Neurology Flashcards
What are the components of GCS?
Eye Opening: spontaneous (4), to speech (3), to pain (2), no response (1)
Verbal response: orientated (5), confused (4), inappropriate words (3), incoherent words (2), no response (1)
Motor Response: obeys commands (6), localises pain (5), withdraws from pain (4), flexes to pain (3), extends to pain (2), no response (1).
How is delirium tremens managed?
Chlordiazepoxide for anxiety and seizure prevention, fluids, antiemetics, pabrinex for vitamin B+C deficiency,
What causes delirium tremens? How does it present? When does it onset? Which neurotransmitter is unopposed?
Withdrawal from alcohol causing confusion, hallucinations, sweating, HeTN, seizures, etc.
Usually begins around 72 hours after last drink and peaks 4/5 days after.
Unopposed glutamate activity.
What are the characteristics of normal pressure hydrocephalus? How is it managed?
Wet (incontinence), wacky (dementia), and wobbly (ataxic).
Ventriculo-peritoneal shunt.
Why might you want to hyperventilate someone with an intracranial bleed?
Hyperventilation = reducing CO2 levels,
Less CO2 = vasoconstriction,
Vasoconstriction reduces bleeding and prevents raised ICP.
What is Cushing’s triad? Why is it dangerous?
HeTN, bradycardia, and irregular breathing/apnoea.
Causes cerebral hypoperfusion, which can cause death.
What are the conditions for CT head <1hour?
- GCS <13 1 hour after injury
- GCS <15 2 hours after injury
- suspected skull base fracture or depressed skull fracture
- seizure
- focal neurological deficit (weakness, paralysis, loss of reflexes, etc)
- > 1 episode of vomiting (>3 in children)
What is deficient in Wernicke’s encephalopathy? What are the sx?
thiamine deficiency - confusion, ataxia, and ophthalmoplegia - doesn’t necessarily mean all three will be present.
What develops in someone who has prolonged/untreated Wernicke’s encephalopathy?
Korsakoff’s Syndrome:
Chronic, irreversible retrograde and anterograde amnesia with confabulation due to prolonged thiamine deficiency/Wernicke’s encephalopathy.
What are the symptoms of cauda equina? What invx is needed?
Saddle anaesthesia, loss of bowel/urinary continence, numbness/paraesthesia down legs.
MRI!!!
What are the signs of signs of a cerebellar neoplasia?
What complication might make it present emergently?
DANISH and signs of space occupying lesion:
- headache,
- night sweats,
- raised ICP, etc
Might present with coning (tonsillar herniation syndrome) due to it being a posterior lesion:
- HeTN/BP instability
- cranial nerve palsies
- Decreasing conciousness
- Flaccid paralysis
- N+V, headache, neck stiffness
How does autoimmune encephalitis present? How is this managed? What are the types?
- Confusion/reduced conciousness/cognitive impairement
- Behavioural changes/emotional lability/psychosis,
- Seizures,
- Movement disorders,
Mx: methylprednisolone (steroids), IV Ig
Types: - Anti-NMDA encephalitis
- Hashimoto’s.
A pt presenting with abnormal sensation and paralysis which started in the feet and has moved more proximal on a background of gastroenteritis is what?
Guillain-Barre (associated with campylobacter).
How do you investigate for/montior GBS? How do you manage Guillain-Barre?
Inx- isolated, raised CSF protein (>5.5), nerve conduction studies, monitor FVC (effect on respiratory system)
Mx: IV Ig and plasmapheresis - monitor FVC to know affect on respiratory system.
Which nerve is affected in Bell’s palsy? How does it present? How is it managed?
LMN CN VII (facial).
- Unilateral facial paralysis: ptosis, facial droop which including forehead
- Taste bud impairment,
- Excessive tearing (epiphroa) OR dry eyes.
Mx - oral pred and artificial tears.
Keratcoconjunctivitis Sicca is a complication of what palsy?
Bells’ - dry eyes cause failure of lid to close properly leading damage to the eye - eyedrops prevent this.
What is Trigeminal Neuralgia? How can it be managed?
Severe shooting/stabbing pains in the distribution of the trigeminal nerve divisions. Worsened by touching face, brushing hair and teeth, etc.
Mx - Carbamazepine and refer for MRI if no discernible cause.
Which way does the tongue deviate in a hypoglossal nerve palsy?
Deviation of tongue to side of lesion on protrusion.
What are medical vs surgical causes of CN III palsy? What is the characteristic appearance of the eye?
Medical- vasculopathic ischaemia (e.g., diabetes), these always spare the pupil.
Surgical- compression (e.g., aneurysm, tumour, etc), this always involve the pupil (e.g., anisocoria).
Both show ‘down and out’ appearance of the eye.
What is meralgia paraesthesia?
compression of the lateral cutaneous nerve of the thigh, causing sensitivity to heat and touch, paraesthesia, and numbness.
What are dissociative/psychogenic seizures?
non-epileptic, involuntary movements (e.g., limb/trunk jerking) and behaviours due to psychological distress.
What is 1st line for myoclonic seizures?
Sodium valproate
Temporal lobe seizures are usually preceeded by what? What do the seizures look like?
Preceded by aura, followed by weakness/blankness, automatisms (e.g., lip smacking).
What is a complication of recurrent temporal lobe seizures?
Damage to the hippocampus (memory learning and emotions problems) and mesial temporal lobe (memory,emotion, social behaviour problems).
Most commonly see memory problems.
What do parietal lobe seizures usually look like?
Sensory symptoms (e.g., pins and needles)
What is the difference between a simple and complex febrile seizure?
Simple is <5minutes and singular event,
Complex >5minutes or recurrent in a short space of time.
What causes serotonin syndrome? What are the symptoms?
Results from serotonin increasing drugs such as SSRIs.
- Restlessness,
- Diaphoresis (sweating) and hyperthermia
- Clonus and hypertonia,
- Hyperreflexia.
What is Neuroepileptic malignant syndrome? What is the classic tetrad? What blood result is usually elevated?
Reaction to starting/increasing antipsychotic drugs such as risperidone (most commonly 1st gens), usually within weeks.
Tetrad - hypertonia, hyperthermia, autonomic instability, mental state change.
CK usually elevated - can get muscle necrosis and rhabdomyolysis (and ATN) if severe.
What is 1st line pharmacological agent for ADHD?
Methylphenidate
What are the pharmacological options for Alzheimer’s?
1) Donepezil - cholinesterase inhibitor
2) Memantine - glutamate receptor antagonist
How does fronto-temporal dementia usually present? What investigation is used and what does it show?
Youngish (50s) pts with memory problems, personality changes, and constructional apraxia (inability to complete movesments related to specific complete tasks).
MRI shows atrophy of frontal and temporal lobes.
Wallenberg Syndrome (aka lateral medullary syndrome) is an infarct of what vessel? What does it cause?
Posterior inferior cerebellar artery affecting medulla oblongata…
- Autonomic dysfunction e.g., Ipsilateral Horner’s,
- Vestibulocerebellar sx e.g., vertigo, diplopia, multidirectional nystagmus
- Sensory symptoms: contalateral loss of pain/temp senation
- Bulbar weakness: hoarsness, dysphagia, dyshonia
Lateral pontine syndrome is an infarct where? What does it cause?
Anterior inferior cerebellar artery.
Wallenberg’s sx + involvement of cranial nerve nuclei.
Basilar artery occlusion causes what?
Locked in syndrome (quadriparaesis with sustained consciousness and ocular movements), complete loss of consciousness or death.
What is Weber’s Syndrome?
Medial midbrain stroke:
- Ipsilateral oculomotor palsy (diplopia and ptosis)
- Contralateral hemiparesis.
A total anterior cerebral infarction (TACI) causes what?
- Contralateral homonymous hemianopia,
- Contralateral hemiplegia,
- Higher cognitive dysfunction (hemispatial neglect, dysphagia, etc)
What is a partial anterior cerebral infarction (PACI)?
2 of TACI components or just higher cognitive dysfunction.
What symptoms do you get from a posterior circulation stroke?
DANISH
What is Amaurosis Fugax?
TIA affecting the eye - loss of vision that suddenly returns.
What is a Lacunar Infarct?
Occlusion of a single branch of a large cerebral artery often in basal ganglia, thalamus, or internal capsule.
Sx can be purely motor, purely sensory, sensorimotor, ataxic hemiparesis, dysarthria-clumsy hand syndrome.
What is the underlying pathology of cerebral amyloid angiopathy? What is the most common clinical manifestation and how is it seen on MRI?
Amyloid-beta deposits in the walls of…
- leptomeningeal arteries,
- cortical arteries,
- and cortical capillaries.
Spontaneous lobar intracerebral haemorrhage.
Cortical superficial siderosis and lobar microbleeds on MRI.
What sx are associated with intracranial venous thrombosis? What is seen on CT?
Headache, N+V, and other non-specific sx.
Hyperdensity in affected sinus - contrast shows filling defect (empty delta sign).
What is the most important management of haemorrhagic stroke?
BP control - should be <140 systolic within 1 hour of admission.
What are the symptoms associated with a subdural haematoma?
Vomiting, weakness of one side (if unilateral haemorrhage), variable confusion.
How do you know the difference between acute and chronic subdural haemorrhage?
CT:
Acute - bright white
Chronic - dark
What are the risk factors for a subdural haemorrhage?
Old age, chronic alcohol use, trauma, anticoagulant use.
How do you manage cauda equina?
1) 16 mg dex stat, 8 mg BD thereafter.
2) Surgical decompression.
Devic’s Disease (neuromyelitis optica) is characterised by inflammation where? What antibodies is it associated with?
Transverse myelitis (inflammation of the spinal cord), and optic myelits (inflammation of the optic nerve).
+ve NMO-IgG antibodies (against aquaporin 4).
What is Miller-Fisher Syndrome? What antibodies are associated? What is the sx?
Rare form of Guillain-Barre that starts proximally such as at the eyes instead of distally.
Associated with GQ1B antibodies.
Weakness, ataxia, areflexia, opthalmoplegia.
Autoimmune encephalitis can be put into what two categories? How does it present?
Anti-NMDA or Hashimoto’s encephalitis.
Seizures, confusion, movement disorders, behavioural change, cognitive impairment.
What do you get on CSF analysis of autoimmune encephalitis? How is it manged?
CSF shows raised lymphocytes.
Mx - steroids and IV Ig 1st line, immunosuppressants may be considered 2nd line.
What are the symptoms of myasthenia gravis? What time of day are they worse? Wht improves symptoms? What antibodies are associated? What is the management?
- Ptosis and double vision,
- Dysarthria/bulbar muscle weakness (hoarsness, dysphonia),
- skeletal weakness,
Sx often worse at the end of the day but improves with rest.
80% have anti-AchR, can also be associated with muscle specific tyrosine kinase abs.
Mx - steroids, anticholinesterases such as pyridostigmine, and possibly IV Ig acutely.
What is the underlying pathology of MS?
Autoimmune disease of the CNS, demyelination and axonal loss of neurons.
What are the clinical manifestations of MS?
- Optic neuritis: blurred/loss of coloured vision
- Internuclear ophthalmoplegia: failure of ipsilateral abduction and contralateral nystagmus (lesion at the medial longitudinal fasciculus)
- Marcus-Gunn pupil: swinging torch elicits bilateral pupil dilation
- Sensory disease
- Cerebellar ataxia
- Spastic paraparesis (weak/stiff legs)
How do you diagnose MS? How is it managed?
Clinical examination, MRI (white matter lesions), CSF analyses (oligoclonal bands).
Mx - acute attacks with steroids, plasma exchange may also be used.
Beta-interferon may be used for relapsing-remitting MS.
Modafinil and amantadine may be used to manage fatigue sx.
How does bacterial/viral encephalitis present? How is it manged?
Fever, change in mental state, flu-like sx, seizures, and temporal lobe involvement in the case of HSV encephalitis.
Mx - ceftriaxone and acyclovir.
What are Kernig and Brudzinski signs?
Kernig - pain on knee extension
Brudzinski - pain on neck flexion
How do viral and bacterial meningitis show on CSF?
Viral: clear appearance, increased protein, normal glucose, predominantly lymphocytes.
Bacterial: turbid appearance, increased protein, decreased glucose, predominantly leukocytes.
How do you manage cryptococcal meningitis? How do you identify it?
- 2 weeks IV amphotericin B and oral flucytosine. Followed by 8 weeks oral fluconazole and then long term maintenance therapy with low dose fluconazole.
- Immunocompromised pts, subacute onset, raised opening pressure on LP (poor prognostic sign).
How is bacterial and viral meningitis managed?
Bacterial: in primary care IM ben-pen, secondary care IV ceftriaxone with added amoxicillin for listeria cover in age extremeties.
Viral: acyclovir
What is waterhouse-friderichsen syndrome?
Meningococcal sepsis - DIC - bleeding into adrenal glands - adrenal failure.
Very poor prognosis.
Hypotension, altered mental status, multi-organ dysfunction.
What causes a pseudobulbar palsy?
Demyelination of corticobulbar and white matter tracts (UMN lesion) affecting muscles of speech and swallowing.
Relapsing and remitting disease pattern.
What deficiency causes subacute combined degeneration of the spinal cord? How would it present?
B12 deficiency causing demyelination of lateral and posterior columns (dorsal and corticospinal)…
- Clumsiness/unsteady gait/falls
- Brisk reflexes
- Decreased vibration and proprioception sense
- Decreased vision
- Cognition and memory problems
- Depression
- Sleepiness
What is the triad of Parkinson’s? What is the underlying pathology?
Bradykinesia, rigidity, intention tremor.
Death of neurones of substantia nigra.
What pharmacological agent is primarily used in Parkinson’s? What are the SEs?
Levadopa…
SEs - N+V, postural hypotension, hallucinations, dyskinesia, confusion, psychosis.
What are the hallmarks of PSPS (progressive supranuclear palsy)?
Intention tremor, hypertonia (rigidity), bradykinesia, and VERTICAL GAZE PALSY.
This is a parkinson’s plus syndrome.
ALS (amyotrophic lateral sclerosis) is what type of disease?
It is the most common form of motor neurone disease.
What mutation causes familial ALS?
SOD1 mutation
What are the sx of ALS?
UMN - hyperreflexia and increased tone
LMN - fasciculations and muscle atrophy
Myotonic dystrophy is caused by inheritance pattern? What channels are affected?
Autosomal dominant trinucleotide repeat disorder causing dysfunction of muscle specific chloride channels.
What are the features of myotonic dystrophy?
Face: frontal balding, catarcats, bilateral ptosis, long, thin face.
Speech: dysarthria
Neck: STCLM wasting
Hands: percussion myotonia, distal wasting, slow relaxing grip
Internal: metabolic syndromes and insulin intolerance, testicular atrophy, cardiomyopathy/cardioarrhythmias
What is Charcot-Marie Tooth Disease? When/how does it present?
Hereditary motor and sensory peripheral neuropathy.
Often presents in puberty in feet and slowly progresses to upper limbs.
How can we diagnose Charcot-Marie Tooth Disease? What are some signs?
Nerve conduction studies (velocity reduced in type 1), clinical examination, and genetic testing.
Signs..
- Enlargement and thickening of nerves
- Symmetrical muscular atrophy causing ‘champagne bottle’ legs and claw hand.
- Pes cavus (high-arched feet)
What is the inheritance of Huntington’s disease?
Autosomal dominant - CAG trinucleotide repeat with anticipation through spermatogenesis.
What are the characteristics of Huntington’s? What do you see on MRI? What is the prognosis?
Choreoathetosis (unpredictable, writhing movements) and dementia.
MRI - atrophy of caudate nucleus and putamen.
Death within 10 years of sx onset.
Where is the lesion in cerebral palsy?
UMN lesion in pyramidal tracts.
A unilateral sudden onset extreme pain often around the eye, occurring alongside watery eyes is what type of headache?
Cluster headache
What is the Mx for cluster headaches?
Prophylaxis: verapamil
Acute attacks: 100% O2/sumitriptan.
A unilateral headache, associated with photophobia, often preceded with aura is what? Mx?
Migraine - propranolol prophylactically, acute mx with triptans.
Who is CI to triptans e.g., sumatriptan?
HeTN, previous stroke, angina, PVD
What symptoms might be associated with basilar migraine? Mx?
Vertigo, diplopia, dysarthria, tinnitus, bilateral visual sx, and bilateral paraesthesia.
Mx - simple analgesics (NSAIDs, paracetamol).
What is Gerstmann Syndrome? Where is the lesion?
Finger agnosia, acalculia, agraphia, R/L discrimination disorder.
Lesion in the dominant angular gyrus (posterior inferior parietal lobe).
What are the characteristics of Brown-Sequard syndrome?
Hemi-lesion of the spinal cord…
- ipsilateral paralysis, hyperreflexia, loss of vibration/position sense
- Contralateral loss of pain/temperature sense
A lesion in wernicke’s area causes what?
language comprehension disorder
A lesion in Broca’s area causes what?
Problems with speech production.
What is Todd’s paresis?
Weakness following a seizure.
What are examples of autonomic dysfunction someone with Parkinson’s may experience?
Changes in bowel habit, ED, sleep disturbance, low mood.
Ankle, knee, bicep, and tricep reflexes come from whish nerve roots?
S1 and 2 = ankle (buckle my shoes)
L3 and 4 = knee jerk (kick down the door)
C5 and 6 = bicep (pick up the sticks)
C7 and 8 = tricep (keep them straight)
What are the cerebellar signs? How do you test for them?
- Dysdiadochokinesis (hand flip = slow, difficult movement)
- ataxia (walk)
- nystagmus (follow the finger)
- intention tremor (finger-nose test fully outstretched)
- slurred speech (red lorry yellow lorry)
- hypotonia (complete flaccidity)
What are requirements for a diagnosis of MS?
Evidence of damage in both time and space.
By what way does vascular dementia usually progress?
Stepwise progression.
How do you differentiate between Dementia with Lewy Bodies and Parkinson’s Dementia?
If the movement disorder and dementia occur within a year of each other then it is Dementia with Lewy bodies. If they occur greater than 1 year apart, this is Parkinson’s disease dementia.
What is the triad associated with Juvenile myoclonic epilepsy? When do seizures most commonly happen?
- absence seizures
- myoclonic seizures (often making them drop things)
- tonic-clonic seizures
Seizures often occur in the morning.
What management can help prolong life in ALS?
Riluzole (anti-glutamatergic which reduces motor neurone firing)
What can be given to manage choreoathetosis in Huntington’s disease?
Tetrabenazine (reduces monoamine release such as dopamine to reduce sx)
What is the first line medication for absence seizures?
Ethosuximide
What is first line for focal seizures?
Lamotrigine or levetiracetam
Which seizure medication can make myoclonic seizures worse?
Carbamazepine
What is idiopathic intracranial hypertension? Mx?
Tends to affect young, obese women, causing pulsatile, bilateral headaches, visual disturbance and papilledema.
Mx- acetazolamide to reduce CSf.
What visual defect occurs in Idiopathic Intracranial Hypertension?
Enlarged blind spots and constricted visual fields.
What medication often used for acne treatment is considered a RF for IIH??
Isotretinoin
Which part of the brain is damaged to cause a conduction aphasia? How is this seen in a patient?
Articulate fasciculus (joins Wernicke’s and Broca’s).
Inability to repeat words back, and substitution errors.
Damage to which part of the brain causes difficulty with language comprehension?
Wernicke’s area- Superior temporal gyrus.
Damage to which part of the brain causes poor speech production?
Broca’s area- lower frontal gyrus
What can be used to manage the symptoms of vascular dementia?
ACH esterase inhibitors such as donepezil.
What antibiotic is given to close contacts of someone with bacterial meningitis as prophylaxis?
Oral rifampicin or ciprofloxacin.
Which familial gene mutation is associated with both frontotemporal dementia and ALS?
C9orf72: hexanucleotide repeat gene
What is multi-systems atrophy (MSA)?
Parkinson’s plus syndrome demonstrating rigidity, bradykinesia, and resting tremor alongside urinary and bowel disturbance, orthostatic hypotension, erectile dysfunction, and sweating abnormalities.
What is hemiballismus? Where is the lesion?
Unilateral flinging movements.
Contralateral subthalamic nucleus.
What happens to the plantar and ankle reflex in conus medullaris syndrome?
Loss of ankle reflex, upgoing plantar response.
What is the management of Central Venous Sinus Thrombosis?
Anticoagulation (e.g., LMWH) and IV mannitol (to reduce ICP).
What are the most common symptoms seen in Creutzfeldt-Jakob Disease (CJD)
Ataxia, dementia, myoclonic jerks.
How do you mange a tension-type headache?
- Infrequent = NSAIDs and OTCs
- Frequent = 10-25 mg Amitriptyline
Where is a pilocytic astrocytoma most commonly found? Who is it most commonly seen in?
Benign lesion of the cerebellum.
Presents in children with signs of raised intracranial pressure (nausea and headaches).
Which head injury is associated with a lucid interval? What most commonly causes it?
Epidural haemorrhage.
Rupture of middle meningeal artery due to trauma.
