Neurology Flashcards
sensory neuropathy think
alcoholism, b12/folate, CKD, malignancy, DM, vascular disease, drugs
ask about chemo
motor neuropathy think
CBS, charcot marie tooth
if pt has ioniazid neuropathy what do you treat them with?
pyridoxine
how to distinguish between a medical or surgical cause 3rd nerve palsy?
surgical (tumours and anyeursms) affect pupil and can cause pain
medical dont
think of it like a two tubed straw, parasympathetic is on outside and surgical is a knife going - it has to slice the outer tube.
fourth nerve palsy commonly caused by
trauma or MS
6th nerve palsy commonly caused by
raised ICP, MS
not that good at localising
painful horners syndrome?
carotid artery dissection
facial nerve palsy
UMN - stroke or MS
LMN - bells
how do we distinguish?
UMN spares forehead
is forehead sparing concerning?
yes
you have ?7th nerve palsy without forehead sparing, what should you examine?
look on ear for painful vesicles to rule in or out ramsay hunt
LMN DD?
bells
ramsay hunt
infections - lyme
immune - sarcoid, GBS
local malignancy
lesion of 5, 7 and 8 nerve what tumour is likely?
cerebellopontine angle
what can you ask a pt to do to distinguish between ET and Parkinsonism?
get them to write
mx for absence seizures?
ethosuximide
impact of chronic alcohol use for someone with epilepsy?
if they are taking sodium valporate
CHRONIC alcohol use is an enzyme inducer
carbamezapine, gapabentin and phenytoin are better for what sort of seizures?
focal (inc secondary generalised) seizures
carbamezapine may make what sort of seizures wrong?
myoclonic
pt in status epilepticus what do you use to secure the airway?
airway adjuncts - guedel
status epilepticus mx
lorry lorry phnny call ITU
ABCDE
lorzaepam 4mg IV
furhter dose
phenytoin infusion
GA
Mixed UMN and LMN signs is usually caused by
MND
friedrichs ataxia
tabes dorsalis
cervical sponylopathy
syringomyelia
What are the tone, reflex, and key features of UMN lesions?
↑ tone (spastic), ↑ reflexes, Babinski +ve (upgoing)
What are the tone, reflex, and key features of LMN lesions?
↓ tone (flaccid), ↓/absent reflexes, fasciculations
What anatomical areas do UMN lesions involve?
CNS – brain, brainstem, spinal cord
What anatomical areas do LMN lesions involve?
PNS – cauda equina, motor nerve, nerve root, anterior horn cell, NMJ
Where does the lateral corticospinal tract decussate?
Medullary pyramids (90%)
Where does the anterior corticospinal tract decussate?
Spinal cord level (10%)
What motor signs occur if lesion is above vs below medulla?
Above medulla = contralateral signs; Below = ipsilateral signs
What signs are seen in a brainstem lesion?
Ipsilateral CN signs + contralateral limb signs
What signs are seen in a cortical (hemispheric) lesion?
Contralateral CN signs + contralateral limb signs
What does the dorsal column carry and where does it decussate?
Vibration, proprioception, fine touch; decussates in medulla
What does the spinothalamic tract carry and where does it decussate?
Pain and temperature; decussates at spinal cord level
What sensory loss pattern is seen in a hemicord lesion?
Ipsilateral vibration/proprioception loss + contralateral pain/temp loss
What does unsteadiness with eyes open on Romberg’s suggest?
Cerebellar ataxia
What does unsteadiness only when eyes are closed suggest?
Sensory ataxia
What does combined motor and sensory loss suggest?
Either spinal cord lesion (UMN) or peripheral neuropathy (LMN)
What are key features of peripheral neuropathy?
LMN signs (↓ reflexes, hypotonia, fasciculations), glove & stocking sensory loss
What are key features of spinal cord lesions?
UMN signs, sensory/motor loss below level, autonomic loss (e.g. bladder/bowel)
What signs indicate cervical cord lesion?
Arms + legs affected, UMN signs, autonomic symptoms
What signs indicate thoracic cord lesion?
Legs only affected, UMN signs
What signs indicate lumbosacral cord lesion?
Legs only, LMN signs (e.g. cauda equina)
What condition shows less dense cord involvement?
Transverse myelitis
What does dermatomal sensory loss suggest?
Nerve root lesion (radiculopathy)
Which cranial nerves arise in the midbrain?
CN III (oculomotor), CN IV (trochlear)
What signs suggest a midbrain lesion?
Ocular symptoms – eye movement, pupil dilation, ptosis
Which cranial nerves arise in the pons?
CN V–VIII (trigeminal, abducens, facial, vestibulocochlear)
What signs suggest a pontine lesion?
Facial symptoms – sensory or motor
Which cranial nerves arise in the medulla?
CN IX–XII
What signs suggest a medullary lesion (bulbar syndrome)?
Tongue weakness (deviates to lesion), dysphagia, dysarthria
How does CN VII lesion differ in UMN vs LMN?
UMN = forehead spared; LMN = whole face affected
What is the normal CSF opening pressure?
< 20 cm H₂O
What is the normal CSF white cell count (WCC)?
< 5 WBC
What is the normal red blood cell count (RBC) in CSF?
Nil
What is the normal CSF protein level?
< 0.45 g/L
What is the normal CSF glucose level?
~⅔ of plasma glucose
What is the typical CSF finding in Guillain-Barré Syndrome (GBS)?
↑ protein, otherwise normal
What is the typical CSF finding in Multiple Sclerosis (MS)?
Oligoclonal bands present
What are the CSF findings in Subarachnoid Haemorrhage (SAH)?
↑ RBC, xanthochromia
What are the CSF findings in cancer?
↑ WCC, ↑ protein, ↓ glucose
What is the appearance of CSF in bacterial meningitis?
Cloudy
What is the opening pressure in bacterial meningitis?
↑↑
What happens to CSF glucose in bacterial meningitis?
↓↓ (<½ plasma glucose)
What happens to CSF protein in bacterial meningitis?
↑↑
What type of cells are seen in CSF in bacterial meningitis?
↑↑↑ neutrophils
What is the appearance of CSF in viral meningitis?
Clear or cloudy
What is the opening pressure in viral meningitis?
Normal or ↑
What happens to CSF glucose in viral meningitis?
Normal or ↓
What happens to CSF protein in viral meningitis?
Normal or ↑
What type of cells are seen in CSF in viral meningitis?
Lymphocytes
What is the appearance of CSF in fungal meningitis?
Cloudy
What is the opening pressure in fungal meningitis?
↑↑
What happens to CSF glucose in fungal meningitis?
↓↓
What happens to CSF protein in fungal meningitis?
↑↑
What type of cells are seen in CSF in fungal meningitis?
Lymphocytes
What is the appearance of CSF in TB meningitis?
Clear or cloudy
What is the opening pressure in TB meningitis?
↑↑
What happens to CSF glucose in TB meningitis?
↓↓↓
What happens to CSF protein in TB meningitis?
↑↑↑
What type of cells are seen in CSF in TB meningitis?
Lymphocytes
What is a migraine?
A common primary headache disorder with severe, recurrent attacks, more common in women.
What are the diagnostic criteria for migraine (without aura)?
≥5 attacks lasting 4–72 hrs, with ≥2: unilateral
throbbing
moderate/severe
worsened by routine activity.
Plus ≥1: nausea/vomiting or photophobia/phonophobia.
What are common migraine triggers?
Caffeine, stress, poor sleep, skipping meals, cheese, chocolate, alcohol (esp. red wine), bright lights, menstruation, COCP.
What are key presenting features of a migraine?
Severe, unilateral throbbing headache
-nausea/vomiting
-photophobia
-phonophobia, aura
-worsened by movement, relieved by quiet/dark.
What is an aura?
A progressive visual disturbance 5–60 min before headache onset.
What are common associated symptoms on migraine examination?
-Nausea
-vomiting
-photophobia
-phonophobia
-mechanophobia.
When should further investigations be considered in a mirgraine?
Presence of red flags: immunocompromised, cancer Hx, thunderclap headache, new neuro deficit, cognitive dysfunction, LOC, cough/sneeze/valsalva-triggered headache, posture-related change, personality change, recent trauma.
What lifestyle advice is recommended for a migraine ?
Avoid triggers (caffeine, alcohol, missed meals)
maintain hydration
exercise regularly
sleep hygiene.
What is first-line acute treatment for migraines?
Triptan + paracetamol or triptan + NSAID.
What is second-line acute treatment for migraines?
Add antiemetic (metoclopramide or prochlorperazine), switch painkiller (e.g. aspirin).
What is medication-overuse headache?
Headache caused by regular analgesic use — important to screen for in migraine patients.
When is migraine prophylaxis indicated?
≥2 disabling attacks/month.
What are first-line prophylactic options for migraine?
Propranolol (preferred in women), topiramate, or amitriptyline.
What are important considerations for prophylactic agents for migraine ?
Avoid propranolol in asthma/COPD.
Use propranolol in childbearing women or if Hx of renal stones.
Amitriptyline can cause sedation — advise caution with driving/machinery.
What are second-line options for prophylaxis for migraine?
Acupuncture and riboflavin (vitamin B2).
What is a cluster headache?
A headache characterized by intense, sharp pain around one eye, occurring in episodic clusters (several weeks), followed by pain-free periods, typically one cluster per year.
What are the risk factors for cluster headaches?
Male gender, alcohol use.
What are the key features of a cluster headache?
Severe, unilateral, stabbing pain around one eye; triggered by alcohol and sleep.
What are the associated symptoms during a cluster headache attack?
Lacrimation, nasal stuffiness, restlessness, miosis/ptosis.
How long do cluster headache episodes last?
Each episode lasts 15-120 minutes, occurring 2-3 times a day for several weeks or months, followed by pain-free months.
What is seen on examination in cluster headache?
Lacrimation, restlessness/agitation, nasal stuffiness.
What investigations should be done for a cluster headache?
MRI with gadolinium contrast to rule out lesions.
What is the acute treatment for cluster headaches?
100% oxygen therapy + subcutaneous triptan.
What is the prophylactic treatment for cluster headaches?
Verapamil.
When should a patient with cluster headaches be referred?
Referral to neurology for further management.
What is a tension-type headache?
The most common type of episodic recurrent headache.
What are the key features of a tension-type headache?
Bilateral, dull tightness (feels like a tight band or pressure) around the forehead, with low intensity compared to migraines.
What are the associated symptoms of a tension-type headache?
No association with nausea/vomiting (N/V) or aura.
What is the acute treatment for tension-type headaches?
Aspirin, paracetamol, NSAIDs.
What is the prophylactic treatment for tension-type headaches?
Acupuncture.
What is trigeminal neuralgia?
A pain syndrome characterized by severe unilateral pain along the trigeminal nerve (CN V).
What is the pathophysiology of trigeminal neuralgia?
It is usually idiopathic but can also be caused by compression of CN V.
What are the red flags for trigeminal neuralgia?
Onset age < 40, sensory changes in the face
auditory changes
optic neuritis
family history of multiple sclerosis (MS).
What are the key clinical features of trigeminal neuralgia?
Severe unilateral shooting pains along the face, triggered by light touch (e.g., smoking, shaving, washing face, talking, brushing teeth, chewing).
Pain is abrupt and lasts for minutes.
What is the first-line treatment for trigeminal neuralgia?
Carbamazepine.
When should a patient with trigeminal neuralgia be referred to neurology?
If they fail to respond to treatment and/or have red flags, they should be urgently referred to neurology.
What is idiopathic intracranial hypertension (IIH)?
A condition where intracranial pressure (ICP) is raised without an obvious increase in volume.
It is most common in young, obese females.
What are the risk factors for idiopathic intracranial hypertension?
Female gender
obesity
pregnancy
medication (e.g., tetracyclines, COCP, steroids, lithium).
What are the common clinical features of idiopathic intracranial hypertension?
Headache and blurred vision are most common.
What signs may be seen on examination in idiopathic intracranial hypertension?
Papilloedema
Cushing’s triad (↓ HR, wide pulse pressure, irregular breathing)
↑ blind spot, and 6th nerve palsy (unable to abduct eye).
What is the differential diagnosis for idiopathic intracranial hypertension?
Brain tumours
Hydrocephalus
encephalitis
intracranial bleeds (e.g., SAH, subdural, extradural).
What investigations should be done to diagnose idiopathic intracranial hypertension?
CT/MRI brain to rule out space-occupying lesions.
What is the management of idiopathic intracranial hypertension?
-Weight loss
-acetazolamide (carbonic anhydrase inhibitor to reduce CSF production)
- possibly topiramate, and surgery (e.g., lumbar puncture/VP shunt, optic nerve decompression).
What is a seizure disorder?
A neurological disorder characterized by recurrent episodes of sensory disturbances
- TLOC
- convulsions (fits or faints)
- caused by abnormal electrical activity in the brain.
How are seizures differentiated from syncope and psychogenic non-epileptic seizures (PNES)?
Seizures have a longer duration (2-5 mins), rhythmic limb jerking, and post-ictal confusion.
Syncope is brief (<1 min) with pale skin and quick recovery. PNES have gradual onset, pelvic thrusting, and elevated prolactin levels.
What are the causes of seizures?
Epilepsy (no medical cause)
vascular causes (TIA, stroke)
toxic causes (withdrawal seizures)
structural causes (brain tumours
brain bleeds)
infectious causes (meningitis, encephalitis) metabolic causes (hypoxia, hypoglycaemia electrolyte disturbances)
febrile convulsions in children.
How are seizures classified?
Seizures are classified as focal (unilateral) or generalized (bilateral).
What are the types of focal seizures?
Focal seizures can be aware (with auras but preserved awareness) or unaware (loss of awareness with random movements/noises).
Focal seizures can spread to become bilateral (focal to bilateral).
What are the types of generalized seizures?
- Tonic-clonic (grand mal)
- absence (petit mal)
- myoclonic seizures.
What are the clinical features of seizures?
- Fits (seizures)
- faints (TLOC)
- blank stares
- sensory auras (smells, tingling, visual changes)
- post-ictal confusion or lethargy
What are the signs during a seizure?
- Tongue biting
- cyanosis
- epileptic cry
- salivary frothing
- Localizing signs include automatisms (lip smacking, grabbing) in temporal lobe seizures and jerky movements in frontal lobe seizures.
What investigations should be done for seizures?
Acute: FBC, CRP, U&E, glucose, ECG.
First-fit clinic: EEG, MRI brain to classify type and identify structural causes.
What is the acute treatment for seizures?
Benzodiazepines (e.g., IV lorazepam) if seizure lasts >5-10 mins.
If no venous access, use PR diazepam or buccal midazolam.
If refractory, use IV Kepra (Levetiracetam), phenytoin, or phenobarbital.
What is the management after a second seizure?
Unless there is a neuro deficit, structural abnormality, or EEG confirms epilepsy, treatment may involve antiepileptics based on seizure type.
What is the treatment for tonic-clonic seizures?
Males: sodium valproate
Females: lamotrigine or levetiracetam.
What is the treatment for myoclonic seizures?
Males: sodium valproate
Females: levetiracetam.
What is the treatment for focal seizures?
First-line: lamotrigine or levetiracetam;
Second-line: carbamazepine, oxcarbazepine, or zonisamide.
What is the treatment for absence seizures?
First-line: ethosuximide
Second-line: sodium valproate (males), lamotrigine (females).
What is the side effect of lamotrigine?
Lamotrigine can cause a skin rash and mucosal blisters, which may progress to Steven Johnson Syndrome.
What is status epilepticus?
A medical emergency defined as one seizure lasting >5 minutes or two or more seizures within 5 minutes without returning to normal in between.
How is status epilepticus managed?
ABCDE approach
- IV lorazepam, followed by phenytoin or phenobarbital infusion if not resolving.
- If refractory, general anesthesia may be required.
What are the DVLA rules for driving after a seizure?
After the first seizure, no driving for 6 months (12 months if EEG/MRI positive).
For diagnosed epilepsy or multiple unprovoked seizures, driving is allowed after 12 months seizure-free
normal license restored after 5 years without a seizure.
What is syncope?
Syncope is a transient loss of consciousness (TLOC) characterized by rapid onset
brief duration
spontaneous complete recovery
usually due to temporary cerebral hypoperfusion.
What are the types of syncope?
- Vaso-vagal (reflex), triggered by emotional or situational factors.
- Cardiogenic, caused by arrhythmias or structural heart conditions.
- Orthostatic, due to autonomic failure, such as standing up too quickly.
What are the triggers of vaso-vagal syncope?
Emotional triggers (stress, emotion, pain) and situational triggers (coughing, weeing, GI straining).
What are the signs of cardiogenic syncope?
Palpitations, heart skipping a beat, or a racing heart, often associated with arrhythmias or structural heart issues like valvular disease or HOCM.
What are the clinical features of syncope?
TLOC with brief duration (<1 min)
- floppy drop
- brief myoclonic jerks
- spontaneous complete recovery without confusion.
Vaso-vagal syncope is associated with dizziness, nausea, and visual blurring.
Cardiogenic syncope may have palpitations or murmurs.
What should be seen on examination in a patient with syncope?
Pale appearance, possible arrhythmia, or cardiac murmur if cardiogenic cause is suspected.
What investigations should be done for syncope?
Cardiovascular (CV) and neurological exams to rule out cardiac and neurological causes.
ECG (consider 24-hour monitoring for arrhythmias), table tilt test, carotid massage test, and postural BP readings.
How should syncope be managed?
Treat underlying causes.
For cardiogenic syncope, consider interventions like a pacemaker for serious AV block or managing arrhythmias.
What is meningitis?
Inflammation of the meninges (the tissues lining the brain and spinal cord); bacterial meningitis is the most severe form.
How is meningitis classified and what are the main causative agents?
- Viral (self‑limiting): enteroviruses, mumps, HSV.
- Bacterial (30% mortality):
–Neisseria meningitidis, S. pneumoniae
–Listeria monocytogenes in elderly/immunocompromised
–GroupBStrep, E.coli, Listeria in neonates
–Mycobacterium tuberculosis occasionally - Fungal (rare, immunocompromised): e.g. Cryptococcus spp.
What are the classic presenting symptoms of meningitis?
Headache, photophobia, nausea and vomiting.
What key signs are found on examination for meningitis?
- Neck stiffness, fever
- purpuric rash (meningococcal septicaemia)
- Kernig’s sign
- Brudzinski’s sign.
What are Kernig’s and Brudzinski’s signs?
Kernig’s: pain/stiffness on straightening a flexed hip and knee.
Brudzinski’s: involuntary knee flexion on passive neck flexion.
What initial investigations are performed for meningitis ?
FBC, CRP, U&Es, lactate, glucose, clotting profile, then lumbar puncture (LP) for CSF analysis (glucose, protein, cell count, appearance, opening pressure), MC&S and viral PCR.
When should a CT head be done before LP?
If there are signs of raised ICP (focal neuro signs, papilloedema, uncontrolled seizures, GCS <12), meningococcal septicaemia rash, hemodynamic instability or bleeding risk.
When is LP contraindicated or delayed?
Contraindications/delays if:
-signs of raised ICP
- unstable hemodynamics
- meningococcal rash
- significant bleeding risk
- need to defer >1h after hospital arrival.
What is the first‑line management of bacterial meningitis for children over 3 months and adults below 50?
ceftriaxone + IV dexamethasone (unless meningococcal septicaemia, immunocompromised or <3months).
What antibiotic prophylaxis is given to close contacts of bacterial meningitis?
Oral ciprofloxacin or rifampicin for anyone exposed in the preceding 7days.
How is viral meningitis managed?
Supportive care; LP results awaited may receive empirical ceftriaxone until bacterial infection is excluded; specific antivirals (e.g. aciclovir) only if HSV suspected.
What is the most common complication of meningitis?
Sensorineural hearing loss; test with Rinne’s (normal) and Weber’s (lateralizes to the unaffected ear).
What is the first‑line management of bacterial meningitis for childre under 3 months?
IV cefotaxime+ IV amoxicillin if <3months or >50years
What do you add to 1st line management of bacterial meningitis if listeria suspected?
add gentamicin
What is Guillain‑Barré syndrome (GBS)?
An immune‑mediated inflammatory demyelination of the peripheral nervous system
- most often occurring after an infection and causing an acute, symmetrical peripheral neuropathy.
What is the pathophysiology of GBS?
Autoantibodies attack the myelin sheath of peripheral nerves, interrupting nerve conduction and leading to ascending weakness and sensory loss.
Which pathogen is most commonly associated with GBS onset?
Campylobacterjejuni gastroenteritis.
How is GBS classified?
- AIDP (acute inflammatory demyelinating polyneuropathy) – monophasic, resolves in 3–4 weeks.
- CIDP (chronic inflammatory demyelinating polyneuropathy) – relapsing/remitting over months.
- Miller Fisher syndrome – anti‑GQ1b variant.
What is the Miller Fisher syndrome triad?
Ophthalmoplegia, areflexia, and ataxia.
What are the typical presenting symptoms of GBS?
Progressive, symmetrical, ascending limb weakness and sensory loss
- often with back or leg pain
- history of recent gastrointestinal or respiratory infection
- may progress to cranial nerve and respiratory muscle involvement.
What neurological signs are found on examination?
Decreased or absent deep tendon reflexes in all four limbs.
Which conditions are key differentials for GBS?
- Transverse myelitis – presents with four‑limb weakness plus upper motor neuron signs.
- Polymyositis – muscle weakness without sensory loss.
What cerebrospinal fluid (CSF) findings support GBS?
Albuminocytologic dissociation: normal cell count with elevated protein.
What nerve conduction study findings support GBS?
Reduced motor nerve conduction velocity consistent with demyelination.
What is the first‑line management for GBS?
Intravenous immunoglobulins (IVIG) and/or IV corticosteroids.
What is the next step if a patient does not respond to IV IG or steroids?
Plasma exchange (plasmapheresis).
How should respiratory involvement be monitored?
Regular measurement of forced vital capacity (FVC); a falling FVC indicates need for intensive care support or ventilation.
What is encephalitis?
Inflammation of the brain, most often due to infection.
What is the most common cause of encephalitis?
Herpes simplex virus type1 (HSV‑1) accounts for about 95% of cases.
Which brain regions are typically affected in HSV encephalitis?
The temporal lobes and inferior frontal lobes.
What are the key presenting symptoms of encephalitis?
Fever
- headache
- seizures
- confusion/psychiatric symptoms
- vomiting
What focal neurological signs might be found on examination?
Signs depend on lesion location and may include hemianopia, aphasia, and dysphagia.
What cerebrospinal fluid (CSF) findings are typical?
Elevated protein and lymphocytic pleocytosis (↑ white cell count).
Which pathogens should be tested for by CSF PCR?
- HSV
- varicella‑zoster virus (VZV)
- enteroviruses.
What neuroimaging and other tests are indicated?
MRI of the brain to look for characteristic changes, and EEG if seizures or altered consciousness.
What is the first‑line treatment for suspected viral encephalitis?
Intravenous aciclovir.
What is transverse myelitis?
Inflammation of the spinal cord causing motor weakness
- sensory loss
- autonomic dysfunction below the level of the lesion.
What is the pathophysiology of transverse myelitis?
Inflammatory degeneration of spinal cord tissue with possible axonal loss.
What are common causes of transverse myelitis?
It may be idiopathic, post‑infection or autoimmune, part of systemic/inflammatory CNS diseases, or occur in multiple sclerosis.
What motor symptoms occur in transverse myelitis?
Muscle weakness with upper motor neuron signs (spasticity, brisk reflexes, Babinski positive).
What sensory and autonomic features occur?
Sensory: pain and paresthesia below lesion level. Autonomic: bowel and bladder dysfunction.
Which imaging study is essential for suspected transverse myelitis?
MRI of the spinal cord—to confirm cord inflammation and rule out compressive lesions.
What is the role of lumbar puncture in transverse myelitis?
To demonstrate inflammatory changes in CSF and investigate other causes (e.g., multiple sclerosis).
What is first‑line treatment for transverse myelitis?
Intravenous high‑dose methylprednisolone.
What is the next step if steroids are insufficient?
Plasma exchange (plasmapheresis).
What is the typical prognosis and long‑term risk?
Most patients recover fully; 5–10% go on to develop multiple sclerosis.
child dropping thingss are breakfast is a classic buzz stem for what?
juvenile myoclonic epilepsy
Which cranial nerve is affected if a patient reports loss of smell after head trauma?
CN I – Olfactory (e.g. cribriform plate fracture)
A patient presents with bitemporal hemianopia. Which cranial nerve is involved?
CN II – Optic (think: pituitary adenoma compressing optic chiasm)
Which nerve is affected in optic neuritis with an afferent pupillary defect?
CN II – Optic (common in MS)
A diabetic patient has ptosis but a spared pupil. Which nerve is likely involved?
CN III – Oculomotor (ischaemic palsy)
An aneurysm of the posterior communicating artery may cause a pupil-involving third nerve palsy. What symptoms appear?
‘Down and out’ eye, ptosis, dilated pupil – CN III
A patient has vertical diplopia when looking down and tilts their head away from the lesion. Which nerve is affected?
CN IV – Trochlear
A patient presents with severe stabbing pain in the cheek triggered by light touch. What’s the diagnosis and nerve?
Trigeminal neuralgia (CN V)
Which cranial nerve is responsible for the afferent limb of the corneal reflex?
CN V – Trigeminal
A patient with diplopia on lateral gaze and failure to abduct the eye likely has a palsy of which nerve?
CN VI – Abducens
Which cranial nerve palsy is a classic false localising sign in raised ICP?
CN VI – Abducens
A patient has facial weakness, can’t raise eyebrow, has hyperacusis and taste loss. What nerve is involved?
CN VII – Facial (LMN palsy e.g. Bell’s palsy)
In a stroke, the forehead is spared in facial weakness. What nerve is this, and is it UMN or LMN?
CN VII – Facial, UMN lesion
A patient has tinnitus, imbalance, and gradual hearing loss. What condition and nerve are involved?
Acoustic neuroma – CN VIII – Vestibulocochlear
Which cranial nerve is responsible for loss of gag reflex (afferent limb)?
CN IX – Glossopharyngeal
A patient has dysphagia and hoarseness, and their uvula deviates away from the lesion. Which nerve?
CN X – Vagus
Which nerve is responsible for shoulder droop and weak head turning after neck surgery?
CN XI – Accessory
A patient’s tongue deviates toward the side of the lesion. Which cranial nerve is involved?
CN XII – Hypoglossal
