Neurology Flashcards
A patient presents with transient loss of consciousness. What needs to be elicited in the hx?
Witness!
1) Clarify LOC: Was it actually LOC? or light headedness, dizziness, falling (PE, aortic dissection, orthostatic hypothension)
2) Memory of episode: Remember whole episode? Parts of it? for how long?
3) Before: When? Where? Posture (sitting, standing, walking)? Precipitating events? Warning signs (visual disturbance, light headedness, sweating)?
4) During: Duration? Jerking (focal or generalised)? Eyes (open or closed)? Tongue biting? Incontinence? Injury?
5) After? Conscious (directly after or later)? Disorientation/confusion? Drowsiness? Weakness (uni/bilateral)
6) Rule out vasovagal/orthostatic hypotension
How is vasovagal or orthostatic hypotension ruled out when taking a history of transient loss of conciousness?
Has it happened before? (when taking bloods, urinating, opening bowels, standing for extended periods of time)
Relieved by lying down?
Precipitated by feeling hot or sweaty?
With a transient loss of consciousness what examinations would you perform?
Vitals
Cardiology exam
Neurological exam upper and lower limb sensory and motor
Cranial nerve exam
+/- resp
What ECG finding is in this image?
What leads would you see this in?
Brugada Coves in V1-V3
Broad P wave with some PQ prolongation
J point elevation
Coved ST segment elevation
Inverted T wave
Here are all the ECG findings associated with LOC
Here is a delta wave. Where is this seen?
Wolff-Parkinson-White Syndrome
Signifying Ventricular pre-excitation
Here are all the ECG findings associated with LOC
A patient comes with an episode of LOC. on examination there are residual neurological signs. What does this indicate? What is the next course of action?
This may be stroke => admit urgently
A patient presents with transient LOC. Give 5 differentials
These can apply to anything in neuro rly
Vasovagal syncope
Hypoglycemia
Stroke/TIA
Space-occupying lesion
Epilepsy
Dizziness
Orthostatic hypotension
Panic attacks/hyperventilation
Abnormal perceptions (hallucinations) -doesnt count
Vasovagal syncope occurs when there is raised vagal activity leading to peripheral vasodilation + bradycardia => venous pooling => postural hypotension. It is a diagnosis of exclusion. Once there are no other diagnoses, what is required to confirm the diagnosis?
1 of the 3Ps
1) Posture - Prolonged standing before event, relieved by sitting
2) Provoking factors - Pain or medical procedure (taking bloods)
3) Prodromal symptoms -> sweating, feeling warm/hot before event
Syncope that occurs when opening the bowel is called?
Situational syncope
What are the different ways hypoglycaemia may present with LOC?
DM patients on insulin or hypoglycaemic meds (sulfonylureases)
Initially symptoms of hypoglycemia
=> Autonomic changes (pallor sweating, tachycardia) + confusion
Then coma
Then seizures
You are asked to take a history of a patient with a headache. How would you approach it and what would you elicit?
If nothing else, do Socrates + before,during,after (and remember to separate the types)
1) Types -> 1 type of headache or more? take a separate history for each
2) Time -> When? How often? Pattern (episodic or constant or daily), Duration
3) Character -> Site of pain and quality
4) Associated sx -> Nausea, vomititng, visual disturbance, weakness, paraesthesia
5) Predisposing/triggering factors (eg. related to period, loud noises, bright lights)
6) Response -> How do you deal with it e.g. medication or sitting in a quiet room
7) QoL -> Affecting school, work, relationships
8) Must ask: Headaches, funny fits and turns, visual disturbance
while conducting an exam on a patient with headache, you note tenderness over the temporal area. What is this consistent with>
GCA or temporal arteritis
What must be done when asked for examination of a headache
Neuro exam
Cranial nerve exam
Examine the fundus and visual acuity
Palpation of temporal regions (GCA/temporal arteritis), sinuses and neck (stiffness for meningitis)
Check for rash
Give 5 red flags in headache that warrant urgent referral (dont actually memorize)
Meningitis (fever, worsening headache, purpuric non-blanching rash)
Papilloedema
Reduced consciousness
Recent head injury
Suspected temporal arteritis
Weight loss + visual disturbance (pituitary cancer)
Suspected acute glaucoma (e.g. steroids)
Atypical migraine (e.g. with hemiparesis)
Thunderclap headache (Subarachnoid haemorrhage)
A patient presents with a headache, what are your differentials
Acute New Headache:
1) Meningitis
2) Encephalitis
3) Subarachnoid haemorrhage/Thunderclap headache
4) Head injury (epidural/subdural)
5) Sinusitis
Acute recurrent headache:
1) Migraine
2) Cluster headaches
3) Trigeminal neuralgia
4) Glaucoma
Chronic Headache
1) Tension headache
2) GCA/Temporal arteritis
3) Cervicogenic
4) Malignancy (pituitary)
What ddx for headache is associated with fever, photophobia and rash
Meningitis
What ddx for headache is associated with fever, confusion, reduced GCS
Encephalitis
What ddx for headache is associated with a very severe sudden onset headache
Subarachnoid haemorrhage (Thunderclap headache)
What ddx for headache is associated with an aura, visual disturbances and nausea
Migraine
What ddx for headache is associated with reduced GCS, Lucidity, amnesia?
Head injury leading to epidural/subdural haemorrhage
What ddx for headache is associated with extremely painful headaches focused around 1 eye with associated autonomic symptoms on that side including ptosis, miosis, red, watery eye, runny blocked nose and forehead sweating. It is predictable and always occurs after falling asleep and after drinking alcohol. The headaches last 15minutes to 3 hours. They occur once daily (can occur as little as once weekly).
Cluster headaches
What ddx for headache is associated with red eye, haloes, and reduced visual acuity
Glaucoma
What ddx for headache is associated with stabbing pain around the TMJ
Trigeminal neuralgia
What ddx for headache is associated with pain like a band around the head, brought on by stress and anxiety. It is a bilateral, pressing, tightening pain of moderate intensity.
No vomiting
Does not prohibit daily activities.
Tension headache
What ddx for headache is associated with pain like band from the neck to the forehead + scalp tenderness
Cervicogenic
What ddx for headache is associated with diplopia?
Malignancy (pituitary)
What ddx for headache is associated with scalp tenderness, raised ESR in a patient >50
GCA/temporal arteritis
What is considered within the Chronic Disease Management Criteria
Any patient aged >18 with
1) A.fib
2) Asthma
3) COPD
4) Diabetes
5) Ischemic heart disease
6) HF
7) Stroke/TIA
Give 3 examples of typical and atypical auras
Typical: Lasting <60 minutes
Visual sx (flickering lights, spots, and LOV)
Sensory sx (paresthesia and numbness)
Speech disturbance
Atypical: Motor weakness, double vision, unilateral visual sx, Poor balance, LOC
What is the typical presentation of a migraine
Moderate to severe unilateral/bilateral throbbing/pulsating headache lasting 4-72 hours.
May occur with or without aura (flickering lights, spots, blurring…)
May also have nausea, vomiting, sensitivity to light/loud noise
What is the pathophysiology of Migraine
Disturbance of cerebral blood flow under the influence of Serotonin
What is the difference between episodic and chronic migraine?
Episodic = <15d/month
Chronic = >15d/month for >3 months
What are 5HT1 agonists? Give an example
Triptans, serotonin receptor agonist, Sumatriptan
What is the management of an acute migraine attack?
Combination therapy including
1) Triptan (Sumatriptan)
2) NSAID/Paracetamol
3) Antiemetic (metoclopramide)
When advising a patient on taking Triptans for acute attacks of migraine, they ask when they should take it. What would you say?
She then asks, what if a second attack is superimposed? Do I take another dose?
On the onset of the headache. It is not effective if taken before (not a prophylactic drug). It stops 70-80% of attacks
Yes, another dose is given in that case (of triptan)
A patient is having an acute migraine attack you give them combination therapy including
1) Triptan (Sumatriptan)
2) NSAID/Paracetamol
3) Antiemetic (metoclopramide)
She cannot take anything orally though. What will you give her?
Nasal spray Sumatriptan (typically used for children)
+Diclofenac PR
+Metoclopramide PR
What is the general advise you should give all patients taking pain killers for migraine?
Taking too many doses can lead to rebound headaches when not using them. Control and only take when needed
What lifestyle advice would you give a patient suffering from migraines?
a) Identify and avoid triggers
b) Headache Diary!!!
c) Instruct on how to take medication and management of an acute attack
d) Advice on relaxation and stress management
Give 5 examples of triggers for migraines
When is prophylactic management of migraines indicated?
What is the medical management to prevent (prophylaxis of) migraines
Considered only if 4+ attacks/month of if very severe (reduces attacks by 50%)
1st line - Propanalol or Topiramate
2nd line - Gabapentin or Accupuncture (10 sessions over 5-8 weeks
3rd line - Referral for Botulinum A toxin injection if 3 drugs did not work
Other: Riboflavin
What is the full management plan for a patient presenting with new episodic migraines who says it is affecting her ability to work in her job as a manager in retail. She has 5 attacks every month.
1) Advice:
a) Identify and avoid triggers
b) Headache Diary!!!
c) Instruct on how to take medication and management of an acute attack
d) Advice on relaxation and stress management
2) Acute attack medications:
a) Triptan (Sumatriptan)
b) NSAID/Paracetamol
c) Antiemetic (metoclopramide)
3) Prophylaxis (4+)
1st line - Propanalol or Topiramate
(2nd line - Gabapentin or Accupuncture (10 sessions over 5-8 weeks
3rd line - Referral for Botulinum A toxin injection if 3 drugs did not work
Other: Riboflavin)
What presentation would make you suspect a menstrual migraine
How is it managed?
Suspect if it occurs 2 days before to 3 days after starting period in 2/3 consecutive months (headache diary always helps)
Triptan on days that it is expected
50% of those with migraine also have tension headaches. What is the typical presentation of a tension-type headache?
What is meant by episodic vs chronic tension-type headaches?
How are they managed?
Acutely
Chronic
Bilateral, pressing/tightening pain of mild/moderate intensity - similar to a band around the head
Not associated with vomiting
Does not prohibit daily/physical activities
Caused by stress, anxiety, or structural abnormalities in the head or neck
Episodic <15d/month or <180d/y
Chronic >15d/month or >180d/y
Acute: Simple analgesia (NSAIDs, paracetamol)
Chronic:
Physiotherapy for structural abnormalities
Relaxation, massage, yoga for stress-induced
Counselling for anxiety
Prophylaxis with Acupuncture (10 sessions over 5-8 weeks)
What is the typical presentation and features of cluster headaches
Differentiate between episodic and chronic cluster headaches
Patients presenting with cluster headaches need to be referred for neuroimaging (MRI) (A)
How are acute cluster headaches managed?
How are chronic cluster headaches managed/prevented?
- extremely painful headaches focused around 1 eye
- associated autonomic symptoms on that side including ptosis, miosis, red, watery eye, runny blocked nose and forehead sweating.
- It is predictable and always occurs after falling asleep and after drinking alcohol. The headaches last 15minutes to 3 hours. They occur once daily (can occur as little as once weekly).
Episodic: Remissions of >1 month
Chronic: Remissions of <1 month in a 12-month period
Acute: 100% oxygen (>12L/min) + 5HT1 (Sumatriptan)
Prophylaxis: Verapamil (non-dihydro) if attacks are frequent
Persistent headache in patients excessively using analgesics for >3 months is called?
How is it managed?
Medication-overuse headache
Management is education and abruptly stopping analgesics for at least 1 week, Noting that it will be worth for the first week before getting better
Give 3 differentials for facial pain
How could this pain be managed?
Trigeminal neuralgia
Dental disorders
Sinusitis
Post-herpetic neuralgia
NSAIDs/Paracetamol escalated to TCAs (amitriptyline) and then if needed
Trigeminal neuralgia is associated with MS. Describe the presentation of trigeminal neuralgia.
What branches are most affected?
What is the management?
Unilateral!! intense stabbing/burning/electric-shock-type pain lasting seconds to minutes in CN-V distribution with no sx in between eisodes. They may be very frequent from 100s/day to years of remission
Mandibular/maxillary > opthalmic
Management: Carbamazepine, Oxcarbazepine, Neurology referral
Define stroke
Focal global disturbance of cerebral functioning lasting >24 hours
What are the causes of stroke?
1) Ischemic = Atherosclerotic occlusion or embolism => A.fib MI, Prosthetic valve, VTE risk, carotid stenosis (anything in Qrisk)
2) Haemorrhagic = Aneurysms, HTN, subarachnoid haemorrhage, Trauma, carotid artery dissection
What are the RFs for Stroke?
Age
HTN
Dyslipidaemia
!!A.fib
Previous TIA/stroke/MI
Smoking
Alcohol
Obesity
low physical activity
Poor diet
What is the presentation of Stroke?
FAST - Facial palsy, Hemiparesis, slurred speech
+
ACA - Upper limb weakness
MCA - Hemiparesis, Hemianaesthesia, Aplasia (dominant hemisphere)
PCA - Homonymous Hemianopia
PICA - Lateral medullary syndrome
+
Urinary incontinence
What is the management of stroke from a GP POV?
Emergency ambulance, admission for thrombolysis therapy
What is the management of stroke in secondary care?
Emergency admission with ABCDE, NPO, 2xlarge bore cannulas, group and hold 4 units, take bloods, exclude hyperglycemia
Non-contract CT brain -> rule out haemorrhage (CI for thrombolysis and CT angio) -> CT angiogram (locate insult/obstruction for thrombectomy)
IV thrombolysis (<4.5hrs): IV alteplase (tPA) 0.9mg/kg up to 90, delivered 10% bolus and 90% over 1 hour.
If major vessel occlusion is present on CT angio => Thrombectomy (<12 hours)
What supports can a GP offer in patients after theyve had a stroke?
1) Occupational therapy -> Aids
2) Social work -> Benefits
3) Speech and language therapy
4) Physiotherapy
5) Counselling (very high rates of depression)
Define TIA
Transischaemic attack
Focal global disturbance of cerebral functioning lasting >24 hours
Patients with TIA have a 20% risk of stroke in the following month with the highest risk in 24 hours. What is your treatment approach to TIAs?
If the patient has ongoing symptoms => Admit as stroke
If the patient does not, commence secondary prevention via Aspirin 300mg STAT + urgent referral to specialised neurovascular clinic
What is Amaurosis Fugax?
Form of TIA with emboli passing through retina presenting as “curtain-like” transient loss of vision.
Managed as TIA obviously + referral to opthalmology
SAH causes spontaneous bleeding into the subarachnoid space causing increased IP => pressure on other vessels => stroke. What are the 2 most common specific etiologies for SAH and what are the causes of SAH?
70% are due to a ruptured congenital berry aneurysm
15% AV malformation
Causes:
Traumatic
Non-traumatic:
Aneurysm (85%)
Extension of Intraparenchymal or intraventricular hemorrhage (10%)
AV malformations (venous sinus thrombosis, Vasculopathy
APS/SLE (RF)
Where do Berry Aneurysms typically occur?
ACA, PCA, Bifurcation of internal carotid and middle cerebral artery (In that order)
These are the most common locations for a SAH
What RF are associated with aneurysm formation (applies to AAA as well)
1) Polycystic kidney disease (ADPKD)
2) Atherosclerosis
3) Ehler Danlos syndrome + Marfan’s
4) HTN
5) Smoking
How does SAH present?
Thunderclap headache: Worst headache of my life => Sudden extreme headache
+/- Vomitting, collapse, LOC, Seizures, Hemiparesis
Neck stiffness after 6 hours (so not on presentation)
What is the management of SAH? (inclue secondary care briefly)
Referral to ED
ABCDE
Non-contrast CT brain -> CT angiogram
Definitive management by interventional radiology
a) Aneurysm coiling
b) Neurosurgical clipping
Epidural haemorrhage is between the dura and bone of skull. Subdural haemorrhage is due to bleeding from bridging veins (shown on CT) resulting in accumulation of blood between the dura and arachnoid. What is the most likely cause of these haemorrhages.
Give 4 RF
Trauma
RF:
1) Age
2) Alcohol
3) Prone to fall (Benzos, poor vision)
4) Epilepsy
5) Anticoag therapy
6) HTN
Give signs of raised ICP
Vomiting, seizures, headaches, sleepiness (Somnolence), neurological signs (hemiparesis, weakness)
How would subdural and epidural haemorrhages present?
Insidious onset GCS after a head injury that produced no LOC +/- physical/intellectual slowing.
+ Sx of raised ICP => Vomiting, seizures, headaches, sleepiness (Somnolence), neurological signs (hemiparesis, weakness)
What is the management of subdural and epidural haemorrhages
Refer to ED for early emergency craniotomy
What does the primary prevention of stroke involve?
For all => Lifestyle measures
1) Healthy diet (mediterranean)
2) Exercise
3) reduce alcohol intake
4) Smoking cessation
+/-
Statin therapy (hyperlipidemia, Qrisk >10%)
ACE/ARBs or CCB/Thiazide-like (if HTN)
Anticoagulation (controversial)
What does the secondary prevention of stroke entail
Lifestyle measures
1) Healthy diet (mediterranean)
2) Exercise
3) reduce alcohol intake
4) Smoking cessation
+
Statin therapy
ACE/ARBs or CCB/Thiazide-like
Anticoagulation (CHADSS Vasc) Or Antiplatelet therapy
What is the medication and dose of antiplatelet therapy in 2ndary prevention of stroke
Clopidogrel 175mg (not 75)
What anticoagulation therapies are available for secondary prevention of stroke
DOAC: Edoxaban
LMWH: Enoxaparin
Anti-Vit K: Warfarin
A patient presents with a stroke at age 45. 50% of strokes occur >70yo. What is the likely etiology behind this and how would you investigate?
APS, SLE
LAC - Lupus anticoagulant
aCL - Anticardiolipin
What are 5 features of parkinsonism
1) Resting tremor “Pill-rolling” in nature
2) Rigidity “Lead Pipe Rigidity” and “Cog-wheel rigidity”
3) Shuffling gate
4) Mask-like expression on face (less blinking, less fidgeting)
5) Difficulty initiating movement
6) Micrographia (small handwriting)
How is lead pipe rigidity demonstrated in Parkinsons?
Limbs resist extension
How is Cogwheel rigidity demonstrated in parkinsons?
Juddering on passive extension/pronation/supination of forearm
What is shuffling gate?
Small steps
What are the causes of Parkinsonism?
Parkinson’s Disease
Drugs: Haloperidol, metoclopramide
Alzheimer’s disease
Trauma
Normal-pressure hydrocephalus
What is Steel-Richardson Syndrome?
Parkinsonism
Dementia
Absent vertical gaze
1st generation antipsychotics such as haloperidol can cause Parkinsonism. If a schizophrenic is on haloperidol and develops parkinsonism, how will you manage
Do not stop medication. Either
1) Give Anticholinergic such as procyclidine
2) Consider a 2nd gen antipsychotic but specialist advice necessary (so option 1 is best in the mean time anyways)
What is Parkinson’s disease? (definition must include pathophysiology)
It is an incurable, progressive, degenerative disease affecting dopaminergic neurons of the Substantia Nigra in the brainstem leading to dopmanine deficiency and hence excess acetylcholine (=> why anticholinergics counter parkinsonism)
How does Parkinson’s disease present? Give 10 and youre good
Parkinsonism =>
1) Resting tremor “Pill-rolling” in nature
2) Rigidity “Lead Pipe Rigidity” and “Cog-wheel rigidity”
3) Shuffling gate
4) Mask-like expression on face (less blinking, less fidgeting)
5) Difficulty initiating movement
6) Micrographia (small handwriting)
+ Non-motor symptoms:
A) Neuropsychiatric: Apathy, anxiety, depression, visual hallucination, dementia, pain, olfactory disturbance
B) Sleep: Excessive somnolence (daytime sleepiness), restless legs (give magnesium)
C) Autonomic: Postural hypotension, Drooling, Hyperhidrosis, Urinary dysfunction, Dysphagia, weight loss
Why do patients with parkinson’s have dysphagia?
Reduced peristalsis
What is hyperhidrosis?
opposite of anhidrosis due to excess acetylcholine
give an example of dopamine receptor agonist. Where is this used?
Bromocroptine for Parkinson’s disease (a/w pulmonary, retroperitoneal, and pericardial fibrosis - X-ray typically done before)
What is the surgical management of Parkinson’s Disease?
Deep brain stimulation
How is Parkinson’s disease managed?
Refer all patients for MDT rehabilitation (all the same roles, social, occupational, physio, neurology…)
Medical:
1) Dopamine Receptor agonist: Bromocriptine
2) Levodopa + Carbidopa
3) Levodopa + Carbidopa + Bromocriptine
4) Levodopa + Carbidopa + Selegiline (MAOI)
Surgical: Deep brain stimulation
What is the role of Carbidopa in the management of parkinson’s disease?
Used to prevent peripheral breakdown of Levodopa => focuses on the brain
