Stroke and acute neurological complaints Flashcards
Case 1:
27y/o man, right-handed, presents with sudden onset severe occipital headache
while at work, sitting in from of computer for 2hrs, stressed with deadlines, drinking too much coffee.
No N or V or LOC. Stopped work, went home and rested (early bed).
PMH: History of migraine.
Examination: in A&E still has headache normal examination, no focal signs, apyrexial, obs stable.
What is your plan?
a) reassure and send home
b) present case and go home “I am year 3”
c) suggest CT, if normal send home
d) suggest CT head then LP
e) sumatriptan 50mg and await response
Suggest CT, if normal send home.
Thunderclap? could be subarachnoid haemorrhage, need to rule out.
Where are the pain receptors that cause headaches as a symptom?
Brain tissue is insensate.
- Traction or dilatation of intracranial vessels.
- Traction of large extra cranial veins.
- Compression, traction or inflammation of cranial and spinal nerves.
- Meningeal irritation and raised intracranial pressure.
- Spasm or trauma to cranial or cervical muscles.
- Disturbance of serotonergic projections.
What is the purpose of headache assessment?
Diagnose headache subtype.
Determine cause (exclude secondary cause).
To explain diagnosis and rationale for treatment.
Optimise treatment.
What is part of the headache assesment
History:
Onset, frequency, duration, quality, intensity, location, triggeres, easers
Associated symptoms:
PMHx,
DHx: over/ counter drugs
SHx: ETOH, smoking, illicit drugs
Examination:
Full neuro
Fundoscopy
Menigism
Systemic exam
Temp
Blood pressure
IMagine and tests
CT, MRI
ESR bloods
LP
How are headaches classified?
What comes under those cathegories
Primary headache (no causative disorder):
- migraine
- tension type
- cluster headache
- other primary headaches.
Secondary headache (causative disorder):
- head or neck trauma
- vascular disorder
- CNS infection
- intracranial pressure disorder
- metabolic disorders
- drug withdrawal disorders
- headache psychiatric disorder
- dental, ENT or ocular problem.
Cranial neuralgias.
What are the headache red flags?
Age of onset: middle-aged to elderly (>50) GCA.
Type of onset: abrupt and severe (thunderclap). Temporal: progressively severe or increasing frequency.
Pattern: significant change in headache pattern.
Neurological signs: meningioma (stiff neck), focal signs, confusion, altered LOC.
Systemic signs: abnormal examination, fever, weight loss.
Triggers: posture, valsalvar, coughing, exertion.
Secondary risk factors: systemic disease, cancer, HIV, 3rd trimester pregnancy/postpartum, recent head injury.
How do patients present with subarachnoid haemorrhage?
- 1/3 present with acute onset severe headache as the only symptom.
- 5-11% misdiagnosed, most commonly as migraine
- Headache onset: abrupt, sudden, acute, thunderclap over seconds or minutes.
What does this show?
subarachnoid hemorrhage
How does the sensitivity of a CT head change with time for a SAH
first 12h 98%
3 days 80%
1 week 50%
after 3 weeks 0%
WHat investigations do you do on a patient, which you think might have a subarachnoid haemorrhage
- CT headhead
- if negative after 12h do an LP and then check for xanthochromia using a spectrophotometer (can not do it by eye)
What are the causes of thunderclap headache?
Intracranial infection:
- meningitis.
CSF pressure related:
- 3rd ventricle colloid;
- cyst
- spontaneous intracranial hypotension (SIH).
Vascular:
- i_schaemic and haemorrhagic stroke;_
- SAH;
- cerebral venous thrombosis;
- cervical arterial dissection;
- reversible cerebral vasoconstriction syndrome (RCVS);
- cerebral vasculitis;
- pituitary apoplexy;
- posterior reversible encephalopathy syndrome.
Others:
- acute hypertensive crisis;
- idiopathic thunderclap headache.
underlined he said are really important to know
List secondary headache conditions which may have normal CT head scans.
- Meningitis.
- SAH.
- Ischaemic stroke.
- Cerebral venous thrombosis.
- Cervical arterial dissection.
- Reversible cerebral vasoconstriction syndrome.
- Cerebral vasculitis and temporal arteritis.
- Pituitary apoplexy.
- Malignant hypertension.
If someone present with vertigo, how do you broadly classify vertigo? What are the main structures involved anatomically?
Peripheral:
Semicircular canals.
Vestibular nerve.
Central
cerebellum
brainstem
What are conditions cause vertigo in the peripheral and in the cental vestibular system
Peripheral:
BPPV
meniere’s
Vestibular neurits
Central
- Isolated vertigo.
- 4% of isolated nystagmus is caused by stroke. Other CNS deficits.
What are the main feature of BPPV
short burst of vertigo
aggravated by head movement
What test is used to identify BPPV
Hallpike maneouvre
What conditions cause dizziness in the peripheral vestibular system?
BPPV. Meniere’s. Vestibular neuritis.
What conditions cause dizziness in the central vestibular system?
Isolated vertigo. 4% of isolated nystagmus is caused by stroke. Other CNS deficits.
How do you identify in a patient with vertigo whether it is central of peripheral
central will present with other CNS deficits
How do classify the different types of pathologies in someone with diplopia
Low motor neurone lesion
- Neuromuscular junction Muscle
- lower motor neurone
Upper motor neurone lesion
- Brain
- Brain stem
- Spinal
Lady can not abduct right eye
What does she have?
abducens nerve palsy
guy can not adduct right eye
and has nystamus like movement on the left eye when trying to look to the right
What does he have?
internuclear ophtalmoplegia
What is fatigability and what condition might it be seen in?
Ptosis develops, eye alignment changes vertically, causes diplopia as eyes are disconjugated.
Myasthenia gravis.
Lady with ptosis, pupil dilation and inability to adduct her right eye
What does she have
3rd nerve palsy
In a 3rd nerve palsy, what is the level of lesion in the nervous system?
Neuromuscular junction.
What is Horner’s syndrome?
Ptosis, miosis, and anhydrosis. Enophthalmos.
patient
weakness on right side of face with sparing of the forehead
Where is the lesion?
UMN lesion
- Frontalis muscle is innervate by both cerebral cortexes and therefore you still get some innervation by the ipsylateral side
If LMN lesion then there would be no innervation and therefore it would not be forehead sparing
What does this patient have?
bell’s palsy
LMN
left facial nucleus
left facial nerve problem
What is bell’s sign
ask patient to shut eyes very tightly
they can not fully close eye - in UMN lesion they usually can close their eye it is just weak
eye ball rotates back - bell’s phenomenon
What does this show
haemorrhage- bright white
person has facial palsy (UMN)
Calcium in choroid plexus- variation - not the abnormality here
What is a stroke?
The sudden death of brain cells due to blockage of blood flow or rupture of an artery to the brain parenchyma. Ischaemic (85%) or haemorrhagic (12%) or SAH (3%).
How does an intra-cerebral haemorrhage cause symptoms of stroke?
Pressure of increasing amounts of blood.
Blood itself (blood is irritating to the brain tissue, causing it to swell.
What are some causes of haemorrhagic stroke?
- Hypertension.
- Rupture of an aneurysm or AVM. (young people)
- Haemorrhagic necrosis (e.g. tumour, infection).
- Venous outflow obstruction (CVT).
- Trauma.
- Altered haemostasis.
What are the types of causes of ischaemic stroke?
- Cryptogenic (30%).
- Large vessel atherosclerosis (20%).
- Small vessel disease (25%).
- Cardio-embolic (20%).
What causes ischaemic stroke?
Thrombus blocks artery to brain, prevents oxygen delivery. Intracranial atherosclerosis. Carotid plaque with emboli. Aortic arch plaque. Cardiogenic emboli. Small artery disease. Carotid stenosis. Atrial fibrillation. Valve disease. Ventricular thrombi.
What are the types of large artery atherosclerosis?
Intracranial stenosis.
Carotid stenosis (>50%).
Aortic arch plaque.
What are the modifiable/ non-modifiable risk factors for large artery atherosclerosis leading to ischaemic stroke?
HT.
DM.
CAD.
Smoking.
Cholesterol.
BMI.
Age.
FMHx.
What is the management plan for patients with large artery atherosclerosis or ischaemic stroke prevention?
Modify lifestyle factors.
Antiplatelet (e.g. aspirin, clopidogrel).
Duplex scan looking for stenosis.
Carotid endarterectomy is of additional benefit for symptomatic carotid disease.
what does this ECG show
AF
What are the cardioembolic causes of ischaemic stroke?
Atrial fibrillation and paroxysmal AF.
Valve disease. Ventricular thrombi.
What are the various complaints in acute stroke? (not in our lecture)
Alteration in consciousness: stupor or coma; confusion or agitation/memory loss; seizures; delirium. Vision and eyes: monocular or binocular; visual field (hemianopia); vertigo, diplopia. Ataxia: poor balance, clumsiness, or difficulty walking. Speech and swallow: slurring of speech or difficulty understanding or expressing language; swallowing problems. Headache: abrupt intense or unusually severe; associated with decreased level of consciousness/neurological deficit; unusual/severe neck or facial pain. Facial weakness or asymmetry: paralysis of facial muscles (e.g. when patients speak or smile); may be on same side (ipsilateral) or opposite side (contralateral) to limb paralysis. Weakness and paralysis. Sensory loss. Unilateral hearing loss, nausea, vomiting.
What neuromuscular syndromes occur in left (dominant) hemisphere stroke?(not in our lecture)
Aphasia. Right hemiparesis. Right-sided sensory loss. Right visual field defect. Poor right conjugate gaze. Dysarthria. Difficulty reading, writing, or calculating.
What neuromuscular syndromes occur in right (non-dominant) hemisphere stroke?(not in our lecture)
Neglect of left visual field. Extinction of left-sided stimuli. Left hemiparesis. Left-sided sensory loss. Left visual field defect. Poor left conjugate gaze. Dysarthria. Spatial disorientation.
What neuromuscular syndromes occur in brainstem/ cerebellum/ posterior hemisphere stroke?(not in our lecture)
Motor or sensory loss in all 4 limbs. Crossed signs. Limb or gait ataxia. Dysarthria. Disconjugate gaze (diplopia). Nystagmus (vertigo). Bilateral visual field defects.
What neuromuscular syndromes occur in small subcortical hemisphere or brain stem stroke (lacunar syndromes)?(not in our lecture)
Pure motor. Pure sensory. Sensory motor. Ataxic hemiparesis. Dysarthria clumsy hand syndrome. (Without abnormalities of higher brain function, sensation, or vision).
What is bright on a CT scan?
Blood Contrast Bone Calcium Metal
What is dark on a CT scan?
Air CSF/water Oedema
Case 1: 24y/o female from Somalia. Gradual onset generalised headache with some nausea and lightheadedness eases with eating. Has had 3-4 attacks in the last month. PMHx: DM (insulin dependent); depression. SHx: refugee, orphaned aged 6. O/E: left homonymous hemianopia. Metal artefact seen on CT. What is the likely cause of the headache?
Hypoglycaemia. Metal artefact caused hemianopia- bullet remained from genocide as a child.
What is the ischaemic cascade?
When brain cells are deprived of sufficient oxygen, a biochemical cascade is initiated, involving several pathways known as the ischaemic cascade, leading towards cell death: necrosis, apoptosis and inflammation.
What are the dynamic changes following ischaemic stroke?
Necrosis and apoptosis. Inflammation. Repair and remodelling (angiogenesis and neurogenesis). Increased density (&darkness) on CT brain.
What is the ischaemic penumbra window of opportunity?
Ischaemic zone surrounds a central core of infarction. Viability of brain tissue is preserved if perfusion is restored within a critical time period. Tissue surrounding the infarct that is salvageable, but at risk.
Case 2: History: sudden onset of diplopia and left-sided weakness of the face, arm and leg. On examination: right eye failure of abduction on right lateral gaze, weakness of CN VII with forehead sparing on the left, tone and reflexes increased on the left, weakness of arm and leg on left side, up going plantar on left. What is this syndrome?
Millard Gilbert syndrome.
guy who presents with right homonomys hemianopia
Where is the lesion?
left occipital lobe lesion
figure 1 - first came in 2-8 hours
figure 2: 7-14 days (brain is liquifying on the left occipital lobe)
What are the options if someone presents acutely with stroke
Thrombolysis or Endovascular thrombectomy
if some one has AF how you determine their risk for Stroke
CHA2DS2VASC score
Congestive heart failure
Hypertension
Age over 75 - 2
Ddiabetes
Stroke or TIA 2
Vascular disease
Aage 65
SC - female
What medication do you use if someone has AF
warfarin
DOAC
What is the strongest risk factor for stroke ?
- AF
- Hypertension
In what window is thrombolysis useful?
How do thrombolysis work
within 90 min fantastic outcome after 4.5 hours not useful
but drastically decrease within afew hours
alteplase´or RTPA - disolve clot
WHat is the ischaemic Penumbra
ischaemia brain surrounding the area of infarction
that will be revived if you thrombolyse the clot
When a call for a stroke comes in, what is all the investigations and management that is done
ALL within 20-30min
- Airway and breathing
- protect from aspiration
- Vitals/BM/ O2
- IV access
- Clinical and neurological Assesment
- Onset and scenario
- Significant comorbidities and medication
- NIHSS scale
- Review contraindication lost for thrombolytics
- Labs
- Glucose, electrolytes, FBC, coags
- Ordern non conrast CT
- obtain CT
What is Multi modal brain imaging?
imaging tool that visualises the areas of the brain that are still salvagable
allows us to do endovascular thrombectomy and thrombolysis much later on (even 24 hours later as oposed to 4.5 hours )
62 year old woman with hypertension and a previous TIA has been found to hsve AF on a 12 Lead ECG
What is the optimal treatment?
warfarin
atenolol
amiodarone
DC cardioversion
Aspirin
Warfarin
a 50 year old cleaner has double vision when looking to the right
on examination there is failure to abduct the right eye
What is the cranial nerve lesion
left Abducens
a 75 year old woman has a sudden onset severe headache 4 hours ago. neuro examination is normal aprt from neck stiffnes
What investigation should be performed first?
ct head
