia
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
178
Name some red flag symptoms for trigeminal neuralgia
Sensory changes
Deafness
Pain only in ophthalmic division(eye socket, forehead and nose) or bilaterally
Optic neuritis
FHx of MS
<40 yrs
179
What is bulbar palsy?
Subtype of LMN lesion impacting the 9/10/12th cranial nerves
180
Name the major causes of bulbar palsy
Motor neurone disease-mc
Myasthenia gravis
Guillain-barre
Brainstem stroke-Wallenberg's/lateral medullary syndrome
Syringobulbia
181
Describe the signs and symptoms of bulbar palsy
Dysarthria and dysphagia
Absent/normal jaw jerk reflex
Absent gag reflex
Flaccid, fasciculating tongue
Nasal speech, often described as 'quiet'
Additional signs suggestive of underlying cause(e.g. limb fasciculations: MND)
182
Name some differentials for bulbar palsy
Pseudobulbar palsy
Brainstem tumour
MS
Polymyositis and dermatomyositis
183
What investigations should be done in a patient with bulbar palsy?
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
184
How is bulbar palsy managed?
Speech and swallowing therapy-manage dysarthria and dysphagia
Nutritional support
Treat underlying cause
185
How can Horner's syndrome be characterised?
Pre-ganglionic
Post-ganglionic
Central
Dependent on location of sympathetic nerve interruption
186
Name some causes of Horner's syndrome
Pancoast tumour: pre-ganglionic
Stroke-central
Carotid artery dissection: post-ganglionic
Trauma, tumours, surgery-central
187
What is a pancoast tumour and how can it case Horner's syndrome?
Non-small cell lung carcinoma
Located at superior sulcus of lung affects lower roots of brachial plexus and sympathetic chain
188
How do patients with Horner's syndrome typically present?
Ptosis-dropping of upper eyelid
Miosis-constriction of pupil
Anhidrosis
Enophthlamos-eye may appear sunken
Heterochromia-eye colour may change, more common in congenital Horner's syndrome
189
Name some differential diagnoses for Horner's syndrome
Oculomotor nerve palsy-will also have ophthalmoplegia
Myasthenia gravis
Bell's palsy
190
What investigations might be done in a patient presenting with Horner's syndrome?
Imaging: MRI/CT head neck and chest to ID structural causes
Bloods: assess for diabetes or AI disorders
Pharmacological pupil testing to confirm diagnosis and differentiate between pre- and post-ganglionic lesions
191
Describe the management of Horner's syndrome
Treat underlying causeIf no casue identified, observation and regular follow up
Cosemtic interventions for ptosis or miosis may be considered
192
Describe the aetiology of Guillain Barre syndrome
1-3 weeks post infection-mc Campylobacter
Others: mycoplasma and EBV
40% idiopathic
Others: CMV, HIC, hepatitis A, vaccinations
193
How do patients with Guillan Barre present?
Progressive ascending symmetrical limb weakness-> lower limbs first
Low back pain from radiculopathy
Paraesthesia
LMN signs in lower limbs: hypotonia, flaccid paralysis, areflexia
Cranial nerve signs: opthlamoplegia, facial nerve palsy, bulbar palsy
Potential autonomic dysfunction
Potential respiratory muscle involvement
194
Name some variants of Guillaim Barre syndrome
Parapetic
Miller-Fischer
Pure motor
Bilateral facial palsy with paraesthesias
Pharyngeal brachial cervical weakness
Bickerstaff's brainstem encephalitis
195
Name some differential diagnoses for Guillain Barre
Vascular: strokesInfective/inflammatory: polio, lyme, CMV, TB, HIV, CIDP, myasthenia gravis
Spinal cord compression
Metabolic-porphyria, electrolyte abnormalities
196
What investigations might be done in a patient with suspected Guillain Barre?
Monitoring of FVC for respiratory muscle involvement
Serological: anti ganglioside antibodies
LP: albuminocytological dissociation
Nerve conduction studies: prolongation or loss of the F wave
ID underlying cuase: stool cultures, serology, CSF virology
197
How is Guillain Barre managed?
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
Give some prognostic factors for Guillain Barre
Speed of onset
Severity
Age
Presence of preceding diarrhoeal illness
199
Describe the pathophysiology of Guillain Barre syndrome
Cross reaction of antibodies with gangliosides in the peripheral nervous system
Correlation between anti-ganglioside antibody and clinical features
Anti-GM1 antibodies
200
Describe the epidemiology of Huntington's disease
Most common neurodegenerative disorder
201
Describe the aetiology of Huntington's disease
Autosonomal dominant mutation involving excessive repetition of CAG nucelotide in huntingtin gene
Gradual degeneration of caudate nucleus and putamen
202
Describe the presentation of a patient with Huntington's disease
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
Give some differential diagnoses for Huntington's disease
Parkinson's
Wilson's disease
Huntington's disease like disorders
Neuroacathocytosis syndromes
204
How is Huntington's Disease diagnosed?
MRI/CT: loss of striatal volume and enlarged frontal horn of lateral ventricles
Genetics: including for at risk family members
205
How is Huntington's disease managed?
Chorea management; tetrabenazine
Depression: SSRI
Psychosis: atypical antipsychotics
Supportive: physical and emotional support from MDT
206
Describe the pathophysiology of Huntington's disease
Autosomal dominant mutaiton results in degeneration of cholinergic and GABAergic neurons in striatum of basal ganglia
207
What is a seizure?
Transient occurences of signs and symptoms due to abnormal excessive or synchronous neuronal activity in the brain
208
Describe the aetiology of epilepsy
Idiopathic generalised epilepsy
Childhood absence
Juvenile absence
Juvenile myoclonic
generalised tonic clonic
Structural:
Stroke
Trauma
Malformations
Genetic
Infectious
Metabolic
Immune
Unknown
209
Name some differential diagnoses for epilepsy
Syncope
TIA
Migraines
Panic disorder
Non epileptic attack disorder
210
What investigations might be done in a patient with a seizure?
History including collateral and neuro examImaging like CT/MRI
EEG
Might consider LP, bloods, advanced imaging depending on background
211
Name some localising features of temporal lobe seizures
Can occur with/without impairment of consciousness or awareness
Usually has an aura: rising epigastric sensation, psychic phenomena
Automatisms: lip smacking, grabbing, plucking
212
Name some localising features of frontal lobe seizures
Frontal lobe-motor
Head/leg movements
Posturing
Post-ictal weakness
Jacksonian march
213
Name some localising features of parietal lobe seizures
Parietal lobe-sensory
Paraesthesia
214
Name some localising features of occipital lobe seizures
Occipital-visual
Floaters/flashers
215
What are focal seizures?
Previously: partial seizures
Start in a specific area on one side of the brain
Level of awareness can vary
216
How can focal seizures be further classified?
Based on awareness:Focal aware(simple partial)
Focal impaired awareness(complex partial)
217
Describe a focal seizure with impaired awareness
Patients lose consciousness, usually post an aure or at seizure onset
Commonly originate from the temporal lobe
218
Describe a focal saware seizure
Patients retain consciousness experiencing only focal symtpoms
Usually no ictal symptoms
219
Describe a secondary generalised seizure
Focal seizure that evolves into a bilateral tonic-clonic seizure
220
Describe the features of a generalised seizure
Involve both sides of the brain at onset
Consciousness lost immediately
Can be further divided into tonic-clonic and absence etc
221
Describe an absence seizure
Brief pauses for <10 seconds
222
Describe a tonic clonic seizure
Loss of consciousness
Stiffening(tonic) and jerking(clonic) of limbs
Post-ictal confusion common
223
Describe a myoclonic seizure
Sudden jerks of a limb, trunk or face
224
Describe an atonic seizure
Sudden loss of muscle tone causing the patient to fall with consciousness retained
225
Describe the treatment of generalised tonic-clonic seizures
Males: sodium valproate
Females: lamotrigine or levetiracetam
226
Describe the management of focal seizures
Lamotrigine/levetiracetam
Carbamazepine
227
Describe the management of absence seizures
Ethosuximide
Lamotrigine/levetiracetam(sodium valproate in males)=
Carbamazepine
228
Describe the management of myoclonic seizures
Males: sodium valproate
Females: levetiracetam
229
Describe the management of tonic/atonic seizures
Males: sodium valproate
Females: lamotrigine
Carbamazepine
230
Name some complications of epilepsy
Status epilepticus
Psychiatric complications-> increased risk of depression and epilepsy
Sudden unexpected death in epilepsy(SUDEP)
231
Name some side effects of topirimate
Abdo pain
Cognitive impairment
Confusion
Muscle spams
mood changes
n+v
tremor
weight loss
232
Name some side effects of lamotrigine
blurred vision
arthralgia
ataxia
diarrhoea
dizziness
headache
insomnia
rash
tremor
233
Name some side effects of carbamazepine
ataxia
blood disorders
blurred vision
fatigue
hyponatraemia
234
name some side effects of sodium valproate
ataxia
anaemia
confusion
gastric irritation
haemorrhage
hyponatraemia
tremor
weight gain
235
name some side effects of phenytoin
acne
anorexia
constipation
hirsutism
insomnia
rash
tremor
236
What are the DVLA rules with regards to epilepsy?
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
Describe the management of status epilepticus
Buccal midazolam or rectal diazepam-can repeat
If IV access: IV lorazepam repeated after 10-20 minutes MAX 2 dose benzos 2nd line: levetiracetam, phenytoin, sodium valproate
Refractory status(20-90 minutes)-general anaesthesia
Propofol
midazolam
infusion
thiopental sodium
238
What investigations might be done in a patient with status epilepticus?
ABG
Bloods: FBC, U&E, LFT, CRP, clotting, bone profile
Toxicologyc screen
Anti epileptic drug
Imaging to determien cause: CT/MRI, LP
239
Describe the epidemiology of MS
Females: 2.3:1
Average onset 30yrs
240
Describe the aetiology of MS
Combination of genetic and environmental factors including potential viral pathogens
CD4 mediated destruction oligodendrogial cells and humoral response to myelin binding protein
241
Describe the symptoms of MS
Visual:
Optic neuritis
Optic atrophy
Uhtoff's phenomenon: worsening of vision following rise in body temperature
Internuclear ophthalmoplegia
Sensory:
Paraesthesia
Lhermittes phenomenon: paraesthesia in limbs on neck flexion
Motor:
Spastic weakness
Cerebellar:
Ataxia
Tremor
Others:
Urinary incontinence
Sexual dysfunction
242
How can MS be classified?
Relapsing remitting-> may become secondary progressive
Primary progressive
243
Name some differentials for MS
SLE
Lyme disease
Neurosarcoidosis
Vitamin B12 deficiency
244
How is MS diagnosed?
MRI showing >2 periventricular white matter lesions disseminated in time and space
Oligoclonal bands in CSF electrophoresis
245
What criteria is used to diagnose MS?
McDonald criteria
246
Describe the acute management of an MS flare?
High dose IV methylprednisolone for 5 days
Reduce duration or relapse not severity
Rule out infection
247
Describe the long term management of MS
Natalizumab-biologics->Ocrelizumab
Beta-interferon-injectable
Symptomatice therapies:PhysioBaclofen and botox for spasticity
Anticholinergics for bladder dysfunction
Sildenafil for ED
248
Name some risk factors that might suggest a worse prognosis for a patient with MS
Older age at onset
Primary progressive
High relapse rate
Rapid accumulation of disability
Comorbid conditions
Smoking
249
Describe the epidemiology of normal pressure hydrocephalus
More common in older adults
Considered a significant cause of reversible dementia
250
Describe the epidemiology of diabetic peripheral neuropathy
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
Describe the aetiology of diabetic peripheral neuropathy
Chronic hyperglycaemia-> accumulation of advanced glycation end products, oxidative stress and inflammatory pathways
252
How can diabetic peripheral neuropathy be categorised?
Distal symmetrical sensory neuropathy
Small fibre predominant neuropathy
Diabetic amyotrophy
Mononeuritis multiplex
Autonomic neruopathy
253
Describe the features of distal symmetrical sensory neuropathy
Most common form of diabetic peripheral neuropathy
Results from loss of large sensory fibres'glove and stocking' distribution affecting touch, vibration and proprioception
254
Describe the features of small fibre predominant neuropathy
Loss of small sensory fibres
Loss of pain and temperature sensation in 'glove and stocking' distribution accompanied by epsiodes of burning pain
255
Describe the features of diabetic amyotrophy
Originates from inflammation of the lumbrosacral plexus or cervical plexus
Characterised by severe pain around thighs and hips and proximal weakness
256
Describe the features of mononeuritis multiplex
Painful
Neuropathies involving >=2 distinct peripheral nerves
257
Describe the features of autonomic neuropathy
Postural hypotension
Gatroparesis
Constipation
Urinary retention
Arrhythmias
Erectile dysfunction
258
Name some differentials for diabetic peripheral neuropathy
Vitamin B12 deficiency
Alcohol induced peripheral neuropathy
CIDP
Hypothyroidism
259
What investigations might be done in a patient with diabetic peripheral neuropathy?
Neuro exam
Nerve conduction tests
Bloods-HbA1c, B12, TFTs, LFTs
260
Name some complicaitons of diabetic peripheral neuropathy
Foot ulcers due to loss of sensation
Autonomic neuropathy-> cardiac, GI and GU disturbances
261
Describe the management of diabetic peripheral neuropathy
Control of blood glucose levels and treat complications(foot ulcers etc)
1)amitriptyline, duloxetine, gabapentin, pregabalin
2)Try other drugs from first line if one fails
3)Tramadol as 'rescue therapy' for exacerbations
Topical capsaicin if localised
262
What is Charcot neuropathy?
Chronic progressive condition characterised by painful or painless bone and joint destruction in limbs that have lost sensory innervation
263
Describe the epidemiology of charcot arthropathy
MC in pts with long standing DM
Middle aged and elderly population
264
Describe the aetiology of Charcot neuropathy
DM(mc)->microvascular disease, autonomic and peropheral neuropathy-> cumulative damage to joints
Also:
Chronic alcohol abuse
Syringomyelia
Syphilis
265
What are the signs and symptoms of Charcot arthropathy?
6D's
Destruction of bone and joint
Deformity
Degeneration
Dense bones
Debris of bone fragments
Dislocation
266
Name some differentials for charcot arthropathy
Osteomyelitis-> important to rule out
267
What investigations are used to diagnose charcot arthropathy
Clinical dx mostlyX-rays 1st line imaging: bone destruction, debris, sclerosis and dislocation
MRI if ostemyelitis suspected
268
How is charcot arthropathy managed?
Conservative: lifestyle, footwear, orthotics
Medications: bisphosphonates, gabapentin
Surgical: resection of bony prominences, amputation if severe
269
Describe the symptoms of cerebellar dysfunction
DANISH
Dysdiadochokinesia
Ataxia
Nystagmus
Intention tremor
Slurred speech
Hypotonia
270
Name the causes of cerebellar syndrome
PASTRIES
Paraneoplastic syndrome
Alcohol
Sclerosis-MS
Tumours
Rare-Friedreich's ataxiaIatrogenic-phenytoin, carbamazepine
Endocrine/metabolic: hypothyroidism/Wilson's
Stroke
271
How is cerebellar dysfunction investigated/diagnosed?
CT/MRI: ID stroke, tumours, trauma
Serology: infectious/inflammatory causes
LP: infection, inflammation, malignancy
Genetics-hereditary
272
How is cerebellar dysfunction managed?
Treat underlying cause
Surgery/meds as required
Lifestyle-alcohol etc
Rehab: OT, physio etc
273
Describe the epidemiology of parkinson's disease
2nd mc neurodegenerative disorder after Alzheimer's
65yrsM>F
274
Describe the pathophysiology of Parkinson's disease
Accumulation of Lewy bodies in the substantia nigra of the basal ganglia-> neuronal cell death of dopaminergic cells
275
What are lewy bodies?
intracellular inclusions composed mostly of misfolded alpha synuclein
276
What are the components of the basal ganglia?
Striatum-> dorsal and ventral
Globus pallidus
Thalamus
Substantia nigra
Subthalamic nucleus
277
Describe the direct movement pathway in the substantia nigra
Excitatory
Increases thalamus activity-> increase movement
278
How does parkinson's affect the direct movement pathway?
Decreased levels of dopamine
Decreases direct pathway
Can't initiate increased movement->decreased movement
279
Describe the indirect motor pathway in the substantia nigra
Inhibitory
Decreases thalamus activity
Decreases movement
280
How does parkinson's affect the indirect movement pathway?
Less dopamine
Increases indirect pathway
Can't prevent excessive movement pathway
Decreases movement
281
Name some risk factors for Parkinson's disease
Family hx-especially when onset <50yrs
Previous head injury
282
Name some protective factors for Parkinson's disease
Smoking> including past smoking
Caffeine intake
Physical activity
283
Describe the tremor associated with Parkinson's disease
Resting tremor'pill rolling'
Asymmetrical
3-5Hz
284
How does bradykinesia present in a patient with Parkinson's disease
Parkinsonian gait->shuffling, slowness of movement especially on initiation and turning
285
How does muscle rigidity present in Parkinson's disease?
'Cogwheel rigidity'
Decreased arm swing
Stooped posture
286
Name some motor symptoms of Parkinson's disease
Triad of:
Tremor
Bradykinesia
Muscle rigidity
Also:
Postural instability->increased falls
Hypomimic facies
Hypokinetic dysarthria, speech impairment, dysphagia
Micrographia
287
Name some non motor symptoms of Parkinson's disease
Autonomic dysfunction
Sleep dysfunction(REM behavioural disorder)
Olfactory loss
Psychiatric->depression, anxiety, hallucinations, psychotic episodes, paranoid delusions
288
How is Parkinson's disease diagnosed?
Most clinical and positive response to treatment trials(excluded by absolute failure to respond to 1-1.5g levodopa daily)
If doubt:MRI head-absence of swallow tail sign
Dopamine transporter scan
289
Name some differentials for Parkinson's disease
Essential tremor
Multiple system atrophy
Lewy body dementia
290
How is essential tremor differentiated from Parkinson's disease tremor?
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
Name some complications of Parkinson's disease
Autonomic dysfunction
Recurrent falls
Cognitive imapirment
292
How does levodopa work for Parkinson's disease
Dopaminergic
Precursor to dopamine->converted in CNS and periphery
293
What drug is levodopa often dosed with for treating Parkinson's disease patients and why?
Carbidopa
Decreases conversion of levodopa in periphery-> increases CNS availability and decreases peripheral side effects
294
Name some peripheral side effects of levodopa
Postural hypotension
Nausea and vomiting
295
Name some central side effects of levodopa
Hallucinations
Confusion
Dyskinesia
Psychosis
296
What are 2 problems with long term levodopa therapy other than side effects?
End of dose effect
On and off phenomenon
297
Aside from levodopa, what medication groups might be used to treat Parkinson's disease?
Monoamine oxidase B inhibitors(MAO-B inhibitors)
COMT inhibitors
Dopamine agonists
Amantadine
Anticholinergics
298
Give some examples of MAO-B inhibitors and how they can help in Parkinson's disease
Rasagiline and selegilin
Decrease dopamine breakdown peripherally so increase central uptake
299
What is an important potential complication of using MAO-B inhibitors?
Can cause serotonin syndrome
300
Give some examples of COMT inhibitors and how they are used in Parkinson's disease treatment
Entacapone and tolcapone
Extend use of levodopa-> good for wearing off effect of levodopa
301
Give some examples of dopamine agonists and how they are useful for Parkinson's disease
ropinirole
rotigotine
apomorphine-most potentmimic dopamine
302
What is an important side effect of apomorphine?
Haemolytic anaemia
303
Aside from medications, what treatments are available for Parkinson's disease?
Deep brain stimulation
Physio, SALT, OT
304
Name some situations in which hypoxic-ischaemic encephalopathy can occur
Neonates: pperinatal asphyxia
Adults: secondary to cardiac arrest/severe systemic hypoxia
305
Describe the pathophysiology of hypoxic-ischaemic encephalopathy
Primary: immediately after event-> anaerobic respiration, lactic acidosis and cytotoxic oedema
Latent phase: brain appears to recover
Secondary: hours to days later-> renewed accumulation of toxic metabolites and free radicals causing further neuronal death
306
How does hypoxic-ischaemic encephalopathy present clinically?
Altered consciousness ranging from lethary to coma
Seizures
Abnormal tone and reflexes
307
How is hypoxic-ischaemic encephalopathy managed?
Supportive: maintain normal body temp and blood glucose levels
Seizure control
Neonates within 6 hours of birth: therapeutic hypothermia
308
What investigations might be done in hypoxic-ischaemic encephalopathy?
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
Name some complications of hypoxic-ischaemic encephalopathy
Cerebral palsy
Seizure disorders
Cognitive impairment
Motor deficits
Sensory impairments
Microcephaly
Behavioural disorders
Multisystem organ failure of severe: CVR, renal, hepatic, resp
310
What is a brain abscess?
Collection of pus within the brain parenchyma linkes with significant morbidity and mortality
311
Describe the aetiology of a brain abscess
Usually contiguous spread of infection from sinusitis, otitis media or dental infection
Haematogenous spread from distant sources; endocardities etc
Direct inoculation: trauma/neurosurgery
312
Name some risk factors for developing a brain abscess
Immunocompromised states
Congenital heart defects and endocarditis
Chronic otitis/sinusitis
IVDU
Dental head and neck procedures
313
Describe the pathogenesis of a brain abscess
4 stages:Early/initial cerebritis: 1-3 days
Late cerebritis: 4-9 days
Early capsule formation: 10-13 days
Late capsule formation: 14 days onwards
314
Describe the signs and symptoms of a brain abscesss
Headache
Focal neurological deficits
Infeciton signs: fever, n+v, meningism
Raised ICP: headache, 3rd nerve palsy, papilloedema, seizures
315
Name some differentials for a brain abscess
Space occupying lesions-cancer, vascular
CNS infections
Stroke
316
How is a brain abscess diagnosed?
MRI with gadolinium contrast-> better at detecting early cerebritis
CT for complications like hydrocephalus
Stereotactic needle aspiration
LP CONTRAINDICATED
317
Describe the management of a brain abscess
A-E and consider sepsis 6
Surgery: craniotomy-aspiration/excision
IV abx: 3rd gen: cephalosporin + metronidazole
Sx management: dexamethasone for raised ICP
318
Name some complications of a brain abscess
Seizures
Meningitis
Ventriculitis
Hydrocephalus
Cerebral oedema
Herniation
Death
Permanent neuro deficits
319
Name some causes of space occupying lesions
Neoplasia: metastatic and primary CNS tumours
Vasulcar: avms/aneurysms
Infective: abscesses, TB etc
Granulomatouus disease: neurosarcoidosis
320
What is Cushing's reflex?
Hypertension
Bradycardia
Irregular respirations
Sign of raised ICP
321
Describe some potential signs/symptoms of brain metastases
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
What investigations might be used for brain metastases
CT head-1st line in acute settings e.g. if presenting with seizures
MRI brain for details
PET scan
Biopsy
323
How are brain metastases treated?
Often not treatable with surgrical intervention
Chemo/radiation may be used
If metastases, often indicates stage 4 disease-> palliative care
Manage raised ICP-steroids, osmotic agents
324
What is a glioblastoma multiforme?
Mc primary brain tumour in adults
Malignant and highly aggressive
Associated with a poor prognosis-1 yr
325
How does a glioblastoma multiforme appear on imaging?
Solid tumours with central necrosis and a rim that enhances with contrast
Disruption of blood brain barrier and vasogenic oedema
326
How is a glioblastoma multiforme treated?
Surgical with postoperative chemo and/or radiotherapy
Dexamethasone for oedema
327
Describe the features of a meningioma
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
How is a meningioma diagnosed and treated?
CT-contrast enhancement and MRI
Observation, radiotherapy or surgical resection
329
What is a vestibular schwannoma?
Previously acoustic neuroma
Benign tumour arising from the 8th cranial nerve
Often seen in cerebellopontine angle
330
What is a pilocytic astrocytoma?
Mc primary brain tumour in children
331
What is a medulloblastoma?
Aggressive paediatric brain tumour that arises withn the infratentorial compartment
Spreads through CSF system
332
What is an oligodendroma?
Benign slow growing tumour common in the frontal lobes
333
What is a haemangioblastoma and what is it associated with?
Vascular tumour of the cerebellum
Associated with von Hippel-Lindau syndrome
334
What is a pituitary adenoma?
Benign tumours of the pituitary gland
Either secretory or non-secreotry
Can be microadenomas(<1cm) or macroadenomas(>1cm)
335
How do patients with pituitary adenomas present?
Consequences of hormone excess
Cushing's: ACTH
Acromegaly: GH
Compression of optic chiasm: bitemporal hemianopia due ot crossing nasal fibres
336
How is a pituitary adenoma diagnosed?
Pituitary blood profile
MRI
337
How can pituitary adenomas be treated?
Hormonal
Surgical: transphenoidal resection
338
What is a craniopharyngioma?
Most common paediatric supratentorial tumour
Solid/cystic tumour of the cellar region derived from the remnants of Rathke's pugh
Can be in adults too
339
How might patients with craniopharyngioma present?
Hormonal distrubance
Hydrocephalus
Bitemporal hemianopia
340
How is a craniopharyngioma diagnosed?
Pituitary blood profile
MRI
341
How is a craniopharyngioma treated?
Typically surgical +/- postoperative radiotherapy
342
Describe the epidemiology of herpes zoster ophthalmicus
Primarily older adults: 60-70yrs
Immunocompromised
343
Name some risk factors for herpes zoster ophthalmicus
Age: >60yrs
Immunosuppression
Past hx of chickenpox
344
Describe the aetiology of herpes zoster ophthalmicus
Varicella zoster virus which remains dormant in the trigeminal ganglion following chickenpox, reactivates andn spreads along the opthlamic division of the trigeminal nerve
345
Describe the presentation of a patient with herpes zoster ophthalmicus
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
Name some differentials for herpes zoster ophthalmicus
Bacterial conjunctivitis
Uveitis
Keratitis
347
What investigations are used to diagnose herpes zoster ophthalmicus
Ophthalmic exam to assess extent of ocular involvement and potential complications
Viral culture/PCR testing from skin lesions/ocular specimens to confirm dx
348
How is herpes zoster ophthalmicus mnaged?
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
In what age groups does shingles commonly occur?
Elderly
If in young person should prompt investigation for underlying immune condition
350
Describe the presentation of shingles
Tingling feeling in a dermatomal distribution
Progressess to erythematous papules occuring along one or more dermatomes within a few days-> develop into fluid filled vesicles which then crust over and heal
Associated with viral sx: fever, headache, malaise
Herpes zoster ophthalmicus
351
Describe the management of shingles
Oral antiviral(valaciclovir) within 72hr rash onset if immunocompromised or moderate/severe rash/pain or non-truncal involvemets
Hospital and IV antivirals if severe, immunocompromised/ophthalmic sx, suspicion of meningitis/encephalitis
Avoid contact with pregnany women, babies and immunocompromised until lesions are fully crusted over
Pain management with NSAIDs, back up amitryptyline, duloxetine, gabapentin
352
Name some complications of shingles
Secondary bacterial infection of skin lesions
Corneal ulcers, scarring and blindness if eye involved
Post herpetic neuralgia
353
Describe the features of post herpetic neuralgia
Pain occuring at site of healed shingles infection
Can cause neuropathic pain(burning, pins and needles)
Can cause allodynia(perception of pain from a normally non-painful stimulus like light touch)
354
Name some risk factors for normal pressure hydrocephalus
SAH
Meningitis
Traumatic brain injury
Intracranial tumours
Ventricular shunting or LP
355
Describe the pathophysiology of normal pressure hydrocephalus
Ventricular dilation without an apparent increase in intracranial pressure-> periventricular stress-> disruption of blood brain barrier-> inflammatory response-> cerebral perfusion changes
356
Describe the clinical features of normal pressure hydrocephalus
'Wet, wacky and wobbly'
Incontinence
Dementia
Magnetic gait-often appear as though 'stuck' can't lift feet off floor
357
Name some differentials for normal pressure hydropcephalus
Alzheimer's
Parkinson's
Other dementias
358
How is normal pressure hydrocephalus investigated?
CT/MRI imaging: dilated lateral ventricles-can also be seen in demenita
LP: measure walking ability and cognition before and after
359
Describe the management of normal pressure hydrocephalus
Therapeutic LP
Ventriculoperitoneal shunt-redirect excess CSF to abdomen
360
Describe the epidemiology of idiopathic intracranial hypertension
Young and obese women
9:1 women
361
Name some risk factors for idiopathic intracranial hypertension
Femal gender
Obesity
Pregnancy
362
Describe the clinical features of idiopathic intracranial hypertension
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
Name some differentials for idiopathic intracranial hypertension
Brain tumour
Venous sinus thrombosis
Sleep apnoea
Migraines
364
What investigations might be done in a patient with suspected idiopathic intracranial hypertension
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
Describe the management of idiopathic intracranial hypertension
Weight losss
Carbonic anhydrase inhibitors-acetazolamide-poorly tolerated
Topirimate and candesartan
Invasive: therapeutic LP, surgical CSF shunting, optic nerve sheath fenestration-prevent progressive visual loss
366
Describe the prognosis of idiopathic intracranial hypertension
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
What gene is narcolepsy associated with?
HLA-DR2
368
Describe the clinical features of narcolepsy
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
How is narcolepsy investigated/diagnosed?
Multiple sleep latency EEG
370
Describe the management of narcolepsy
Daytime stimulants(e.g. modafanil)
Nighttime sodium oxybate
371
Describe the epidemiology of motor neurone disease
M>F
50-60yrs
90% sporadic, 10% familial
372
Name some genes associated with familial MND
SOD1
FUSC9
ORF72
373
What condition overlaps with MND?
Fontotemporal dementia
C90RF72 mutation found in both
374
Name some UMN signs
Spasticity
Hyperreflexia
Upgoing plantars(although often downgoing in MND)
375
Name some LMN signs
Fasciculations
Muscle atrophy
376
Describe the general presentation of a patient with MND
Combination of lower and upper MN signs
Fasciculations
Asymmetric limb weakness
Wasting of small hands muscles
Absence of sensory signs/sx
377
What are the different types of MND?
Amyotrophic lateral sclerosis(ALS)-most common
Primary lateral sclerosis
Progressive muscular atrophy
Progressive bulbar palsy
Spinal muscular atrophy
378
Describe the features of amyotrophic lateral sclerosis(ALS)
Typically LMN signs in arms and UMN in legs
If familial: gene is on chromosome 21 and codes for superoxide dismutase
Can have bulbar onset in some cases
379
Describe the features of primary lateral sclerosis
UMN signs only
380
Describe the features of progressive musclular atrophy
LMN signs only
Distal muscles before proximal
Best prognosis
381
Describe the features of progressive bulbar palsy
UMN and LMN signs
Palsy of tongue, muscle of masticaiton and facial muscles due to loss of function of brainstem motor nuclei->dysphagia/dysarthria
Carries worst prognosis
382
Name some differentials for MND
MS
Chronic inflammatory demyelinating neuropathy
Myasthenia gravis
Brainstem lesions
Paraproteinaemias
383
How is MND investigated/diagnosed?
Clinical
Nerve conduction studies-> normal motor conduction so exclude a neuropathy
EMG: reduced number of action potentials with increased amplitude
MRI: brasintem lesions/cervical cord compression/myelopathy
384
Describe the management of MND
Mostly supportive
Riluzole-> extends life expectancy by about 3 months, used mainly in ALS
Respiratory care: BIPAP at night
Nutrition: PEG as bulbar disease progresses
Discuss advanced care early
Anticholinergics for drooling
385
How does riluzole work?
Prevents stimulation of glutamate receptors
386
Describe the prognosis of MND
Poor: 50% die within 3 years
Most <5yrs
Most die from respiratory complications
387
Describe the features of myopathy
Symmetrical muscle weakness(proximal >distal)
Problems rising from chair/getting out of bath
Normal sensation, normal reflexes, no fasciculation
388
Name some causes of myopathy
Inflammatory: polymyositis
Inherited:
Duchenne/Becker muscular dystrophy,
myotonic dystrophy
Endocrine: Cushing's,
thyrotoxicosis
Alcohol
389
Name some risk factors for degenerative cervical myelopathy
Smoking
Genetics
Occupation->high axial loading
390
Describe the presentation of a patient with degenerative cervical myelopathy
Variable-fluctuating but progressive
Pain-neck, upper, lower limbs
Loss of motor function-hard to do up shirts/use a fork
Loss of sensory function->numbness
Loss of autonomic function-> urinary/faecal incontinence and impotence
Hoffman's sign
391
How is degenerative cervical myelopathy diagnosed?
MRI cervical spine: disc degeneration and ligament hypertrophy with accompanying cord signal change
392
Describe the management of degenerative cervical myelopathy
Urgent assessment by specialist spinal services-> early treatment to prevent progression
Surgical decompression
Physio-only by specialist services to avoid further damage
393
What conditions affect the dorsal column?
Tabes dorsalis(neurosyphilis)
Subacute combined degeneration of spinal cord
394
What is a spinal cord compression and how is it different to cauda equina?
Form of myelopathy caused by pressure on cord-> causes an UMN lesion
Cauda equina: compression below level of L1-> LMN
395
Name some causes of spinal cord compression
Trauma: mc-vertebral fracturas/dislocation of facet joints
Malignancy
Infection: TB and abscess formation
Epidural haematoma
Intervertebral disco prolapse-rare
396
Describe the symptoms of a patient with spinal cord compression
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
Name some signs seen in a patient with spinal cord compression
Hypertonia
Hyperreflexia(may be absent at level compressed)
Clonus
Upgoing plantars
Sensory loss
398
Name some differentials for spinal cord compression
Transverse myelitis
Cauda equina
Peripheral neuropathy
Spinal metastases
Sciatica
399
How is spinal cord compression investigated/diagnosed?
MRI whole spine-urgent if suspected MSCC
Bladder scan if suspected urinary retention
EEG and baseline bloods
If MSCC: ix to find primary cancer
400
Describe the management of spinal cord compression
Immobilise and spinal precautions
Analgesia for pain
VTE prophylaxis
Catheterise if retention
Treat underlying cause
Neurosurgery-> consider surgical decompression
401
Describe the management of metastatic spinal cord compression
Hihg dose steroids: 16mg dexamethasone to reduce oedema and compression +PPI + monitor glucose
Refer to neuro: surgical decompression(vertebroplasty/kyphoplasty)
Oncology input
402
In patients with metastatic spinal cord compression where do the metastases most commonly come from?
Lung
Breast
Prostate
403
What is cauda equina syndrome?
Lumbosacral nerve roots that extend below the spinal cord(L1/L2 level) are compressed
404
Name some causes of cauda equina syndrome
Lumbar disc herniation at L4/5 or L5/S1-mc
Tumours-primary/metastatic
Trauma
Infection: abscess, discitis
Epidural haematoma
405
Describe the symptoms of cauda equina syndrome
Low back pain
Radicular pain-often symmetrical
Leg weakness
Difficulty walking
Saddle anaesthesia
Bowel incontinence/constipation
Urinary incontience/retention
Erectile dysfunction or sexual dysfunction
406
Describe the signs of cauda equina syndrome
Loss of lower limb power
Hypotonia in lower limbs
Hyporeflexia in lower limbs
Sensory loss/paraesthesias in legs
Reduced perianal sensation
Loss of anal tone
Bladder palpable and dull to percussion in urinary retention
407
Name some differentials for cauda equina syndrome
Compression of conus medullaris
Spinal cord compression
Sciatica
408
How is cauda equina syndrome diagnosed?
Urgent whole spine MRI
409
Describe the management of cauda equina syndrome
Surgical decompression
410
Name some complications of cauda equina syndrome
Permanent paralysis of lower limbs
Sensory loss
Bladder/bowel dysfunction
Sexual dysfunction
Pressure ulcers
VTE due to immobility
411
If damage to the DCML occurs in the spinal cord, what side will the symptoms be?
Same side
412
Describe the aetiology of sub-acute combined degeneration of the spinal cord
Anything that can cause B12 deficiency:
Pernicious anaemia
Malabsorption syndromes
Dietary deficiencies
Recreational nitrous oxide inhalation
413
Describe the signs and symptoms of a patient with sub-acute combined degeneration of the spinal cord
Symmetrical distal sensory sx, usually start at feet and progress to hands
Varying degrees of ataxia
Mixed UMN and LMN sings: exaggerated/diminished/absent reflexes
Autonomic bowel/bladder sx
Haematological manifestations may be present/absent
414
How is sub-acute combined degeneration of the spinal cord investigated/diagnosed?
Assess B12 and folate
Homocysteine: raised level despite normal B12-> functional B12 deficiency
MRI of spine-exclude myelopathy
Nerve conduction studies: axonal neuropathy
415
Describe the management of sub-acute combined degeneration of the spinal cord
Urgent Vitamin B12 replacement using hydroxocobalamin 1mg IM alternate days until no further improvement
Maintainence tx with hydroxocobalamin 1g IM every 2 months
416
What are muscular dystrophies?
Group of inherited genetic disorders characterised by progressive degeneration and weakening of muscles
417
Name some types of muscular dystrophies
Duchenne Muscular Dysrophy
Becker muscular dystrophy
418
Describe the aetiology of Duchenne muscular dystrophy
X linked recessive-> mutation in dystrophin genes
419
Describe the epidemiology of Duchenne muscular dystrophy
Males predominnalty affected with females are carreirs(X linked)
420
Describe the symptoms of Duchenne muscular dystrophy
Progressive proximal muscle weakness from 5 years
Calf pseudohypertrophy
intellectual impairment
Gower's sing: child uses arms to stand from a squatted position
421
Describe the features of Becker's muscular dystrophy
Presents later in childhood with muscle wasting and weakness
Wheelchair bound in teens and can survive into thirties
422
How is Duchenne muscular dystrophy investigated/diagnosed?
Raised creatinine kinase
Genetics-replaced muscle biopsy
423
Describe the management of Duchenne muscular dystrophy
Supportive: low impact exercise, mobility aids, OT, physio
Manage complications: dysphagia, chest infections etc
Glucocorticoids: slow muscle regeneration for 6 months-2 years
Newer: ataluren and creatinine supplements
Genetic counselling
424
Name some complications of Duchenne muscular dystrophy
Joint contractures
Respiratory muscle failure-hypoventilation, poor cough and recurrent pneumonia(cause of death)
Dilated cardiomyopathy
Anaesthetic complications(rhabdo and malignant hyperthermia
425
Describe the epidemiology of migraine
CommonF>M
Peak: 30-39yrs
426
Name some triggering factors for migraines
Tiredness/stress
Alcohol
COCP
Lack of food/hydraiton
Cheese, chocolate, red wines, citrus fruits
Menstruation
Bright lights
427
How might migraines present in children?
May be shorter lasting
Bilateral headaches
More prominent GI disturbance
428
Describe the symptoms of a migraine
Aura: visual/sensory sx preceding headache
Unilateral throbbing headache
Photophobia/phonophobia
Nausea and/or vomiting
429
Name some differentials for a migraine
Tension type headache
Cluster headache
SAH/stroke
Giant cell arteritis
430
Describe the features of a hemiplegic migraine
Migraine variant in which motor weakness is a manifestation of aura in at least some attacks
Strong family history in 50%
Very rare, most common in adolescent females
431
What aura symptoms of a migraine might prompt further investigation/referral?
Motor weakness
Double vision
Visual sx in only one eye
Poor balance
Decreased level of consciousness
432
Describe the acute management of a migraine
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
Describe the prophylactic management of migraines
Propanolol-CI in asthma
Topirimate-not for women of childbearing age/onc ontraceptive
Amitryptaline
Candesartan
Injections:Greater occipital nerve block
Botulinum toxin injections
Acupuncture
434
Describe the general management if migraines with regards to drug classes
5 HT receptor agonists for acute5 HT receptor antagonists for prophylaxis
435
Describe the treatment of migraines in pregnancy
Paracetemol 1g first line NSAIDS
second line in 1st and 2nd trimester
Avoid aspirin and opioids like codeine
436
How does a PMH of migraines affect COCP and HRT use?
COCP: absolute contraindication in patients with aura due to risk of stroke
HRT: safe to prescribe but may make migraines worse
437
Name some red flags for headaches
<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
Describe the epidemiology of a cluster headache
Middle aged men
Smokers
Related to nocturnal sleep
Can be triggered by alcohol
439
Name some risk factors for cluster headaches
Male
>30yrs
Alcohol consumption
Prior brain surgery/trauma
Fhx
440
Describe the clinical features of a cluster headache
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
How are cluster headaches diagnosed/investigated?
Generally clinical diagnosis but neuroimaging done in most patients-underlying brain lesion can be found in some patients
MRI with gadolinium contrast
442
Describe the acute management of a cluster headache
100% oxygen-usually effective in <10 minutes
SC triptan
443
Describe the prophylactic treatment for cluster headaches
Verapamil
Topirimate
Sometimes tapering dose of prednisolone
444
Describe the epidemiology of tension headaches
Mc cause of chronic recurring head pain
Women?men
445
Name some contributing factors to tension headaches
Stress
Poor posture
Eye strain
446
Describe the clinical features of a tension headache
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
How is a tension headache managed?
Stress management
PT
Analgeisa: paracetemol or NSAIDS then step it up
Be careful of mediaction overuse headaches
448
What is a central venous sinus thrombosis?
Occlusion of venous vessels in sinuses of the cerebral veins
449
Describe the epidemiology of central venous sinus thrombosis
F>M20-35yrs
450
Name some risk factors for central venous sinus thrombosis
Hormonal(pill, pregnancy etc)
Prothrombotic haem conditions/malignancy
Systemic disease(dehydration/sepsis)
Local(skull abnormalities, trauma, local infection
451
Describe the presentation of central venous sinus thrombosis
Very variable
Headache
Confusion/drowsiness/impaired consciousness
IMpaired vision
N+V
Focal neuro deficits
Cranial nerve palsies
Papilloedema
452
How is central venous sinus thrombosis investigated/diagnosed?
NCCT head: hyperdenstiy in affected sinus
CT venogram-filling defect-empty delta sign
453
How is central venous sinus thrombosis treated?
LMWH
Adress underlying risk factors that increase risk of clotting
After initial therapy with LMWH can be bridged to warfarin
454
How do patients with central venous sinus thrombosis present?
Chemosis
Exophthalmos
Peri-orbital swelling
455
What is Brown-Sequard syndrome?
Lateral hemisection of the spinal cord
456
Descirbe the clinical features of Brown-Sequard syndrome
Ipsilateral weakness below lesion
Ipsilateral loss of proprioception and vibration sensation
Contralateral loss of pain and temperature sensation
457
Name some causes of Brown-Sequard syndrome
Cord trauma-penetration injury mc
Neoplasms
Disc herniation
Demyelination
Infective/inflammatory lesions
Epidural haematomas
458
Describe the management of Brown-Sequard syndrome
Depends on causative pathology
Medical management preferred if infective/inflammatory/demyelinating
Surgical if pathologies causing extrinsic cord compression
459
Describe the causes of mononeuropathies
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
What are the general symptoms of mononeuropathies
Depends on underlying cause and affected nerve
Sensory: numbness, pain, tingling
Motor: weakness, atrophy, loss of coordination
461
How are mononeuropathies generally treated?
Conservative: rest, heat, avoid/remove causative activity, NSAIDs, bracing
Oral/injected corticosteroids
Surgical decompression
462
What is carpal tunnel syndrome?
Compression of median nerve in the carpal tunnel
463
In what circumstances is carpal tunnel commonly seen in?
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
Describe the symptoms of carpal tunnel syndrome
Pain and paraesthesia in thumb index and middle finger-impingement of palmar digital branch of median nerve
Symptoms worse at night or after activities involving wrist flexion
465
Name some differentials for carpal tunnel syndrome
Cubital tunnel syndrome
Thoracic outlet syndrome
Radial tunnel syndrome
Ulnar neuropathy
466
How is carpal tunnel diagnosed?
EMG and nerve conducton studies: motor+sensory prolongation of action potential
467
Describe the management of carpal tunnel syndrome
Conservative: splints at night, NSAIDS, corticosteroid injecitons, adjust activities
Surgical decompression: flexor retinaculum division
468
How can radiculopathy be classified?
Cervical
Lumbar
469
Describe the sympotms of cervical radiculopathy
Pian in neck, shoulders, upper back or arms
470
What age group is most commonly affected by cervical radiculopathy
30-60yrs
471
Name some causes of cervical radiculopathy
Disc degeneration
Sponylosis
Bone disease
Cancer
Herniated disc
472
Name 2 examples of lumbar radiculopathy
Sciatica-mc
Cauda equina syndrome
473
Describe the symptoms of sciatica
Pain and numbness from spinal nerve root location to legs or feet
474
Name some causes of lumbar radiculopathy
Disc herniation
Bone spurs
Bone disease
Cancer
475
Describe the treatment for radiculopathy
OTC anaglesia
PT: lower pain, improve posture, strengthen muscles
Steroid injections
Oral steroids
Anti-epileptics
Surgical spinal decompression
476
