TO DO NEURO Flashcards
(196 cards)
1
Q
STROKE
Give an example of how chronic HTN can cause a stroke.
A
- Charcot-Bouchard aneurysms most often in the basal ganglia
2
Q
STROKE
What are some important differentials of stroke?
A
- Metabolic (hypo or hyperglycaemia, electrolytes)
- Intracranial tumours, hemiplegic migraine
- Infection (meningitis)
- Head injury, seizure (focal > Todd’s paralysis)
3
Q
STROKE
What classification system can be used for strokes?
A
- Oxford stroke (Bamford) classification
4
Q
STROKE
How would a Total Anterior Circulation Infarct (TACI) present?
A
(involves middle and anterior cerebral arteries)
- unilateral hemiparesis +/- hemisensory loss of face, arm and leg
- homonymous hemianopia
- higher cognitive dysfunction e.g. dysphagia
5
Q
STROKE
how would a Partial Anterior Circulation Infarct present?
A
2 of the criteria are present:
- unilateral hemiparesis +/- hemisensory loss of face, arm and leg
- homonymous hemianopia
- higher cognitive dysfunction e.g. dysphagia
6
Q
STROKE
how does a lacunar infarct (LACI) present?
A
presents with one of the following:
- unilateral weakness (+/- sensory deficit) of face, arm and leg or all 3
- pure sensory stroke
- ataxic hemiparesis
7
Q
STROKE
what vessels are affected in a lacunar infarct?
A
perforating arteries around the internal capsule, thalamus and basal ganglia
8
Q
STROKE
how would a posterior circulation infarct (POCI) present?
A
presents with one of the following:
- cerebellar or brainstem syndromes
- loss of consciousness
- isolated homonymous hemianopia
9
Q
STROKE
what is the presentation of lateral medullary syndrome?
A
IPSILATERAL
- ataxia
- nystagmus
- dysphagia
- facial numbness
- cranial nerve palsy
CONTRALATERAL
- limb sensory loss
10
Q
STROKE
what vessels are affected in lateral medullary syndrome?
A
posterior inferior cerebellar artery
(also known as Wallenberg’s syndrome)
11
Q
STROKE
what is the presentation of Weber’s syndrome?
A
- ipsilateral CN III palsy
- contralateral weakness
12
Q
STROKE
How would a PCA stroke present?
A
visual issues
- Contralateral homonymous hemianopia
- Cortical blindness
- Visual agonisa
- Prosopagnoisa
- Dyslexia
- Unilateral headache
13
Q
STROKE
How would a brainstem/basilar artery infarct present?
A
- Locked in syndrome – complete paralysis BUT eye movement + awareness preserved
14
Q
STROKE
How would a haemorrhagic stroke appear on CT head?
A
- Acute = hyperdense
- Subacte = isodense
- Chronic = hypodense
15
Q
STROKE
What other investigations may you do in stroke?
A
- ECG 72h tape to look for paroxysmal AF, MI.
- ECHO to check for endocarditis or CHD
- CTA/MRA or carotid doppler USS to look for dissection or carotid stenosis
16
Q
STROKE
What is the treatment for an ischaemic stroke?
A
Immediate management:
- CT/MRI to exclude haemorrhagic stroke
- aspirin 300mg
Antiplatelet therapy
- aspirin 300mg for 2 weeks
- clopidogrel daily long term
Anticoagulation (e.g. warfarin) for AF
thrombolysis
- within 4.5 hrs of onset
- IV alteplase
- lots of contraindications (can cause massive bleeds)
mechanical thromboectomy
- endovascular removal of thrombus
17
Q
STROKE
What other treatment can be given in ischaemic stroke either alongside alteplase or after the time frame?
A
- Thrombectomy (mechanical retrieval of clot)
- Proximal anterior circulation stroke within 6h (with IV alteplase if <4.5h) or within 24h if potential to salvage brain tissue
- Proximal posterior circulation stroke within 24h (with IV alteplase if <4.5h) if potential to salvage brain tissue
18
Q
STROKE
What other management is given for ischaemic strokes?
A
- Control BP
- 300mg aspirin OD 2w post-stroke + then lifelong 75mg clopidogrel
19
Q
STROKE
What medication and general management may be given in stroke prevention?
A
- Antiplatelets (lifelong clopidogrel or aspirin + dipyridamole if cardiac disease)
- Anticoagulation if have AF but wait 2w post-stroke
- Manage co-morbidities (HTN, DM)
- Cholesterol >3.5mmol/L diet + 80mg atorvastatin
- VTE assessment + monitor for infection
20
Q
STROKE
What is the CHA2DS2-VaSc score
A
- Congestive heart failure
- HTN
- Age 65-74 (1), ≥75 (2)
- Diabetes
- Prev stroke/TIA (2)
- Vascular disease
- Sex female
- 1 = consider anticoagulation, ≥2 = anticoagulate
21
Q
SAH
What is the pathophysiology of a subarachnoid haemorrhage (SAH)?
A
- tissue ischaemia - less blood, O2 and nutrients can reach the tissue due to bleeding loss -> cell death
- raised ICP - fast flowing arterial blood is pumped into the cranial space
- space occupying lesion - puts pressure on the brain
- brain irritates meninges - these inflame causing meningism symptoms. This can obstruct CSF outflow -> hydrocephalus
- vasospasm - bleeding irritates other vessels -> ischaemic injury
22
Q
SAH
What are the investigations for SAH?
A
- urgent non-contrast CT head = starburst sign
- ECG
to consider
- lumbar puncture = xanthochromia (if CT negative, perform >12hrs after symptom onset)
- CT angiogram
23
Q
SAH
What is the management of SAH?
A
1st line
- nimodipine 60mg 4hrly
- endovascular coiling (2nd line = surgical clipping)
- if raised ICP = IV mannitol, hyperventilation + head elevation
- conservative = bed rest, stool softeners
24
Q
EDH
What is the pathophysiology of extra-dural haematoma (EDH)?
A
- Often fractured temporal/parietal bone leads to blood accumulating between bone + dura mater over minutes to hours
After a lucid interval there is:
- rapid rise in ICP
pressure on the brain
- midline shift
- tentorial herniation
- coning
25
EDH
What are some differentials for EDH?
- Epilepsy,
- CO poisoning,
- carotid dissection
26
EDH
What are the investigations for EDH?
Non-contrast CT head - hyperdense biconvex (lemon shape)
Skull x-ray - may show fracture lines
LP is contraindicated
27
EDH
What is the management for EDH?
- bed position = tilted to 30 degrees
- intubation if low GCS
- maintain cerebral perfusion (hyperventilation, inotropes + vasopressors, fluids, hypertonic saline or IV MANNITOL)
- hypothermia
- burr hole
DEFINITIVE
- Craniotomy + haematoma evacuation
28
SDH
What is the most common cause of subdural haematoma (SDH)?
- Rupture of a vein running from hemisphere to the sagittal sinus of the dural venous sinuses (bridging veins) that's beneath the dura leading to haematoma between arachnoid + dura mater
29
SDH
What are the investigations for SDH?
Non-contrast CT head
- crescentic collection
- not limited by suture lines
acute = hyperdense (light)
subacute = isodense
chronic = hypodense (dark)
30
SDH
What is the management of SDH?
SURGERY
1* = irrigation via burr-hole craniostomy
2* = craniotomy
IV MANNITOL - to reduce ICP
address cause of trauma
31
STATUS EPILEPTICUS
What is the step-wise management of status epilepticus?
PRE-HOSPITAL/EARLY STATUS (<10 MINS)
- in community 1st line = buccal midazolam (2nd line = rectal diazepam)
- in hospital 1st line = 4mg IV lorazepam (2nd line = IV diazepam)
two doses of benzodiazepine given 10 mins apart
ESTABLISHED STATUS (>10 MINS)
- alert on-call anaesthetist
- one of following: phenytoin, levetiracetam, sodium valproate
if one fails, try another agent on list
REFRACTORY STATUS (>30 MINS)
- phenobarbitone
- general anaesthesia with propofol, midazolam or thiopental
32
LOC
What are the potential causes of LOC?
CRASH
- Cardiogenic (more alarming)
- Reflex (neurally mediated)
- Arterial
- Systemic
- Head
33
NEAD
what is the management of NEAD?
correct Dx vital,
speak to pt,
reassure them,
wait for seizure to pass,
CBT,
avoid AEDs as can be fatal if mistreated excessively (respiratory depression)
34
PARKINSON'S DISEASE
what are the clinical features of Parkinson’s disease
MOTOR SYMPTOMS
- bradykinesia (slow movements, festinant gait due to reduced arm swing + turning en bloc)
- tremor (resting, pill-rolling, 4-6Hz)
- cogwheel rigidity (tremor superimposed on a rigid movement)
- lead-pipe rigidity (stiffness throughout entire movement)
NON-MOTOR SYMPTOMS
- anosmia (early symptom)
- sleep disturbance
- depression
- anxiety
- dementia (usually develops after motor symptoms)
- constipation
- postural instability
35
PARKINSON'S DISEASE
How can you differentiate Parkinson's resting tremor from benign essential tremor ?
- Asymmetrical vs symmetrical
- 4–6Hz vs 5–8Hz
- Worse at rest vs improves at rest
- Improves with intentional movement vs worse with intentional movement
- No change with alcohol vs improves with alcohol (also Rx = propranolol)
- Parkinson's vs. autosomal dominant condition
36
PARKINSON'S DISEASE
What are 4 differential diagnoses to consider in Parkinson's disease?
Parkinson's plus syndromes –
- Progressive supranuclear palsy
- Multiple system atrophy
- Lewy Body dementia
- Corticobasal degeneration
37
PARKINSON'S DISEASE
What is progressive supranuclear palsy?
- Early falls, cognitive decline or both sides being equally affected
- Occurs above nuclei of CN3, 4 + 6 so difficulty moving eyes
- Impaired vertical gaze (down worse = issues reading or descending stairs)
- Ocular cephalic reflex present (caused by supranuclear issue) where they tilt/turn their head to look at things rather than moving eyes
38
PARKINSON'S DISEASE
What is multiple system atrophy?
- Neurones in multiple systems in the brain degenerate
- Degeneration in basal ganglia > Parkinsonism
- Degeneration in other areas > early autonomic (postural hypotension + falls, bladder/bowel dysfunction) + cerebellar (ataxia) dysfunction
39
PARKINSON'S DISEASE
What is Lewy Body dementia associated with?
- Associated with Sx of visual hallucinations, delusions, REM sleep disorders, fluctuating consciousness, progressive cognitive decline + Parkinsonism
40
PARKINSON'S DISEASE
What is corticobasal degeneration?
- Early myoclonic jerks, gait apraxia, agnosia + alien limb
41
PARKINSON'S DISEASE
What is the management of Parkinson's disease?
- Lifestyle: education, exercise, physio, MDT
1st line:
- if motor symptoms are affecting QoL = L-DOPA (CO-CARELDOPA)
- if motor symptoms not affecting QoL = dopamine agonist (ROPINIROLE) or MAO-B inhibitor (SELEGILINE or RASAGALINE)
2nd line
- COMT inhibitor (ENTACAPONE)
- amantadine
- SC apomorphine (in advanced disease with severe motor symptoms)
- deep brain stimulation
42
HUNTINGTON'S DISEASE
What is the pathophysiology of Huntington's disease?
- Less GABA causes less regulation of dopamine to striatum causing increased dopamine levels resulting in excessive thalamic stimulation and subsequently increased movement (chorea)
43
HUNTINGTON'S DISEASE
How does Huntington's disease present?
● Main sign is hyperkinesia
● Characterised by:
○ Chorea, dystonia, and incoordination
● Psychiatric issues
● Depression
● Cognitive impairment, behavioural difficulties
● Irritability, agitation, anxiety
- rigidity
- dysarthria (speech problems)
- dysphagia (swallowing problems)
44
HEADACHES
What is the management of cluster headaches?
ACUTE
- SC or intranasal sumatriptan
- 100% oxygen at 15L/min via non-rebreather mask
- avoid triggers
- avoid paracetamol, NSAIDs, opioids, ergots + oral triptans
PROPHYLAXIS
- verapamil
45
TRIGEMINAL NEURALGIA
What is the pathophysiology of trigeminal neuralgia?
What is affected?
- Compression of trigeminal nerve results in demyelination + excitation of the nerve resulting in erratic pain signalling
- Affects all 3 ophthalmic (V1), maxillary (V2) + mandibular (V3) branches but V3 mostly
46
TRIGEMINAL NEURALGIA
How would you manage trigeminal neuralgia?
Carbamazepine - suppresses attacks
Less effective options = phenytoin, gabapentin and lamotrigine
Surgery = microvascular decompression, gamma knife surgery
47
MIGRAINE
What is the pathophysiology of migraines?
- Changes in brainstem blood flow leads to unstable trigeminal nerve nucleus + nuclei in basal thalamus
- Leads to release of vasoactive neuropeptides CGRP + substance P > neurogenic inflammation > vasodilation + plasma protein extravasation leading to pain propagating all over the cerebral cortex
48
MIGRAINE
What are the triggers of migraines?
CHOCOLATE –
- Chocolate
- Hangovers
- Orgasms
- Cheese/caffeine
- Oral contraceptives
- Lie-ins
- Alcohol
- Travel
- Exercise
49
MIGRAINE
What is the acute management of migraines?
- PO (or nasal in paeds) triptan like sumatriptan plus paracetamol or NSAID
- Antiemetic like metoclopramide or prochlorperazine if vomiting occurs
50
MIGRAINE
What is the prophylaxis for migarines?
- Propranolol or topiramate are first line
- Topiramate is teratogenic + can reduce efficacy of hormonal contraceptives though
- Also, amitriptyline, botulinum toxin or acupuncture.
- 400mg OD of riboflavin (B2) may help
- NOT gabapentin
- Avoid indentified triggers (?headache diary)
51
MND
What is ALS?
What is a long-term consequence?
- Loss of motor neurones in motor cortex + anterior horn of cord so mixed signs
- Long term consequence is progressive spastic tetraparesis
52
MND
What is progressive bulbar palsy?
What does it affect?
What does it need to be differentiated from?
- Only affects CN 9–12 (brainstem motor nuclei) so LMN of them
- Primarily affects muscles of talking, chewing, tongue palsy + swallowing
- Progressive pseudobulbar palsy = destruction of UMN so same as bulbar but small spastic tongue with no fasciculations
53
MND
What is...
i) progressive muscular atrophy?
ii) primary lateral sclerosis?
i) Anterior horn cells affected so LMN signs only, distal > proximal
ii) Loss of cells in motor cortex so UMN signs only
54
MND
What is the general clinical presentation of MND?
SYMPTOMS
- progressive weakness
- falls
- speech + swallow issues
SIGNS
- UMN + LMN issues
- spastic paraparesis
- fasciculations
- dysarthria
- dysphagia
- muscle wasting
NO SENSORY abnormalities
NO EXTRAOCULAR involvement
NO CEREBELLAR involvement
sphincter dysfunction is rare and only late feature
55
MND
What are UMN signs?
Hypertonia or spasticity,
brisk reflexes
upgoing plantars,
muscle wasting
56
MND
What are some investigations for MND?
EMG = fibrillation potentials
nerve conduction studies = reduction in amplitude
MRI spine (exclude spinal pathology)
pulmonary function tests
57
MND
What medication may be given in MND?
- RILUZOLE – Na+ blocker inhibits glutamate release
- Drooling - ORAL PROPANTHELINE or ORAL AMITRIPTYLINE
- Dysphagia: NG tube
- Spasms: ORAL BACLOFEN
- Non-invasive ventilation
- Analgesia e.g. NSAIDs - DICLOFENAC
58
MULTIPLE SCLEROSIS
What are some classic sites for MS?
- Periventricular white matter lesions
- Predilection for distinct sites – optic nerves, corpus callosum, brainstem + cerebellar peduncles
59
MULTIPLE SCLEROSIS
What is the diagnostic criteria for MS?
McDonald criteria –
- >2 relapses
- Multiple CNS lesions (≥2)
- Sx that last >24h
- Disseminated in space (Clinically or on MRI) and time (>1m apart)
60
MULTIPLE SCLEROSIS
What are the symptoms of MS?
SYMPTOMS
- blurred vision + red desaturation (optic neuritis)
- numbness + tingling
- weakness
- bowel + bladder dysfunction
- Uhtoff's phenomenon (worsening symptoms following temperature rise e.g. hot bath/shower)
SIGNS
- visual (pale optic disc + inability to see red, relative afferent pupillary defect)
- internuclear ophthalmoplegia
- sensory loss
- UMN signs (spastic paraparesis)
- cerebellar signs (ataxia + tremor)
- Lhermitte's phenomenon (electric shock sensation on neck flexion)
61
MULTIPLE SCLEROSIS
In terms of the symptoms of MS, what is the pattern of motor weakness?
i) Pyramidal pattern so extensors weaker than flexors in upper limb, flexors weaker than extensors in lower
62
MULTIPLE SCLEROSIS
What are some signs of MS?
- UMN = spastic paraparesis, brisk reflexes, hypertonia
- Sensory = loss of sensation, cerebellar signs
- Relative afferent pupillary defect
- Internuclear ophthalmoplegia
- Optic atrophy (pale optic disc) in chronic MS
63
MULTIPLE SCLEROSIS
What are the investigations for MS?
- MRI head + spinal cord to show demyelination plaques = diagnostic
- Lumbar puncture may show oligoclonal bands of IgG on CSF electrophoresis
- Evoked potentials = delayed visual, auditory + somatosensory potentials
64
MULTIPLE SCLEROSIS
What is the management of MS relapses?
How does this affect disease prognosis?
- oral/IV methylprednisolone for 5 days
- plasma exchange (for sudden, severe relapses not responding to steroids)
65
MULTIPLE SCLEROSIS
What is the management of MS remissions?
DMARDs
- natalizumab
- ocrelizumab
- fingolimod
- beta-interferon
- glatiramer acetate
66
MENINGITIS
What are the clinical signs of meningitis?
- Meningism
- +ve Kernig's = pain or unable to extend leg at knee when it's bent
- +ve Brudzinski = involuntary flexion of hips + knees when neck flexed
- Non-blanching purpuric rash = later sign in meningococcal septicaemia
67
MENINGITIS
What are some complications following meningitis?
- Hearing loss is key complication
- Seizures + epilepsy
- Sepsis or abscess
- Hydrocephalus
- Cognitive impairment + learning disability
68
MENINGITIS
What is the management of bacterial meningitis
1st line = ceftriaxone/cefotaxime (+ amoxicillin if <3m or >55)
IV dexamethasone (avoid in meningococcal sepsis)
if penicillin allergic = IV chloramphenicol
69
BRAIN ABSCESS
What are the most common causative organisms?
- Staph. aureus + strep. pnuemoniae
70
BRAIN ABSCESS
What is the management of brain abscess?
1ST LINE
- empirical antibiotics (IV ceftriaxone + metronidazole)
- treat underlying cause
2ND LINE
- abscess drainage/excision
71
BRAIN DEATH + COMA
What are the components of 'eyes' in GCS?
E4 = opens spontaneously
E3 = opens to verbal command
E2 = opens to pain
E1 = no response
72
BRAIN DEATH + COMA
What are the components of 'verbal' in GCS?
V5 = orientated in TPP, answers appropriately
V4 = confused conversation, odd answers
V3 = inappropriate words (random, abusive)
V2 = incomprehensible sounds (groans)
V1 = no response
73
BRAIN DEATH + COMA
What are the components of 'motor' in GCS?
M6 = obeys commands
M5 = localises pain
M4 = withdraws away from painful stimulus
M3 = flexion to pain
M2 = extension to pain
M1 = no response
74
BRAIN DEATH + COMA
What is abnormal flexion to pain?
What does it indicate?
- Decorticate posturing – arm adducted + flexed, wrist flexed, internal rotation, plantar flexed + stiff appearance
- Indicates significant damage to cerebral hemispheres, internal capsule + thalamus
75
BRAIN DEATH + COMA
What is abnormal extension to pain?
What does it indicate?
- Decerebrate posturing – arms + legs extended, head extension, plantar flexion, internal rotation, pt rigid with teeth clenched
- Indicates brainstem damage + so lesions in cerebellum or midbrain
76
MYASTHENIA GRAVIS
What are the risk factors of myasthenia gravis?
- female gender
- family history
- autoimmune (RA and SLE)
- thymoma or thymic hyperplasia
77
MYASTHENIA GRAVIS
What are the clinical features of myasthenia gravis?
SYMPTOMS
- lethargy
- muscle weakness (worse at end of day)
- double vision
- slurred speech
- dysphagia
- shortness of breath
SIGNS
- proximal muscle weakness with fatiguability
- ptosis exacerbated on upward gaze (uni/bilateral)
- complex ophthalmoplegia
- head drop
- myasthenic snarl (snarling expression when attempting to smile)
78
MYASTHENIC CRISIS
What is the management of myasthenic crisis?
- Urgent review by neurologists + anaesthetists
- IV immunoglobulins or parapheresis
- intubation
- corticosteroids
79
MYASTHENIA GRAVIS
What is the management of myasthenia gravis?
1st line = acetylcholinesterase inhibitors (pyridostigmine)
2nd line = prednisolone
3rd line = azathioprine
other = methotrexate or rituximab
Thymectomy if thymoma present
80
GUILLAIN-BARRE
What is the pathophysiology of GBS?
- B cells produce antibodies against the antigens on the pathogen causing the preceding infection and these antibodies also match proteins on the nerve cells leading to demyelination and potentially axonal degeneration
81
GUILLAIN-BARRE
What is Miller-Fisher syndrome?
- GBS variant which affects CNS + eye muscles
- Characterised by ophthalmoplegia + ataxia
82
GUILLAIN-BARRE
What is the clinical presentation of GBS?
SYMPTOMS
- tingling + numbness in hands and feet (often precedes muscle weakness)
- symmetrical ascending progresive weakness
- unsteady when walking
- back and leg pain
- SOB
- facial weakness and speech problems
SIGNS
- reduced sensation in affected limbs
- symmetrical weakness
- ataxia with hyporeflexia
- autonomic dysfunction (tachycardia, HTN, postural hypotension, urinary retention)
- respiratory distress
- cranial nerve involvement and bulbar dysfunction (diplopia, facial droop)
83
GUILLAIN-BARRE
What are the investigations for GBS?
BLOODS
- U&Es
- B12 + folate
- TFTs (exclude hypothyroidism)
- anti-ganglionside antibodies
CULTURES
- stool or sputum
LUMBAR PUNCTURE
- raised protein with normal WCC
To consider
- nerve conduction studies (not required for diagnosis)
- MRI brain + spinal cord
84
GUILLAIN-BARRE
What is the main treatment for GBS?
1st line
- IV immunoglobulin (IVIG) = 5 day course commenced within first 2 weeks of symptom onset
or
- plasma exchange = 5 treatments of 2-3L over 2 weeks commenced within first 4 weeks of symptom onset
ADDITIONAL OPTIONS
- thromboprophylaxis
- physiotherapy
- ICU support (if ventilatory failure)
85
BRAIN TUMOURS
What focal signs would you get if the tumour was located in the frontal lobe?
Personality + intellect change, hemiparesis, expressive dysphasia
86
NEUROPATHY
What is the pathophysiology of mononeuritis multiplex?
- Inflammation of vasa nervorum can block off blood supply to nerve causing sudden deficit
87
NEUROPATHY
What are the causes of peripheral neuropathy?
ABCDE –
- Alcohol
- B12 deficiency
- Cancer + CKD
- Diabetes + drugs (isoniazid, amiodarone)
- Every vasculitis
88
NEUROPATHY
In terms of peripheral neuropathy, what conditions show a...
i) mostly motor loss?
ii) mostly sensory loss?
i) GBS, chronic inflammatory demyelination polyneuropathy (chronic GBS), Charcot-Marie-Tooth disease
ii) DM, CKD, deficiencies
89
NEUROPATHY
What is Charcot-Marie-Tooth disease?
- Autosomal dominant condition.
- Characterised by high-arched feet, distal muscle weakness + atrophy (inverted champagne bottle legs), hyporeflexia, foot drop + hammer toes
90
NEUROPATHY
Where is Baum's loop located?
Where is Meyer's loop located?
How can you remember which is superior/inferior?
- Parietal lobe
- Temporal lobe
- PITS – Parietal Inferior Temporal Superior
91
NEUROPATHY
What does a CN5 lesion cause?
- Loss of sensation to face
- Weak muscles of mastication
- Loss of corneal reflex (afferent)
- Jaw deviation to weak side
92
NEUROPATHY
What does a CN7 lesion cause?
Face, ear, taste, tear –
- Muscles of expression
- Stapedius
- Anterior 2/3rd tongue
- Parasympathetic fibres to lacrimal + salivary glands
93
CORD COMPRESSION
What is myelopathy?
Injury to the spinal cord due to severe compression resulting in UMN signs + specific symptoms based on compression
94
CORD COMPRESSION
What are the causes of spinal cord compression?
- Malignancy (mostly secondary, 5Bs = breast, bronchus, byroid, bidney, brostate)
- Infection (epidural abscess), spinal osteophytes
- Disc prolapse (slower onset), haematoma (warfarin)
- Lumbar degeneration due to trauma or age (conservative Mx or steroid injections)
- Myeloma
95
CORD COMPRESSION
What are the signs of spinal cord compression?
- Motor, reflex + sensory level = normal ABOVE lesion
- LMN signs = AT level
- UMN signs = BELOW level
- Tone + reflexes usually reduced in acute cord compression
- ?Sign of infection like tender spine, pyrexia
96
CORD COMPRESSION
How does degenerative cervical myelopathy present?
- Pain, loss of motor or sensory function affecting neck, upper or lower limbs
- Loss of autonomic function
- Hoffman's sign +ve
97
CORD COMPRESSION
What are the investigations of spinal cord compression?
- PR to assess loss of sphincter control
- Screening bloods (FBC, CRP/ESR, B12, LFT, U+Es)
- MRI spine gold standard
- If mass, ?biopsy/surgical exploration
98
SPINAL CORD INJURY
What is Brown-Sequard syndrome?
- Lateral hemisection of spinal cord
- Ipsilateral weakness below the lesion (lateral corticospinal)
- Ipsilateral loss of fine touch, proprioception + vibration (DCML)
- Contralateral loss of pain + temp (lateral spinothalamic)
99
ANTERIOR CORD SYNDROME
What is anterior cord syndrome?
- Anterior spinal artery occlusion or compression
- Bilateral spastic paresis (lateral corticospinal)
- Bilateral loss of pain + temp (lateral spinothalamic)
100
SPINAL CORD INJURY
What is posterior cord syndrome?
- Trauma or posterior spinal artery occlusion
- Loss of fine touch, proprioception + vibration (DCML)
101
SPINAL CORD INJURY
What is central cord syndrome?
- Hyperextension injury, often elderly with underlying cervical disease
- Sensory + motor deficit (upper extremities > lower)
102
MYOPATHY
How do myopathies present?
- Symmetrical proximal pattern of muscle weakness (hairs, stairs + chairs)
- Weakness > wasting
- Reflexes + sensation normal, no fasciculations
103
MYOPATHY
How does myotonic dystrophy present?
- type 1 = distal weakness more prominent
- type 2 = proximal weakness more prominent.
- May have cataracts, testicular atrophy, cardiac lesions (heart block, cardiomyopathy), DM
104
HYDROCEPHALUS
How does normal pressure hydrocephalus present?
'Wet, wacky, wobbly' –
SYMPTOMS
- poor concentration
- poor memory (particularly short term)
- poor insight into deficits
- increasing confusion
SIGNS
- bladder incontinence
- faecal incontinence
- shuffling gait
- magnetic gait (feet appear to be stuck to the floor)
- Sx come on gradually + similar to Alzheimer's so difficult to diagnose
105
IDIOPATHIC INTRACRANIAL HYPERTENSION
What is the management of IIH?
- #1 weight loss (topiramate can be used + has benefit of weight loss)
- Acetazolamide
- Surgery = optic nerve sheath decompression + fenestration to prevent damage
- Lumboperitoneal or ventriculoperitoneal shunt
106
NEURO PHARMACOLOGY
What are some side effects and important information for...
i) carbamazepine?
ii) valproate?
iii) lamotrigine
i) Blurred vision, headache, drowsiness – agranulocytosis, aplastic anaemia, P450 inducer
ii) Teratogenic, hepatitis, hair loss, tremor, weight gain – some interactions with antidepressants
iii) Blurred vision, headache, drowsiness – Steven-Johnson syndrome + risk of leukopenia
107
NEURO PHARMACOLOGY
What are some side effects and important information for...
i) phenytoin?
ii) levetiracetam?
iii) ethosuximide?
i) Megaloblastic anaemia (folate), osteomalacia, teratogenic, P450 interactions – Steven-Johnson syndrome
ii) Headache, drowsiness – some interactions with antidepressants
iii) Night terrors, rashes
108
NEURO PHARMACOLOGY
What is the mechanism of action of Levodopa?
- Levodopa is dopamine precursor which can cross BBB to be converted to dopamine by dopa-decarboxylase
- Must be combined with peripheral dopa-decarboxylase inhibitor like carbidopa so levodopa can reach brain
109
NEURO PHARMACOLOGY
What are the side effects of Levodopa?
- Postural hypotension
- Confusion
- Dyskinesias (abnormal movements)
- Effectiveness decreases with time (even with dose increase)
- On-off effect
- Psychosis
110
NEURO PHARMACOLOGY
Give some examples of dopamine receptor agonists.
What is the mechanism of action?
What are some side effects?
What monitoring is required?
- Bromocriptine, cabergoline, ropinirole
- Increases amount of dopamine in CNS
- Hallucinations (more than levodopa), postural hypotension
- ECHO, ESR, creatinine + CXR prior to Rx
111
NEURO PHARMACOLOGY
What are some adverse effects of dopamine receptor agonists?
- Pulmonary retroperitoneal + cardiac fibrosis
- Bromocriptine associated with gambling + other inhibition disorders (e.g. sexual)
112
NEURO PHARMACOLOGY
What are COMT + MAO-B inhibitors?
What is the mechanism of action?
- Catechol-o-methyltransferase (COMT) inhibitor = entacapone
- Monoamine oxidase-B (MAO-B) inhibitor = selegiline
- Inhibit enzymatic breakdown of dopamine
113
NEURO PHARMACOLOGY
Examples of triptans.
Mechanism of action?
Used for?
- Sumatriptan, naratriptan
- 5-HT (serotonin) receptor agonists + act on smooth muscle in arteries > vasoconstriction, peripheral pain receptors > inhibit activation of pain receptors (vasoactive peptides) + reduce neuronal activity in CNS
- Abort migraines when start to develop
114
STROKE
What is the timeframe for thrombolysis for ischaemic strokes?
- Within 4.5 hours of the onset of symptoms
115
STROKE
what is the mechanism of action for alteplase / streptokinase (thrombolysis drugs for ischaemic stroke)?
- Converts plasminogen > plasmin so promotes breakdown of fibrin clot
- Alteplase (tPA) or can use streptokinase
116
SDH
what are the risk factors of SDH?
- Elderly - brain atrophy, dementia
- Frequent falls - epileptics, alcoholics
- Anticoagulants
- babies - traumatic injury (“shaking baby syndrome”)bridging veins stretched so more likely to rupture,
117
EPILEPSY
How would a partial seizure present in the parietal lobe?
paraesthesia
visual hallucinations
visual illusions
118
NEAD
How can NEAD and a true epileptic seizure be differentiated?
- Vital signs including lying-standing BP
- FBC, U+Es, glucose, LFTs, TFTs (normal CK + prolactin in NEAD)
- 24h 12-lead ECG + ECHO
- EEG + CT/MRI if necessary
119
MULTIPLE SCLEROSIS
In terms of the symptoms of MS, what is Lhermitte's sign?
Neck flexion causes electric shock sensation down spine
120
MULTIPLE SCLEROSIS
In terms of the symptoms of MS, what is Uhthoff's phenomenon?
symptoms worsening in heat e.g. in the shower/exercise
121
MENINGITIS
What are the aseptic causes of meningitis?
MS.
HSV2, SLE, sarcoidosis + skull # can cause recurrent aseptic meningitis
122
ENCEPHALITIS
What are the non-viral causes of encephalitis?
Bacterial meningitis
TB
Malaria
Lyme’s disease
123
MYASTHENIA GRAVIS
What medications can exacerbate myasthenia gravis?
Abx, CCBs, beta-blockers, lithium + statins
124
BRAIN TUMOURS
What focal signs would you get if the tumour was located in the temporal lobe?
Receptive dysphasia, amnesia
125
BRAIN TUMOURS
What focal signs would you get if the tumour was located in the parietal lobe?
Hemisensory loss, dysphasia
126
NEUROPATHY
What can cause mononeuritis multiplex?
Inflammatory or immune mediated vasculitis like granulomatosis with polyangiitis, polyarteritis nodosa, RA or sarcoidosis
127
BELL'S PALSY
what are the symptoms?
unilateral LMN facial weakness (forehead is affected)
altered taste
post auricular pain - pain behind ears
- hyperacusis (noise sensitivity)
- dry mouth
128
BELL'S PALSY
what is the management?
- prednisolone
- aciclovir
- eye protection (eye lubricants or artificial tears should be considered
129
NEUROFIBROMATOSIS
what are the clinical signs of NF1?
- cafe-au-lait spots on the skin
- pea-sized lumps under skin
- skeletal abnormalities
- tumour on optic nerve
130
NEUROFIBROMATOSIS
what are the clincial signs of NF2?
- acoustic neuromas (bilateral)
- family history
- meningioma, schwannoma, juvenile cortical cataracts or glioma
131
NEUROFIBROMATOSIS
what are the causes of neurofibromatosis 1 and 2?
NF1 = chromosome 17 (autosomal dominant)
NF2 = chromosome 22 (autosomal dominant)
132
NARCOLEPSY
what is the management?
1st line = sleep hygiene + lifestyle changes
can also consider pharmacotherapy
- modafinil
- pitolisant
- sodium oxybate
133
RADICULOPATHY
what are the causes?
- intervertebral disc prolapse
- degenerative diseases of the spine
- fracture (trauma or pathological)
- malignancy (metastatic)
- infection (extradural abscesses, osteomyelitis)
134
RADICULOPATHY
what is the management?
1st line
- NSAIDS (ibuprofen)
- physical therapy
2nd line
- epidural steroid injections
- surgery (laminectomy + discectomy)
135
CATAPLEXY
what is the management?
sodium oxybate
tricyclic antidepressants (clomipramine)
SSRIs
136
EPILEPSY
What is the emergency treatment for epilepsy?
ABCDE
check glucose
RECTAL/IV DIAZEPAM or LORAZEPAM
IV PHENYTOIN loading
mechanical ventilation
137
EPILEPSY
what is the treatment for generalised myoclonic epilepsy?
male = sodium valproate
female = levetiracetam
138
PARKINSON'S DISEASE
Give 2 histopathological signs of Parkinson’s disease
1. Loss of dopaminergic neurones in the substantia nigra
2. Lewy bodies
139
PARKINSON'S DISEASE
What surgical treatment methods are there for Parkinson’s disease?
Deep brain stimulation of the sub-thalamic nucleus
Surgical ablation of overactive basal ganglia circuits
140
HUNTINGTON'S DISEASE
What is the triplet code that is repeated in Huntington's disease?
Trinucleotide expansion repeat of CAG in HTT gene on chromosome 4
- >35 = HD
141
MIGRAINE
What is the diagnostic criteria for a migraine?
classified as with or without aura
at least 2 of:
unilateral pain (usually 4-72hrs)
throbbing-type pain
moderate > severe intensity
motion sensitivity
plus at least 1 of:
- nausea/vomiting
-photophobia/phonophobia
there must also be a normal examination and no attributable cause
142
MIGRAINE
How does triptan work?
Selectively stimulates 5-hydroxytryptamine (serotonin) receptors in the brain
143
MND
What are LMN signs?
Hypotonia + muscle wasting,
reduced reflexes,
fasciculations (particularly tongue)
144
MND
What is the diagnostic criteria for MND?
LMN + UMN signs in 3 regions
El Escorial criteria
Presences of LMN and UMN degeneration and progressive history
Absence of other disease processes
145
MYASTHENIA GRAVIS
What can weakness due to myasthenia gravis be worsened by?
Pregnancy
Hypokalaemia
Infection
Emotion
Exercise
Drugs
146
GUILLAIN-BARRE
When is IV immunoglobulin contraindicated in the treatment for Guillain-Barre syndrome?
If a patient has IgA deficiency - can cause severe allergic reaction
147
ANTERIOR CORD SYNDROME
what are the causes?
- iatrogenic - thoracic and thoracoabdominal AA repair
- aortic dissection
- atherothrombotic disease
- emboli
- vasculitis
148
ANTERIOR CORD SYNDROME
what are the symptoms?
- acute motor dysfunction
- loss of pain and temperature sensation below level of infarction
- autonomic dysfunction - neurogenic bowel/bladder
- acute onset back pain
149
ANTERIOR CORD SYNDROME
what are the investigations?
MRI - 'owls eyes' hyperintensities in anterior horns
lumbar puncture, CSF testing, blood and urine to rule out other causes
150
HORNER'S SYNDROME
what are the causes of 1st order horner’s syndrome?
Stroke
Syringomyelia
MS
tumour
encephalitis
anhidrosis to face, arm and trunk
151
HORNER'S SYNDROME
what are the causes of 2nd order horner’s syndrome?
Pancoast's tumour
thyroidectomy
trauma
cervical rib
anhidrosis of face
152
HORNER'S SYNDROME
what are the causes of 3rd order horner’s syndrome?
carotid artery dissection
carotid aneurysm
cavernous sinus thrombosis
cluster headache
no anhidrosis
153
HORNER'S SYNDROME
what are the clinical features of horner’s syndrome?
MAPLE
Miosis
Anhydrosis
Ptosis
Loss of ciliospinal reflex
Endophthalmos (sunken eyeball)
154
BULBAR PALSY
what are the symptoms?
- dysphagia
- reduced/absent gag reflex
- slurred speech
- aspiration of secretions
- dysphonia
- dysarthria
- drooling
- difficulty chewing
- nasal regurgitation
- atrophic tongue
weak jaw/facial muscles
155
STRABISMUS
what are the risk factors?
FHx of strabismus
prematurity
low birth weight
maternal smoking during pregnancy
156
SCIATICA
what are the risk factors?
- previous injury
- overweight
- lack of core strength
- physically demanding job
- diabetes
- osteoarthritis
- inactivity
- smoking
157
SCIATICA
what are the causes?
- herniated/slipped disc - puts pressure on nerve root
- degenerative disc disease
- spinal stenosis
- spondylolisthesis
- osteoarthritis
- trauma
- cauda equina syndrome
158
MYOPATHY
what are the causes of myotonic dystrophy type 1 and 2?
type 1 - DMPK gene mutation on chromosome 19
type 2 = ZNF9 gene on chromosome 3
159
TIA
what are the signs of a carotid TIA?
Amaurosis fugax = retinal artery occlusion –> vision loss
Aphasia
Hemiparesis
Hemisensory loss
hemianopia
160
TIA
what are the signs of a vertebrobasilar TIA?
Diplopia, vertigo, vomiting
Choking and dysarthria
Ataxia
Hemisensory loss
Hemianopic/bilateral visual loss
tetraparesis
loss of consciousness
161
HYDROCEPHALUS
what are the causes of normal pressure hydrocephalus?
excess fluid builds up in the ventricles, which enlarge and press on nearby brain tissue
- injury
- bleeding
- infection
- brain tumour
- brain surgery
162
ESSENTIAL TREMOR
what is the presentation?
HAND TREMOR
- upper limb
- worse on movement
- bilateral
- improves with sedation (alcohol, benzodiazepines, barbiturates + gabapentin)
- head or voice tremor
- difficulty performing fine motor tasks (writing, eating, dressing)
163
ESSENTIAL TREMOR
what is the management?
mild disease
- observation
moderate disease
- 1st line: propranolol or primidone
- 2nd line: gabapentin or benzodiazepines
- 3rd line: deep brain stimulation, MRI guided thalamotomy
164
EPILEPSY
how do lamotrigine and carbamazepine work?
Inhibit pre-synaptic Na+ channels so prevent axonal firing
165
EPILEPSY
how does sodium valproate work?
Inhibits voltage gated Na+ channels and increases GABA production
166
PARKINSONS DISEASE
what is the pathway for dopamine production?
Tyrosine --> L-dopa --> Dopamine
167
HYDROCEPHALUS
What are some causes of non-obstructive hydrocephalus?
- Commonly failure of reabsorption of arachnoid granulations (meningitis, post-haemorrhage)
- increased CSF production (choroid plexus tumour) but very rare
168
DIABETIC NEUROPATHY
what is the management for gastroparesis?
metoclopramide, domperidone or erythromycin
169
EPILEPSY
what are the risk factors?
- premature birth
- genetic (tuberous sclerosis, NF)
- febrile convulsions as a child
- traumatic brain injury
- neurodegenerative disease
- brain tumour
- intracerebral infection
- illicit drug use
- dementia
170
CHRONIC FATIGUE SYNDROME
what is the diagnostic criteria?
FATIGUE with all following features:
- persistent (>4 months)
- new or specific onset (not lifelong)
- unexplained by other conditions
- substancial reduction in activity level
- characterised by post-exertional malaise and/or fatigue
HAVE ONE OR MORE OF FOLLOWING FEATURES:
- muscle or joint pain
- headaches
- painful lymph nodes
- sore throat
- cognitive dysfunction
- worsening symptoms on physical or mental exertion
- general malaise or flu-like symptoms
- dizziness and/or nausea
- difficulty sleeping
- palpitations
171
HUNTINGTON'S DISEASE
where is the genetic mutation located and what type of mutation is it?
- mutation in HTT gene on chromosome 4
- trinucleotide repeat disorder (CAG)
172
BRAIN METASTASES
what are the most common cancers to metastasise to the brain?
- lung cancer
- breast cancer
- melanoma
- colorectal cancer
- renal cell carcinoma
173
BRAIN METASTASES
what is the management?
- corticosteroids (DEXAMETHASONE)
- radiotherapy
- stereotactic radiosurgery
- surgery
- chemotherapy
- targeted therapies
174
CEREBELLAR DISEASE
what are the causes?
- Friedreich's ataxia
- neoplastic (cerebellar haemangioma)
- stroke
- alcohol
- MS
- hypothyroidism
- drugs (phenytoin, lead poisoning)
- paraneoplastic (secondary to lung cancer)
175
IDIOPATHIC INTRACRANIAL HYPERTENSION
what are the risk factors?
- obesity
- female sex
- pregnancy
- drugs (COCP, steroids, tetracyclines, retinoids, lithium)
176
RADICULOPATHY
how can you distinguish an L5 radiculopathy from a common peroneal nerve injury?
both conditions cause foot drop
L5 RADICULOPATHY
- weakness of foot on dorsiflexion
- weakness of toe on extension
- weakness during foot eversion
- lower limb tendon reflex changes
- L5 dermatomal distribution of sensory loss
COMMON PERONEAL NERVE INJURY
- weakness of foot on dorsiflexion
- weakness of toe on extension
- weakness during foot eversion
- no changes to lower limb reflexes
- sensory loss over anterior aspects of foot and leg
177
WERNICKE-KORSAKOFF SYNDROME
what is the clinical triad?
- confusion
- ataxia
- ophthalmoplegia + nystagmus
178
EPILEPSY
what is the management for different types of seizures?
GENERALISED TONIC-CLONIC
- male = sodium valproate
- female = lamotrigine or levetiracetam
FOCAL SEIZURES
- 1st line = lamotrigine or levetiracetam
- 2nd line = carbamazepine, oxcarbazepine or zonisamide
ABSENCE SEIZURES
- 1st line = ethosuximide
- 2nd line (male) = sodium valproate
- 2nd line (female) = lamotrigine or levetiracetam
MYOCLONIC SEIZURES
- male = sodium valproate
- female = levetiracetam
TONIC OR ATONIC SEIZURES
- male = sodium valproate
- female = lamotrigine
179
MONONEUROPATHY
what are the nerve roots for median nerve?
C5-T1
180
MONONEUROPATHY
what are the clinical features of median nerve palsy (carpal tunnel syndrome)?
- sensory loss and/or paraesthesia over palmar + distal aspect of thumb, index, middle and half of ring ringer
- weakness of hand
- weak thumb abduction
- thenar eminence wasting
- hand pain (worse at night)
181
MONONEUROPATHY
what are the investigations for carpal tunnel syndrome?
tinels test
phalens test
182
MONONEUROPATHY
what are the nerve roots for the ulnar nerve?
C8-T1
183
MONONEUROPATHY
what are the clinical features of ulnar neuropathy?
- sensory loss and/or paraesthesia over little finger + medial side of ring finger
- hand weakness (loss of dexterity, grip weakness)
- muscle wasting (hypothenar eminence +/- interossei muscles)
- claw hand deformity
184
MONONEUROPATHY
what are the investigations for ulnar neuropathy
froments test - pinch paper between thumb + index finger
185
MONONEUROPATHY
what are the nerve roots for the radial nerve?
C5-T1
186
MONONEUROPATHY
what are the clinical features of radial neuropathy?
- sensory loss and/or paraesthesia over dorsum or hand (may extend up forearm)
- wrist drop
- weakness in finger extension
- weakness in brachioradialis
187
MONONEUROPATHY
what are the nerve roots of the axillary nerve?
C5-6
188
MONONEUROPATHY
what are the clinical features of axillary neuropathy?
sensory loss over lateral shoulder
189
MONONEUROPATHY
what are the nerve roots for the common peroneal nerve?
L4-S2
190
MONONEUROPATHY
what are the clinical features of common peroneal neuropathy?
- foot drop (weakness of dorsiflexion)
- sensory loss over dorsum of foot + lateral shin
191
MONONEUROPATHY
what are the nerve roots of the tibial nerve?
L4-S3
192
MONONEUROPATHY
what are the clinical features of tibial neuropathy?
- paraesthesia, pain or numbness over the sole of the foot (worse at night + with prolonged standing)
- foot deformities (pes planus, pronated foot, abnormal gait)
193
MONONEUROPATHY
what is meralgia parasthetica?
pain +/- sensory loss over anterolateral thigh due to neuropathy of lateral femoral cutaneous nerve
194
MONONEUROPATHY
what is the management of carpal tunnel syndrome?
- wrist splints
- corticosteroid injections
- surgical decompression (flexor retinaculum decompression)
195
TIA
What is the secondary prevention following a stroke/TIA?
- 1st line = clopidogrel 75mg
- 2nd line = aspirin 75mg + MR dipyridamole
- 3rd line = MR dipyridamole
- 4th line = aspirin 75mg
all patients = high dose statin (atorvastatin 20-80mg)
manage HTN, DM, smoking and CVD risk factors
196
ENCEPHALITIS
what is the management?
IV ceftriaxone
IV acyclovir
