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, fluids, antiemetics, pabrinex for vitamin B+C deficiency, benzos for seizures.
What causes delirium tremens? 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?
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 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? Why complication might make it present emergently?
DANISH, 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 causing HeTN, cranial nerve palsies, etc.
How does autoimmune encephalitis present? How is this managed? What are the types?
Confusion, seizures, movement disorders, behavioural changes, emotional lability, psychosis, cognitive impairment, and reduced consciousness.
Mx: methylprednisolone (steroids), IV Ig
anti-NMDA encephalitis or 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 and 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, including forehead) taste bud impairment, excessive tearing 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 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 and mesial temporal lobe causing problems with long term memory.
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 is serotonin syndrome?
Results from serotonin increasing drugs such as SSRIs.
Restlessness, diaphoresis, clonus, hypertonia, hyperthermia, 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?
Youngish (50s) pts with memory problems, personality changes, and constructional apraxia. MRI shows atrophy or frontal and temporal lobes.
Wallenberg Syndrome (aka lateral medullary syndrome) is an infarct of what vessel? What does it cause?
Posterior inferior cerebellar artery.
Ipsilateral Horner’s, dysphagia, nystagmus, vertigo, and ataxia.
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 and 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.
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?
amyloid-beta deposits in the walls of leptomeningeal arteries, cortical arteries, and cortical capillaries.
Spontaneous lobar intracerebral haemorrhage showing as cortical superficial siderosis and lobar microbleeds on MRI.