A 35-year-old patient presents with an EPILEPSY
PATHOPHYS: decrease in inhibitory pathway
episode of feeling déjà vu followed by (GABA) and increase in the excitatory pathway
a period brief jerking. They state they (glutamate)
cannot remember anything during the CLINICAL FEAT: patients with focal seizures may
have aura before the event, focal and generalised
episode and witnesses say the patient classification, post-ictal phase (in focal with
also had tongue biting and urinary impairment or generalised or secondary generalised
incontinence. The patient has no – patient confused, lethargic), Todd’s paralysis
(temporary paralysis after seizure)
significant PMHx or FHx, they do not INVESTIGATIONS: EEG (may be normal when pt
smoke or drink alcohol. What is the isn’t seizing), 3 Hz spike in patients with absence
seizures, MRI to exclude secondary cause of the
likely diagnosis? seizure, clinical diagnosis, detailed eyewitness
accounts
MANAGEMENT: usually for males (sodium
valproate), for females (lamotrigine or
levetiracetam), for focal (first line is lamotrigine or
levetiracetam, second line carbamazepine), absence
seizures (first line is ethosuximide, second line is
sodium valproate for males and lamotrigine or
levetiracetam for female)
A patient presents with a seizure ALCOHOL WITHDRAWAL SEIZURE
following admission to a hospital 36 PATHOPHYS: patients with hx of alcohol
excess suddenly stop drinking. Chronic alcohol
hours after. The patient has a history consumption enhances GABA mediation
of chronic alcohol consumption. What inhibition in the CNS and inhibit NMDA- type
is the likely diagnosis? How did it glutamate receptors. Alcohol withdrawal is
occur? thought to lead to the opposite
CLINICAL FEATURES: peak incidence of
seizures at 36 hours, tremor, sweating,
tachycardia, anxiety, delirium tremens at 48-
72 hours
MANAGEMENT: pt with hx of complex
withdrawals admitted to hospital for
monitoring, first line (long-acting
benzodiazepines, lorazepam in patients with
hepatic failure), carbamazepine also effective
A patient presents with gradual onset PSYCHOGENIC NONEPILEPTIC
of violent thrashing movements with SEIZURE
jaw thrusts for 3 minutes, with crying PATHOPHYS: attacks that appear similar
after. She has family member with to seizures but not caused by abnormal
electrical activity in the brain
epilepsy. What is the likely diagnosis?
CLINICAL FEATURES: pelvic thrusting,
family member with epilepsy, much more
common in females, crying after seizure,
don’t occur when alone, gradual onset,
duration > 2 mins
INVESTIGATIONS: video EEG, IX for
physical causes and psychiatric
assessment. NO RAISED PROLACTIN
(unlike in epileptic seizures)
MANAGEMENT: no response to
antiepileptics, psychological treatment
A 20-year-old patient complains of MIGRAINE
PATHOPHYS: most likely due to cortical spreading
severe headaches on the left side of depression theory. An area of the brain gets
her face. She describes it as a hyperexcitable which spreads through the cerebral
throbbing headache. She explains she cortex -> can lead to auras (esp scotomas). This
triggers nociceptors to release VP, CGRP and
also gets nauseous and cannot substance P-> mast cells release inflammatory
tolerate bright lights, so she has to go molecules (histamines and prostaglandins) and leads
to vasodilation -> the trigeminal nerve -> signal to
to a quiet room to alleviate it. Before thalamus -> cortex -> meninges irritated -> pain.
the attack, she explains she saw There is also a decrease in 5HT which leads to
blurry spots in her field of vision. She vasodilation
CLINICAL FEAT: pulsatile photophobia,
doesn’t have any significant PMHx, of phonophobia, one-day duration, unilateral, N&V,
, FHx and she is currently on oral disabling
AURA: paraesthesia, scotoma, zig-zag lines,
contraception. What is the likely weakness, diplopia, vertigo, decreased hearing,
diagnosis? dysarthria
TRIGGERS: stress, chocolate, cheese, red wines,
genetics, OCP, alcohol, menstruation, bright lights
INVESTIGATION: clinical diagnosis, MRI, migraine
diagnostic criteria, bloods
MANAGEMENT: acute (oral triptan and NSAID or
oral triptan and paracetamol, anti-emetics if pt N&V),
prophylaxis (given if patient is experiencing >2
attacks per month, topiramate or propranolol-
propranolol in women of childbearing age-
acupuncture)
A patient presents with a ‘tight band’ TENSION-TYPE
PATHOPHYS: triggers cause muscle in the
headache around his head which pericranial area to become tight, stiff and tender ->
lasted for around 40 minutes. There is activate blood vessels near muscles -> CN V present
no nausea or vomiting. What is the near -> send info to cerebral cortex -> pain in
trigeminal location
most likely diagnosis? CLINICAL FEAT: bilateral, frontal and temporal,
non-pulsating, band-like, “vice”, tightening, >30
mins- 1 week, no N&V/photo/phonophobia
INVESTIGATION: clinical diagnosis, >2 of non-
pulsatile, no N&V, no photo/phonophobia, not worse
on exertion, no aura
MANAGEMENT: acute (aspirin, paracetamol,
NSAID), prophylaxis (acupuncture, some use
amitriptyline but NICE guidelines do not recommend)
A 45-year-old patient presents with CLUSTER HEADACHE
PATHOPHYS: hypothalamus is activated which
one-sided, pain around his eyes that stimulates sphenopalatine ganglion (SPG). The SPG
last around 15 minutes and it can has a parasympathetic effect and causes
occur twice a day. He describes it as a lacrimation, nasal secretion, vasodilation
(conjunctival hyperaemia, neurogenic infl). The
sharp, stabbing pain and he says he is neurogenic inflammation -> trigger CN V-> cortex ->
restless when it happens. He notices meninges irritated -> pain. The cavernous sinus wall
also inflamed -> pressure on sympathetic fibres to
his eyes get teary and red. He is a pupil -> miosis and ptosis
current smoker. What is the likely CLINICAL FEAT: pain once or twice/day, 15-2 hours,
diagnosis? intense, sharp, stabbing pain, one eye, restless,
redness of the eye, lacrimation, lid swelling, nasal
stuffiness, miosis and ptosis, rhinorrhoea
TRIGGERS: smoking, red wine, male, increased
stress
MANAGEMENT: acute (15L non-rebreather, SC
triptan), prophylaxis (verapamil, tapering dose of
prednisolone)
A 47-year-old Japanese patient comes SUBARACHNOID HAEMORRHAGE
CAUSES: berry aneurysm rupture (80%), arterio-
into the emergency department venous malformation (15%), trauma, arterial
complaining of a sudden-onset dissection, vasculitis, encephalitis
headache. He describes the headache RISK FACTORS: HTN, smoking, alcohol, drugs,
females, Japanese, Finnish, FHx, polycystic kidney
as “like being hit by a bat”. He states disease, Ehlers-Danlos
he also has discomfort when lights are CLINICAL FEATURES: headache (‘thunderclap’,
on, and his neck feels stiff. He has a ‘baseball bat’, ‘worse in my life’), N&V, meningism,
coma, seizures sudden death, CN III nerve palsy
PMHx of HTN and polycystic kidney INVESTIGATION: URGENT CT, LP is CT is negative
disease. What is the likely diagnosis? (perform at least 12 hours following onset of
symptoms) to allow breakdown of RBC’s so that
positive sample has xanthochromia
MANAGEMENT: refer ALL proven SAH to
neurosurgery immediately, surgery (coil or
craniotomy and surgical clipping), supportive care
(re-examine CNS often, bed rest, well-controlled BP,
avoid straining, measure obs), vasospasm
prevention (21-day course of nimodipine, triple H
therapy)
A 35-year-old patient presents with BELL’S PALSY (IDIOPATHIC FACIAL NERVE
PALSY)
weakness of the right side of the face. CLINICAL FEATURES: abrupt onset, complete
She explained that it came on unilateral facial weakness, ipsilateral numbness or
pain around the ear, altered taste (ageusia),
