Neurology Flashcards
Femoral nerve:
- Nerve Roots
- Motor function
- Reflex 4) Sensory
- Clinical causes of neuropathy
- Lumbar plexus L2-4
- Knee extension, hip flexion
- Knee jerk
- Anterior thigh and medial lower leg (saphenous nerve)
- Diabetes, femoral nerve block, pelvic fractures, THR, childbirth, psoas abscess, posterior abdoinal neoplasms
Multiple sclerosis is a disease primarily of the …
Oligodendrocytes
MS involves the attack of the following proteins..
Myelin basic protein and myelin oligodendrocyte glycoprotein (MBP and MOG)
Function of oligodendrocytes
Creates the myelin sheath in the CNS (Schwann cells are the myelin sheath in the PNS)
HLA associated with MS
HLA-DR15 (only 2-3x fold increase risk)
Internuclear opthalmoplegia to right clinical finding
If R) sided INO - R) eye cannot adduct and horizontal nystagmus to the right
transverse myelitis clinical features
Rapid onset of weakness, sensory alterations and or bowel,bladder dysfunction
Usually sensory level is detected
Initially flaccid then spastic weakness
transverse myelitis on MRI - signal change in which sequence?
T2 hyperintense signal change
transverse myelitis on LP
Pleocytosis +/- OCB
causes of transverse myelitis
post-infectious (50%) neuroinflammatory conditions (inc MS) autoimmune conditions
diagnosis of MS + updates in 2017 criteria
demonstrate CNS demyelination with dissemination in space and time updates in 2017 criteria: - demonstrating oligoclonal bands (CSF specific)
typical MS lesions
Juxtacorticaol lesions Dawson’s fingers Pontine lesions Spinal cord lesions GAD-enhancing lesions
clinically isolated syndrom
Objective evidence for a single attack typical for MS related demyelination Isolated to a single attack in time (not necessarily space) Risk of progression to MS
radiologically isolated syndrome
Incidental brain or spinal cord MRI findings that are highly suggestive of MS in an asymptomatic patient - no hx/sx of MS
Treatment in MS (disease modifying treatment) principles
Escalation vs induction therapy (Starting with less effective medication and progressing to more potent DMT vs starting with a potent DMT at the beginning) Some risk factors (e.g. disease burden on MRI and lots of enhancing lesions)
Natalizumab (Tysabri)
300mg IV monthly infusion Monoclonal antibody that binds to alpha4 subunit of 2 integrin adhesion molecules. Tries to prevent the extravasation of inflammatory cells through the BBB into the CNS Risk - PML
PML vs MS relapse
PML worsens over weeks where as MS relapse worsens over days
Diagnosis of PML
MRI and JCV PCR in CSF
How often to monitor JCV
Serum JCV every 6 months
Biggest risk factor for PML on Tysabri
Duration (over 2 years) Previous exposure to other immunosuppressants
PML imaging
See Rosenfeld lecture Sharply demarcated border at grey-white junction
Ocrelizumab
IV 300mg infusion twice 2 weeks apart then 600mg 6 months Humanised monoclonal antibody against CD20 (B cell action) Approved for RRMS and PPMS Adverse effects: infections, PML (see Rosenfeld lecture)
Cladribine
Tablet taken over 2 years - no evidence for further courses Mechanism: synthetic deoxyadenosine analogue - reduction in peripheral T and B lymphocytes and resting cells as well Adverse effect: signficant lymphopenia
Alemtuzumab
Probably most effective Binds CD52 - expressed on loymphocytes, natural killer cells, monocytes and dendritic cells Safety concerns - unveils autoimmune diseases - ITP, Autoimmune thyroid disease, Goodpasture’s syndrome; pancreatitis Needs monitoring for autoimmune sequelae for 4 years post treatment
Malignancy screening for MS DMTs
Population screening
Fingolimod
0.5mg daily Binds sphingosine-I-phosphate receptor causing it to be internalised from cell surface. Lymphocyte retention Adverse effects: macula degen - requires OCTs 3 monthly
Interferon beta
Decreases T cell activity Many adverse effects
Glatiramer acetate
Shifts population of T cells from Th1 T cells to Th2 T cells Alters macrophage function
Tecfidera
Oral tablet Mechanism is unclear Reports of PML
Teriflunomide
Oral tablet - active metabolite of lefluomide Inhibits proliferation of actively proliferation cells through inhibition of DHODH Teratogenic
MS in pregnancy
Encourage conception when stable Relapse declines during pregnancy but increases post partum Control disease activity prior conception
What MS meds are not recommended during pregnancy
fingolimod and tysabri (natalizumab) - both have high risk of rebound Teriflunomide (VERY TERATOGENIC) - need chelation and drug elimination prior contraception and also alemtuzumab (high risk of autoimmune thyroiditis)
NMO spectrum disorder clinical features + mechanism
Inflammatory demyelinating disease of the CNS AQP4 Ab in 80% AQP4 is a water channel protein located in the spinal cord grey matter, periaqueductal and periventricular regions and astrocytic foot processes Clinical features: longer segment transverse myelitis; relapsing; OCB in 30%
NMOSD treatment
Steroids, PLEX Steroid sparing agent considered
Anti-MOG disease
Diagnosis via antibodies Rosenfeld lecture
Approved for PPMS
ocrelizumab
intracranial haemorrhage with blood along floor of the anterior cranial fossa - suspicious for?
anterior communicating artery aneurysm
intracranial haemorrhage with blood around the Sylvia fissure - suspicious for?
MCA aneurysm
Low CBV on CT perfusion
Irreversibly damaged dead tissue
Delayed TTP
Collateral territory
Risk of stroke in the first week after TIA (untreated)
10%
when to have delayed MRI for investigation of intracerebral haemorrhage
~8 weeks
Antithrombotics for minor stroke/TIA
DAPT for 3-4 weeks as per CHANCE/POINT trials unless atrial fibrillation
When to do PFO closure in strokes
otherwise cryptogenic stroke age <60
When to do left atrial appendage closure for AF
contraindication to anticoagulation
Blood pressure management in ischaemic stroke
Acute: - Gently lower <185/105 if thrombolysis - Otherwise only treat if >220/120 Longer term: - Aim SBP <140 mmHg
Symptomatic carotid stenosis 70-99%
carotid endarterectomy between 2 days and 2 weeks if not alr severely disabled
Symptomatic carotid stenosis 50-70%
carotid endarterectomy if low surgical morbidity and good life expectancy
Symptomatic carotid occlusion/trickle flow
low risk of recurrent stroke - generally not suitable for surgery
Rate of ololingual angiooedema post tPA
2% (5% if taking ACEI)
Age limits for thrombectomy
Age shouldn’t affect thrombectomy (Goyal Lancet 2016)
IV thrombolysis in parallel with endovascular thrombesctomy?
Yes if eligible
What criteria for extended timing for endovascular thrombectomy (6-24hr)
<70ml core (and other generic thrombectomy criteria)
Perimesencephalic haemorrhage
SAH not associated with aneurysm + midbrain blood
Reversible vasoconstriction syndrome clinical features
Month-6 weeks of episodic thunderclap headaches. Most have good prognosis and a very small proportion can have cerebral ischaemia and have neurological sequalae Treatment is expert opinion. Usually CCB
Causes of lobar haemorrhages
Amyloid (elderly) AVM Pretty much anything else aside from HTN
Mechanism of trigeminal neuralgia
Microvascular compression
Clinical features of trigeminal neuralgia
Electric sudden pain, recurrent, often triggered by sensory stimulus in other affected area ephaptic transmission of sensory/compression input Can rarely be seen in patient in MS
Treatment for trigeminal neuralgia
carbamazepine
Characteristic of migraine aura
Starts off as central visual disturbance, then spreads and expands. The edge has a shimmering quality and zim zag (fortification spectra). Persists for ~20min. Key features is that it migrates. Generally preceds headaches
Cause of migraine aura
Neuronal dysfunction - spreading depression of Leao
New migraine mAb
CGRP inhibitor (Erenumab)
MOA for tripans
5HT1B and 5HT1D agonist Those things are thought to inhibit the release of CGRP
What CN is affected in IIH
CN VI due to its long and vertical course and predisposition to be compressed by the increased pressure (lateral visual palsy)
Ventricle size in IIH
Small unlike NPH
Acute management of cluster headache
High flow oxygen at least 8L/min Triptan - sumitriptan by subcut injection
Long term management of cluster headache
Verapamil - start at 160mg, uptitrate up to 720mg+ (need ECGs) Can use prednisolone (75mg) as transitional therapy GON block
Where does surface electrode for median nerve go
APB abductor pollicis brevis
What are DML and PML in NCS
Distal motor latency and proximal motor latency
Are amplitudes of sensory conduction responses bigger or motor responses
Motor because you are getting the response from the whole muscle rather than over a nerve directly
Can you do a direct calculation of velocity from motor latencies or sensory latencies
Sensory because there’s no NM junction
Are sensory or motor nerves first affected by a peripheral neuropathy
sensory and distal before proximal sural nerve often used
Nerve compression pathology
focal demyelination localised slowing
NCS finding of guillian barre/conduction block
decreased amplitudes across different segments
What does very very slow conduction velocities suggest
Inherited demyelinations - e.g. charcot marie tooth
Critical illness myopathy - why does it produce low amplitude on NCS
low amplitude due to decrease in muscle mass
Normal EMG findings
No response at rest Gradual recruitment of individual muscle fibres Interference pattern when multiple muscle units are recruited
Findings of deinnervation and reinnervation of EMG
Deinnervation = fibrillation and reinnervation - larger amplitude fibrillation happens first
Findings of myopathy is EMG
No fibrillation (not generally), no spontaneous activity. Activity is low amplitude and brief Often polyphasic because the the muscle fibre is damaged and there is re-innervation between the muscle fibres
What myopathies do you see fibrillation
When there is a lot of degeneration going on ICU myopathy, duchenne in active phase, active myositis, necrotising myositis
EMG for Myasthenia gravis
Fast repetitive stimulation to see decremental response (Lambert eaton is incremental response)
Single muscle EMG in myasthenia
lack of activation of the second fibre (blocking) as the acetylcholine becomes insufficient to reach the action potential required to active adjacent muscle fibres Another sign is “jitter” because there is an exaggerated difference in the response of the second recruited muscle
Fasciculations meaning
single motor unit firing by itself happens in chronic deinnervation
myokymia
post radiotherapy common in limbs due to spontaneous firing of individual fibres
demyelination
increased latency and dispersion (Due to different degrees of demyelination in different nerves)
painful neuropathy
generally small fibre B6 toxicity proximal/small fibre amyloid paraneoplastic HIV assoc cryoglobuliaemia
B6 toxicity
painful neuropathy
where is demyelination more common in GBS
proximal demyelination lesions so f waves are important in GBS
anti GQ1 positive GBS variant
ataxia bulbar ophthalmoplegia
diver bomb EMG
myotonia
what is spared in MND
diplopia and micturition as the theory is that only monosynaptic pathways are involved
split hand syndrome
in MND APB and 1st interosseous and more affected preserved ulnar side and hypothena muscles are not affected must thought it’s because the first 4 fingers have a greater representation in the hand
brachioradialus weakness
listen to recordinf
C7 radioculopathy signs
slight weakness in wrist and ifnger extension (grade 2/3) weakness of elbow extension overlap with radiopalsy typically lose triceps jerk sensation middle or sometimes index finger too
inflammatory brachial plexopathy
very painful, restless pain preceeds weakness selects out individual peripheral/adjacent nerves commonest cause of a winged scapula also called neuralgic amyopathy
differentiating between L5 nerve root injury and peroneal nerve injury
hip abduction - significant L5 component ankle jerk is present in peroneal but absent in tibial but the exam ans is tibialis posterior
most common cause for foot drop post hip replacement
stretch of sciatic nerve the sciatic nerve has already divided into the peroneal and tibial branches
