Neuro - ix Flashcards
Dx of Myasthenia Gravis is based on
- Clinical features (fatiguable muscles, facial paresis, ptosis, double vision, dysphagia, dysarthria, proximal limb weakness, SOB)
- Benefit of cholinesterase inhibitors
- Detection of specific autoantibodies (anti-AChR, anti-MuSK, anti-LRP4)
- Electrophysiological tests
Ix for Myasthenia Gravis
- Tensilon test
Gold standard investigation for dx of MG
Tensilon = edrophonium bromide = short acting anti-cholinesterase
Given IV - transiently improves muscle weakness by allowing the prolonged action of Ach
Effects best seen after asking the patient to perform repetitive movements to cause muscle fatigue Generally avoided due to risk of bradycardia
*Serum acetylcholine receptor (AChR) antibodies
First-line investigation
*Muscle-specific tyrosine kinase (MuSK) antibodies
For patients negative for AChR antibodies
- Low density lipoprotein receptor related protein 4 (LRP4)
- Blood CK - to exclude myopathies
*Neurophysiological testing on symptomatic muscles
- repeated nerve stimulation
First line ix
Can help establish the diagnosis in seronegative patients with suspected MG
Positive response - >10% decline in compound muscle action potential amplitude bn 1st + 4th potential in a train of 10 stimulations of the motor nerve
*EMG (more sensitive than neurophysiological testing)
Single fibre EMG may demonstrate “jitter” (variability in latency from stimulus to muscle potential between 2 different single motor fibres of the same motor unit) indicating fluctuation in neuromuscular conduction
*CXR
To visualise thymic hyperplasia>thymoma in the mediastinum or malignancies in the lung
*Ice test
Distinguishes MG from other causes of ptosis
Ice on eye for 3 mins leads to improvement of ptosis in pt w MG
*Serum pulmonary function tests
Indicated if SOB or suspected MG crisis
MG crisis: low FVC, negative inspiratory force
Lambert eaton syndorme - anti-voltage gated calcium channel antibody
Ix of meningitis
Ix must not delay treatment
* Bloods
2 sets of blood cultures
*Imaging
- CT
Considered before LP if there are signs of increased ICP (focal neurological signs, depressed consciousness)
Reserved for those with specific adverse clinical features or when an underlying cause is suspected e.g. mastoiditis
*LP - most important ix
Dx can only be confirmed by LP + lab examination of the CSF (MCS)
Performed immediately (<1h)
Should be performed before starting abx - definitive diagnosis of causative organism + definitive treatment
CSF
- may be normal in the early stages of meningitis
- repeat if symptoms + signs persist
Contraindications to LP
- signs of increase ICP (decreased consciousness, bad headache, frequent fits)
- Coagulopathy
- focal neurology
- severe shock
- sepsis
- open skin lesion at the site of entry
Results of LP in bacterial/viral/TB meningitis
CSF, neutrophils/lymphocytes, protein, glucose
Bacterial
- Turbid CSF
- High neutrophils (>500) - polymorphs
- High protein >1g/L
- Low glucose <2.2
Viral meningitis
- Clear/cloudy CSF
- High lymphocytes 100-500 - mononuclear
- High/Normal protein <1g/L
- Normal glucose
TB meningitis
- Fibrinous CSF
- High lymphocytes (<1000) - mononuclear
- High protein 0.1-0.5
- Low glucose 1.6-2.5
If pt <16 y/o w unexplained petechial rash + fever
- FBC
- CRP
- Coagulation screen
- Blood culture
- Whole blood PCR for N. meningitis
- Blood glucose
- ABG
CSF in bacterial meningitis
Appearance
Cells
Glucose
Protein
Turbid/Cloudy
Increased neutrophils (polymorphs)
Decreased glucose
High protein
Cushing’s reflex/triad
What is it sign of?
Bradycardia
HTN
Irregular breathing
Sign of increased ICP
CSF in viral meningitis Appearance Cells Glucose Protein
Clear
Increased lymphocytes (mononuclear)
Normal glucose
Normal or increased protein
CSF in TB meningitis Appearance Cells Glucose Protein
Fibrin web
Increased lymphocytes (mononuclear)
Low glucose
High protein
Extradural haematoma non contrast CT scan shape
Lemon shaped (lentiform)
Does not cross suture lines
Subdural haematoma non contrast CT scan shape
Banana shaped (crescent)
Crosses suture lines
SAH ix
Urgent non-contrast CT head within 12h
- Presence of hyperdense appearance of blood in the subarachnoid space/basal cisterns
- Hyperattenuation around the circle of willis
If CT normal + still suspecting SAH
LP after 12h have passed, examined by spectrophotometry (photospectrometry)
- xanthochromia + oxyhaemoglobin
- Exclude SAH if both CT + LP are negative
- CT/MR angiography in pt w confirmed SAH required to identify the cause
• U+Es – hyponatramia is the most common abnormality in SAH, assosciated with SIADH
• Hyperglycaemia – feature of any acute brain injury
• ECG – common cardiac findings in SAH (due to massive catecholamine release resulting in overwhelming sympathetic activation – as a result, transient myocardial ischaemia and failure may occur)
o Arrhythmias + ischaemic changes
o Prolonged QT interval
o ST segment/T-wave abnormalities
Ischaemia vs haemorrhage on the CT
Ischaemia - black
Haemorrhage - white
Seizure ix
EEG
Bloods
Brain imaging (CT, MRI)
Stroke ix
• Non contrast CT head
o First line investigation to differentiate haemorrhagic from ischaemic stroke
o In many cases, the CT is normal within the first few hours of an ischaemic stroke
o Less accurate than MRI for determining the site + extent for ischaemic damage
• MRI brain
o Provides more accurate information about the stroke lesion compared with CT
o Clearly highlights the area of ischaemic infarct
o May provide further clues about the causes
• Serum glucose
o To exclude hypoglycaemia as a cause for focal neurological signs
o Hyperglycaemia has been assosciated with risk of haemorrhagic transformation of ischaemic stroke
o Every pt with TIA or stroke should be screened for DM (fasting plasma glucose, HbA1c, oral glucose tolerance test)
• FBC
o May reveal a cause for arterial occlusion (e.g. polycythaemia vera, thrombocytosis)
o Haemorrhage
o To detect conditions that may be potential contraindications for some acute stroke treatments (thrombolytics, anticoagulants, antithombotics)+ interventions (e.g. anaemia or thrombocytopenia)
• U+Es
o Serum electrolytes - To exclude electrolyte imbalance as a cause for focal neurological signs
o Serum urea + creatinine - Renal failure may be a potential contraindication to some stroke interventions
• Prothrombin time + PTT w INR
• ECG
o Performed to exclude cardiac arrhythmia or ischaemia – relatively common in ischaemic stroke
o AF - potential cause of emboli (fast, irregular, no p-waves)
• Cardiac enymes
o Stroke may be assosciated with concomitant MI
• Carotid duplex US
o In stroke/TIA in carotid territory
• People with acute stroke should have their swallowing screened before being given any oral food, fluid, medication
TIA Ix
Primary care
• Urinalysis/Serum glucose
o Every pt with TIA or stroke should be screened for DM (fasting plasma glucose, HbA1c, oral glucose tolerance test)
o Hypoglycaemic events can elicit global symptoms e.g. confusion/syncope which can lead to focal symptoms
• FBC
o Polycythaemia, extreme thrombocytosis, extremely high WBC - can contribute to risk of poor cerebral perfusion
o Thrombocytopenia - RF for intracranial haemorrhage
• U+Es
o Severe hyponatraemia can trigger seizures or induce generalised weakness
o Hypokalaemia + hypercalcaemia - can also cause generalised weakness
• Prothrombin time, INR, PTT
o If neurological deficit persists at time of presentation, abnormal coagulation suspected, thrombolytic therapy for stroke is being considered
• ECG (may show AF - RF for embolic cerebral ischaemia, MI, evidence of myocardial ischaemia, HF - RF for atherosclerosis)
• MRI
o To localise infarct, suggest aetiology + distinguish TIA from stroke
o If unavailable, use CT head
• CT!!!
o New focal deficits need to have ischaemia distinguished from haemorrhage Specialist service
- Doppler US of carotid + vertebral arteries for presence of stenosis
- Echocardiogram – atrial thrombus, aneurysm of the anterior wall of the LV w mural thrombus, atrial myxoma, L-side valve disease
- Telemetry/Holter monitor – performed in all patients with TIA to evaluate for AF and other arrhythmias
- ESR if suspecting giant cell arteritis
If a patient is on warfarin/a DOAC/ or has a bleeding disorder and they are suspected of having a TIA, they should be admitted immediately for imaging to exclude a haemorrhage
What is the ABCD2 score?
Identifies patients at high risk of stroke following TIA
What does he ABCD2 score include?
Age 60+ (1)
BP SBP 140+ or SBP 90+ (1)
Clinical features - speech disturbance with no weakness (1), unilateral weakness (2)
Duration of symptoms - <10min (0), 10-59mins (1), 60+ min (2)
Diabetes (1)
What is a significant ABCD2 score?What does it mean?How do you manage the risk?
4+
High risk of stroke following a TIA
Aspirin 300mg daily
Admit for inpatient assessment regarding suitability for carotid entarterectomy
Secondary prevention
Hydrocephalus ix
• CT – first line
o Dilated lateral + 3rd ventricle with:
N 4th ventricle – aqueduct stenosis
Abnormal 4th ventricle – posterior fossa mass
o General ventricular dilation – communicating hydrocephalus
o May also pick up cause (e.g. tumour)
• LP – performed after confirming with imaging that hydrocephalus is communicating
o To measure pressure of the CSF
o May suddenly relieve symptoms – Therapeutic in NPH [this is considered diagnostic – if pt’s symptoms relieved by LP, he probably has hydrocephalus]
o Contraindicated if increased ICP
• CSF
o From ventricular drain/LP
o May indicate pathology (e.g. TB)
o MC+S, protein glucose
• Levodopa challenge – ordered in all patients w suspected PD
o Pt given therapeutic trial of levodopa + asked to note improvement in gait symptoms – if symptoms are responsive, then NPH can be ruled out
