Acute neurological complaints Flashcards
How common is headaches as a problem?
4.4% per year consult GP for headache
1-3% of all hospital admission
24% of acute admissions to acute neurology service 13% primary headache 2.5 % CNS infections 1% SAH 0.2% Head injury 7.3% other
If brain tissue is insensate, why do we get headaches?
Places where there are pain receptors:
- Disturbance of serotonergic projections
- Spasm or trauma to cranial or cervical muscles
- Meningeal irritation and raised intracranial pressure
- Compression, traction or inflammation of cranial and spinal nerves
- Traction of large extra cranial veins
- Traction or dilatation of intracranial vessels
What is the purpose of a headache assessment?
Diagnose headache subtype
Determine cause (exclude secondary cause)
To explain diagnosis and rational for treatment
Optimise treatment
What is the classification of headaches?
Primary (no causative disorder)
Secondary (causative disorder)
Cranial neuralgias
What are primary headaches?
Migraine
Tension Type
Cluster Headache
Other primary head aches
What are some secondary headaches?
Head or neck trauma Vascular disorder CNS infection Intracranial Pressure disorder Metabolic disorders Drug withdrawal disorders Headache psychiatric disorder Dental, ENT or ocular problem
What do you need to know in a headache history?
Onset Frequency Duration Quality Intensity Location Triggers Easers
Associated symptoms
PMHx & systems review
DHx over/under counter
SHx ETOH, smoking , illicit drugs
What examinations would you do for a headache?
Full neuro exam Fundoscopy Miningism Systemic exam Temperature Blood pressure
What testing and imaging would you do for headaches?
CT
MRI
ESR bloods
LP
How common is a SAH?
1/3 present with acute onset severe headache as the only symptom
5 to 11 % misdiagnosed (most commonly as migraine)
Headache onset- Abrupt, sudden, acute, thunderclap (over seconds or minutes)
What are the red flags of headache?
Age (middle aged/ elderly >50)
Onset (thuderclap, abrupt and severe)
Temporal (Progressive or increased frequency)
Pattern (Significant change in headache pattern)
Neuro signs (Meningism, focal signs, confusion, LOC)
Systemic features (abnormal exam, fevers, weight loss)
Triggers (Posture, valsalvar cough, exertion)
Secondary risk factors (systemic disease, cancer, HIV, preg, recent head injury)
When will you likely catch a SAH on a CT?
12 hours (98%) 3 days (80%) 1 week (50%)
Decreases chance of pickup rate over time
When would LP be abnormal in SAH?
After 12 hrs- we see xanthochromia (loo
Should be carried out 12 hours from symptom onset for detection of xanthochromia
From 12 hours up to 2 weeks xanthochromia is reliable for the presence of SAH using Spectrophotometry
RBC count on 1,2 and 3 tubes and visual inspection IS NOT RELIABLE
What are the causes of a thunderclap headache?
[IMPORTANT] Intracranial infection (meningitis)
CSF pressure related
Vascular
Others
What are the CSF pressure related causes of thunderclap?
3rd Ventricle Colloid cyst
Spontaneous intracranial hypotension (SIH)
What are the vascular causes of thunderclap headache?
[IMPORTANT}
Ischaemic and haemorrhagic stroke
SAH
Cerebral venous thrombosis
[LESS IMPORTANT]
Cervical arterial dissection
Reversible Cerebral Vasoconstriction Syndrome (RCVS)
Cerebral vasculitis
Pituitary apoplexy
Posterior reversible encephalopathy syndrome
Which secondary headaches might have a normal CT?
[more important] Meningitis SAH Ischaemic stroke Cerebral venous thrombosis
Cervical arterial dissection
Reversible Cerebral Vasoconstriction Syndrome (RCVS)
Cerebral vasculitis and Temporal arteritis
Pituitary apoplexy
Malignant hypertension
Others
What are the common types of primary headache?
Migraine
Tension headache
Trigeminal neuralgia
Cluster headache
How do you assess dizziniess?
Onset Frequency Duration Quality Intensity Location Triggers Easers
Associated symptoms
PMHx & systems review
DHx over/under counter
SHx ETOH, smoking , illicit drugs
What examinations do you do for dizzinesss?
Full neuro exam Fundoscopy Cardioexam Systemic exam Temperature Blood pressure Lying and standing
What imaging might you do for dizziness?
ECG
CT, MRI
ESR bloods
LP
What are the places that can be disrupted to cause nystagmus?
Peripheral- inner ear (semicircular canals, vestibular nerve)
Central- vestibular system (brainstem and cerebellum)
What is the vestibular system?
The vestibular system is a set of sensory inputs consisting of three semicircular canals, sensing changes in rotational motion, and the otoliths, sensing changes in linear motion.
The brain combines visual cues with sensory input from the vestibular system to determine adjustments required to retain balance
What is Peripheral vertigo caused by?
Vertigo that is caused by problems with the inner ear or vestibular system, which is composed of the semicircular canals, the vestibule (utricle and saccule), and the vestibular nerve is called “peripheral”, “otologic” or “vestibular” vertigo.
What is the most common cause of vertigo?
The most common cause is benign paroxysmal positional vertigo (BPPV), which accounts for 32% of all peripheral vertigo
What are less common causes of vertigo?
Other causes include Ménière’s disease (12%), superior canal dehiscence syndrome, labyrinthitis, and visual vertigo
What might cause vertigo?
Any cause of inflammation such as common cold, influenza, and bacterial infections may cause transient vertigo if it involves the inner ear, as may chemical insults (e.g., aminoglycosides) or physical trauma (e.g., skull fractures).
What is motion sickness?
Motion sickness is sometimes classified as a cause of peripheral vertigo
What might peripheral vertigo present with?
Patients with peripheral vertigo typically present with mild to moderate imbalance, nausea, vomiting, hearing loss, tinnitus, fullness, and pain in the ear.[14] In addition, lesions of the internal auditory canal may be associated with facial weakness on the same side.[14] Due to a rapid compensation process, acute vertigo as a result of a peripheral lesion tends to improve in a short period of time (days to weeks).[14]
What are central causes of nystagmus/ vertigo?
Other CNS deficits
But 4% of isolated nystagmus is caused by stroke
What would you find on examination of a third nerve palsy?
- Ptosis (70% of L paplebrae by Parasympathetic III fibres) – may be complete
- Mydriasis with decreased direct and consensual constriction
- Inferio-lateral deviation of eye in primary position
- Diplopia on upwards and inwards gaze
- Loss of accomodation
Sudden onset with papillary sparing – sudden infarction of the nerve ‘MEDICAL’ - Diabetes - Hypertension
What would you find in an examination in 6th nerve palsy?
Normal eye position in primary position.
Diplopia and strasbismus on lateral gaze towards the side of the lesion.
True horizontal diplopia. Often the strabismus is not appreciable; check the diplopia is true (disappears when you test one eye) the direction of maximal diplopia, and the eye responsible for the outermost image.
How may ocular myasthenia gravis (NMJ problem) be found?
Element of fatiguability
How does right intra nuclear opthalmoplegia present?
If the right medial longitudinal fasciculus is damaged, and patient is instructed to look to the left, the right eye will not look to the left (fails to adduct) while the left eye has horizontal nystagmus.
This is because the medial longitudinal fasciculus function is for concurrence contraction of medial rectus muscle and lateral rectus muscle on adduction gaze.
Any lesion that damages the unilateral medial longitudinal fasciculus can produce INO.
When do patients present with monocular nystagmus?
Most nystagmuses are biocular unless in a medial pontine stroke, where the unilateral medial longitudinal fasciculus is affected. Patient will present with contralateral internuclear opthalmoplegia (INO).
What are the 4 parts of horner’s syndrome (sympathetic dysfunction)?
Mild ptosis
Miosis
Anhydrosis
Enophalmos
What is a forehead sparing facial nerve palsy?
UMN of the facial nerve tract (left pre central gyrus, left corona radiata or left posterior limb of internal capsule)
What does a LMN facial nerve palsy present as?
full one sided facial nerve palsy
What is bright on a CT?
Blood Contrast Bone Calcium Metal
What is dark on a CT?
Air
CSF/ H2O
Oedema
What is a stroke?
The sudden death of brain cells due blockage of blood flow or rupture of an artery to the brain parenchyma
What are the causes of an intra cerebral haemorrhage?
Hypertension Rupture of an aneurysm or AVM Haemorrhagic necrosis (eg tumour, infection) Venous outflow obstruction (CVT) Trauma Altered haemostasis
Pressure of increasing amounts of blood Blood itself (blood is irritating to the brain tissue, causing it to swell)
What are the ischaemic causes of stroke?
Cryptogenic Large vessel atherosclerosis Small vessel disease Cardio embolic Other
What is the ischaemic cascade?
Oxygen deprivation causes a biochemical cascade leading to cell death
Water comes into cell and swells/ bursts resulting in lower density areas on a brain scan
What are the risk factors for large artery atherosclerosis?
HT DM Smoking Cholesterol BMI CAD FMHx Age
Intracranial stenosis
Carotid stenosis
Aortic Arch Plaque
What is a carotid artery endarterectomy?
Carotid endarterectomy (CEA) is of additional benefit for symptomatic carotid disease
How do you manage ischaemic strokes?
Anti platelets
Lifestyle changes
What are the big causes of stroke?
Atrial fibrillation (AF) and paroxysmal AF (PAF)
Valve disease
Ventricular thrombi
What are the Vascular risk factors?
Patient’s history Clinical symptoms and signs Baseline ECG PAF = AF 24,48,72 hour, 7 day, cont ECG monitoring
[ADD PICTURE slide 55]
What is the ischaemic penumbra risk?
Ischemic 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.
Help using rt-PA
How do we save it: Collateral circulation Systemic circulation Temperature Glucose Time
What gets done in a thrombolysis call?
Airway and Breathing Protect from aspiration and hypoxemia Vitals/BM / O2 IV access (Two green venflons) Clinical and neurological Assessment Onset and scenario Significant comorbidities and medications NIHSS scale Review contraindication list for thrombolytics Labs Glucose, electrolytes, FBC , coags Consent Order Non- Contrast Head CT Obtain CT
