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DPD Stuff > Acute neurological complaints > Flashcards

Acute neurological complaints Flashcards

1
Q

How common is headaches as a problem?

A

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
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2
Q

If brain tissue is insensate, why do we get headaches?

A

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
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3
Q

What is the purpose of a headache assessment?

A

Diagnose headache subtype

Determine cause (exclude secondary cause)

To explain diagnosis and rational for treatment

Optimise treatment

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4
Q

What is the classification of headaches?

A

Primary (no causative disorder)
Secondary (causative disorder)
Cranial neuralgias

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5
Q

What are primary headaches?

A

Migraine
Tension Type
Cluster Headache
Other primary head aches

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6
Q

What are some secondary headaches?

A 
Head or neck trauma
Vascular disorder
CNS infection
Intracranial Pressure disorder
Metabolic disorders
Drug withdrawal disorders
Headache psychiatric disorder
Dental, ENT or ocular problem
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7
Q

What do you need to know in a headache history?

A 
Onset 	
Frequency
Duration      
Quality 
Intensity      
Location
Triggers        
Easers

Associated symptoms
PMHx & systems review
DHx over/under counter
SHx ETOH, smoking , illicit drugs

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8
Q

What examinations would you do for a headache?

A 
Full neuro exam
Fundoscopy
Miningism
Systemic exam
Temperature
Blood pressure
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9
Q

What testing and imaging would you do for headaches?

A

CT
MRI
ESR bloods
LP

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10
Q

How common is a SAH?

A

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)

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11
Q

What are the red flags of headache?

A

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)

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12
Q

When will you likely catch a SAH on a CT?

A 
12 hours (98%)
3 days (80%)
1 week (50%)

Decreases chance of pickup rate over time

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13
Q

When would LP be abnormal in SAH?

A

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

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14
Q

What are the causes of a thunderclap headache?

A

[IMPORTANT] Intracranial infection (meningitis)
CSF pressure related
Vascular
Others

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15
Q

What are the CSF pressure related causes of thunderclap?

A

3rd Ventricle Colloid cyst

Spontaneous intracranial hypotension (SIH)

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16
Q

What are the vascular causes of thunderclap headache?

A

[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

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17
Q

Which secondary headaches might have a normal CT?

A 
[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

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18
Q

What are the common types of primary headache?

A

Migraine
Tension headache
Trigeminal neuralgia
Cluster headache

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19
Q

How do you assess dizziniess?

A 
Onset 	
Frequency
Duration      
Quality 
Intensity      
Location
Triggers        
Easers

Associated symptoms
PMHx & systems review
DHx over/under counter
SHx ETOH, smoking , illicit drugs

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20
Q

What examinations do you do for dizzinesss?

A 
Full neuro exam
Fundoscopy
Cardioexam
Systemic exam
Temperature
Blood pressure  Lying and standing
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21
Q

What imaging might you do for dizziness?

A

ECG
CT, MRI
ESR bloods
LP

22
Q

What are the places that can be disrupted to cause nystagmus?

A

Peripheral- inner ear (semicircular canals, vestibular nerve)
Central- vestibular system (brainstem and cerebellum)

23
Q

What is the vestibular system?

A

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

24
Q

What is Peripheral vertigo caused by?

A

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.

25
Q

What is the most common cause of vertigo?

A

The most common cause is benign paroxysmal positional vertigo (BPPV), which accounts for 32% of all peripheral vertigo

26
Q

What are less common causes of vertigo?

A

Other causes include Ménière’s disease (12%), superior canal dehiscence syndrome, labyrinthitis, and visual vertigo

27
Q

What might cause vertigo?

A

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).

28
Q

What is motion sickness?

A

Motion sickness is sometimes classified as a cause of peripheral vertigo

29
Q

What might peripheral vertigo present with?

A

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]

30
Q

What are central causes of nystagmus/ vertigo?

A

Other CNS deficits

But 4% of isolated nystagmus is caused by stroke

31
Q

What would you find on examination of a third nerve palsy?

A
  • 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

32
Q

What would you find in an examination in 6th nerve palsy?

A

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.

33
Q

How may ocular myasthenia gravis (NMJ problem) be found?

A

Element of fatiguability

34
Q

How does right intra nuclear opthalmoplegia present?

A

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.

35
Q

When do patients present with monocular nystagmus?

A

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).

36
Q

What are the 4 parts of horner’s syndrome (sympathetic dysfunction)?

A

Mild ptosis
Miosis
Anhydrosis
Enophalmos

37
Q

What is a forehead sparing facial nerve palsy?

A

UMN of the facial nerve tract (left pre central gyrus, left corona radiata or left posterior limb of internal capsule)

38
Q

What does a LMN facial nerve palsy present as?

A

full one sided facial nerve palsy

39
Q

What is bright on a CT?

A 
Blood
Contrast
Bone 
Calcium
Metal
40
Q

What is dark on a CT?

A

Air
CSF/ H2O
Oedema

41
Q

What is a stroke?

A

The sudden death of brain cells due blockage of blood flow or rupture of an artery to the brain parenchyma

42
Q

What are the causes of an intra cerebral haemorrhage?

A 
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)
43
Q

What are the ischaemic causes of stroke?

A 
Cryptogenic
Large vessel atherosclerosis
Small vessel disease
Cardio embolic 
Other
44
Q

What is the ischaemic cascade?

A

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

45
Q

What are the risk factors for large artery atherosclerosis?

A 
HT
DM
Smoking
Cholesterol
BMI
CAD 
FMHx
Age

Intracranial stenosis
Carotid stenosis
Aortic Arch Plaque

46
Q

What is a carotid artery endarterectomy?

A

Carotid endarterectomy (CEA) is of additional benefit for symptomatic carotid disease

47
Q

How do you manage ischaemic strokes?

A

Anti platelets

Lifestyle changes

48
Q

What are the big causes of stroke?

A

Atrial fibrillation (AF) and paroxysmal AF (PAF)
Valve disease
Ventricular thrombi

49
Q

What are the Vascular risk factors?

A 
Patient’s history 
Clinical symptoms and signs
Baseline ECG
PAF = AF
24,48,72 hour, 7 day, cont ECG monitoring

[ADD PICTURE slide 55]

50
Q

What is the ischaemic penumbra risk?

A

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
51
Q

What gets done in a thrombolysis call?

A 
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

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