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phase 3a > 3a Neurology > Flashcards

3a Neurology Flashcards

1
Q

Define stroke

A

Rapid onset of focal / global neurological dysfunction where Sx last ≥ 24hrs / lead to death

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2
Q

Causes of a stroke…

A

Cardiac:
AFib
Infective endocarditis
Paradoxical emboli - (Embolus from DVT enters left circulation through heart defect)
Vascular:
Vasculitis
Aortic dissection
Haematological:
Atherosclerosis
Polycythaemia
Sickle cell

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3
Q

Risk factors for stroke…

A

Increased age
FHx
HTN
Smoking
Diabetes
Hypercholesteronaemia
Similar to Atherosclerosis R.F

Carotid artery stenosis

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4
Q

Arteries inc. in anterior circulation of the brain

A

Anterior cerebral artery (ACA)

Middle cerebral artery (MCA)

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5
Q

Arteries inc. in posterior circulation of brain

A

Posterior cerebral artery (PCA)

Basilar arteries

Vertebral arteries

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6
Q

What part of the body is affected if ACA is affected

A

Lower extremities > upper extremities

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7
Q

What part of the body is affected if MCA is affected

A

Upper extremities > lower extremities

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8
Q

How can you tell what part of the body is affected when there is a disruption to the ACA/MCA?

A

Think motor Homunculus.

Each area of brain controls different region of body.
More medial… controls lower extremities
&
More lateral… controls upper extremities

ACA —> Medial part of brain —> controls lower extremities!
MCA —> Lateral part of brain —> controls upper extremities!

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9
Q

Describe stroke signs when ACA is affected

A

Contralateral hemiparesis +/ hemisensory loss in
Lower extremities > upper

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10
Q

Describe stroke signs when MCA is affected

A

Contralateral Hemiparesis +/ hemisensory loss in
Upper extremities > lower

Contralateral homonymous hemianopia

Aphasia (if dominant hemisphere affected)

Hemispatial neglect (if non-dominant hemisphere affected)

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11
Q

Why is contralateral homonymous hemianopia a stroke sign in MCA infarct?

A

MCA supplies region where optic tracts lie.

Left hemisphere processes the right visual field

Right hemisphere processes the left visual field

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12
Q

Why is Aphasia a stroke sign in MCA infarct?

A

Broca’s area and Wernicke’s area are both supplied by the MCA.

These areas (particularly Broca’s) are found in the dominant hemisphere
I.E. Right-handed = left hemisphere dominant
So
Px could present with aphasia if in a right handed patient, they have a left hemispheric infarct…

Left-handed is a bit more complex - allow it!

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13
Q

What is hemispatial neglect

A

When person can see but can not process a side of their vision.
So they neglect that side…

Can see when Px is asked to draw a clock… they write all the numbers 12-11 on one side and leave the other half (which they cannot process) as empty but they can see that side they just cannot acknowledge it

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14
Q

Why is hemispatial neglect a stroke sign for MCA infarcts?

A

The area is supplied by MCA but found in the non-dominant hemisphere.
So, if in a…

Right-handed Px —> Right hemisphere is affected —> contralateral hemispatial neglect (left side is ignored)

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15
Q

Give an associated effect in a stroke when there’s a PCA infarct

A

Contralateral homonymous hemianopia with macular sparing

Contralateral loss of pain +/ temperature
(due to thalamic infarction; thalamus is supplied by PCA and spinothalamic tract runs through thalamus hence Sx of pain + temp loss…)

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16
Q

Why is Contralateral homonymous hemianopia with macular sparing a stroke sign of PCA infarct

A

Macular sparing = they still have central vision

Area of brain responsible for macular = occipital pole; found right at the back of brain.
It has 2 blood supplies; PCA + MCA, therefore, if PCA supply is disrupted, the macular still has blood supply from MCA

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17
Q

Give 3 associated signs of a stroke when vertebrobasilar arteries are affected

A

Cerebellar signs; D.A.N.I.S.H

Quadriplegia or Hemiplegia

Dysdiadokinesia / dysmetria.
Ataxia.
Nystagmus.
Intention tremor.
Slurred speech
Hypotonia.

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18
Q

If basilar artery supply to the pons is interrupted, what condition could you get

A

Locked-in syndrome

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19
Q

Describe what locked-in syndrome is…

A

Px is completely conscious (cortex is intact)
But…
Complete paralysis with only eye movement (motor tracts in pons disrupted)

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20
Q

What artery supplies the pons

A

Mainly pontine arteries which are branches of the basilar arteries

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21
Q

What is a ROSIER score and what’s it used for

A

Recognition Of Stroke In the Emergency Room
Score > 0 = suspected stroke
Do CT head

Features ( /score)
Loss of consciousness/syncope (-1pt)
Seizure activity (-1pt)

new, acute onset…
Asymmetrical Facial weakness (+1pt)
Asymmetrical Arm weakness (+1pt)
Asymmetrical Leg weakness (+1pt)
Speech disturbance (+1pt)
Visual field defect (+1pt)

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22
Q

What tool is used to identify stroke in the community

A

Face
Arms
Speech
Time (act fast, call 999)

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23
Q

What tool is used to identify stroke in the emergency department

A

ROSIER

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24
Q

What are the types of stroke

A

Ischaemic (most common type)
Reduced blood supply —> reduced O2 + glucose —> abnormal cellular ion homeostasis

Haemorrhagic
Rupture blood vessel —> blood accumulation in brain tissue + subarachnoid space —> increased intracranial pressure + compression on tissue etc

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25
Q

Stroke classification system

A

Oxford’s stroke classification
AKA
Bamford’s classification.

Classifies strokes according to area affected

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26
Q

What does oxford’s stroke classification state?

A

Categorises strokes based on their initial Sx
Remember as… Triple H

Hemiparesis +/ Hemisensory loss of face, arms, legs
Hhomonymous hemianopia
Higher cognitive dysfunction (dysphasia)

Total Anterior Circulation Infarcts (TACI);
All 3 of above criteria is present

Partial Anterior Circulation Infarcts (PACI);
2 of above criteria are present

Lacunar Infarcts (LACI);
One-of the following criteria
Pure sensory stroke (thalamus).
Unilateral pure motor stroke
Sensori-motor stroke.
Ataxic hemiparesis. - Ataxia

Posterior Circulation Infarcts (POCI);
Involves vertebrobasilar arteries and presents with one of the following…
cerebellar or brainstem syndromes - D.A.N.I.S.H
loss of consciousness
Isolated homonymous hemianopia

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27
Q

State 4 Sx you more likely to see in haemorrhagic > Ischaemic

A

Reduced levels of consciousness

Headaches

N & V

Seizures

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28
Q

Vessels affected in lacunar stroke

A

Perforating arteries
surrounding thalamus, basal ganglia, internal capsule.

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29
Q

Lesion to what part of brain causes locked-in syndrome

A

Basilar artery infarct

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30
Q

Lesion to what part of the brain causes amaurosis fugax

A

Retinal ophthalmic artery

Transient darkening… and it is used by doctors to describe a temporary loss of vision through one eye, which returns to normal afterwards.

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31
Q

Lesion to what part of the brain can lead to Wellenberg’s syndrome

A

Posterior inferiorly cerebellar artery

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32
Q

Define wellenberg’s syndrome

A

Essentially a stroke in the brain stem…
Posterior inferiorly cerebellar artery affected

Spinal trigeminal Nucleus; Ipsilateral: facial pain + temperature loss

Spinothalamic Tract; Contralateral: limb/ torso pain + temperature loss

Cerebellum; Ataxia, nystagmus

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33
Q

Define Weber’s syndrome

A

Essentially stroke of the midbrain

Ipsilateral CNIII Palsy
Out and Down,
Ptosis (droopy eyelid)
Pupil mydriasis (pupil dilation)
+
Contralateral Hemiparesis

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34
Q

Lesion to which part of the brain causes lateral pontine syndrome

A

Anterior inferior cerebellar artery = lateral pontine syndrome

_____________________________________________________________________

Remember; Posterior inferior cerebellar artery infarct = Wellenberg’s syndrome

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35
Q

Define lateral pontine syndrome

A

Similar presentation to Wellenberg’s syndrome -
*Posterior Inferior Cerbellar Artery stroke*

Plus…

Ipsilateral CNIII Palsy
Out and Down,
Ptosis (droopy eyelid)
Pupil mydriasis (pupil dilation)
+
Contralateral Hemiparesis

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36
Q

Lesion in what part of the brain can cause Amaurosis fugax

A

Retinal ophthalmic artery

_______________________________________________________________________

”transient darkening” - temporary vision loss through one eye!

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37
Q

Describe symptoms of cerebellar syndrome

A

Remember D.A.N.I.S.H

D - Dysdiadochokinesia, Dysmetria (past-pointing), patients may appear ‘Drunk’

A - Ataxia (limb, truncal)

N -Nystamus (horizontal = ipsilateral hemisphere)

I - Intention tremor

S - Slurred staccato speech,Scanning dysarthria

H -Hypotonia

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38
Q

What investigations are done for suspected stroke?

A

1st line: Non-contrast CT head - to differentiate haemorrhagic from Ischaemic stroke
Urgently > 1hr
_______________________________________________________________________

Bedside:
Blood glucose - rule out hypoglycaemia; can cause neurological deficit
ECG - not needed immediately; helps with management if aFib detected

Bloods:
U&Es - rule out hyponatraemia

Imaging:
1st line: Non-contrast CT head - to differentiate haemorrhagic from Ischaemic stroke - Urgently > 1hr
CT Angiogram - can be used for thrombectomy
______________________________
MRI
CXR - if swallowing compromised
Echocardiogram
Carotid Doppler - carotid artery stenosis

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39
Q

What is 1st line investigation for stroke

A

Non-contract CT head

Imaging be done within 1hr of hospital admission

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40
Q

What presents in non-contrast CT head for ischaemic stroke

A

hypodensity in affected region with hyperdense vessels

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41
Q

What presents on non-contrast CT head in haemorrhagic stroke

A

Typically hyperdensity (blood) surrounded by hypodensity (oedema)

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42
Q

Px comes in with a stroke… how are you managing it?

A

Absolutely rule out intracranial haemorrhage before starting

If Px presents ≤ 4.5 hrs of Sx onset:
٠ Start thrombolysis (with IV tPA) - Alteplase
٠ Give Aspirin 300mg daily for 2 weeks starting from following day
٠ Aim for BP < 180/110
٠ Can OFFER thrombectomy via CT angiogram - if Sx onset < 6hrs
٠ Can CONSIDER Thrombectomy via CT angiogram - if Sx onset < 24hrs
ـــــــــــــــــــــــــــــــــــــــــــــــــــــــــــــــــــــــــــــــــــــــــــ
If Px presents > 4.5hrs of Sx onset:
٠ Start Aspirin 300mg immediately, and daily for next 2 weeks
٠ CONSIDER Thrombectomy via CT angiogram - if Sx onset < 24hrs
ــــــــــــــــــــــــــــــــــــــــــــــــــــــــــــــــــــــــــــــــــــــــــ
All Px start anticoagulation (Aspirin 300mg) for 2 weeks as directed above & Clopidergrol 75mg lifelong after the 2 weeks of Aspirin!!
Px with aFib - give anticoagulation such as Rivaroxaban

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43
Q

What is the long-term management of an ischaemic stroke

A

Clopidogrel 75mg lifelong

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44
Q

MoA for thrombolysis + its risk/ contraindication

A

MoA:
plasminogen —> plasmin
Promotes the breakdown of fibrin clots

Risk
Haemorrhage

Contraindication
Haemorrhagic stroke,
Active internal bleeding,
Recent surgeries,
Active cancer

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45
Q

Give 2 examples of a thrombolytic agent

A

Alteplase
Streptokinase

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46
Q

Stroke Px is allergic to 1st line long-term management… what is given alternatively?

A

1st line longterm:
Clopidogrel 75mg

Alternative:
Aspirin + Dipyramidol (given together, not individually)

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47
Q

Tx for haemorrhagic stroke

A

Immediate neurosurgical referral…

Surgical decompression - Endovascular clipping / coiling

Aggressive BP control - 130-140mmHg systolic

Stop anticoagulants + warfarin reversal if required (Vit K + beriplex)

IV _Hyper_tonic saline - if evidence of raised ICP

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48
Q

2º prevention for stroke

A

Clopidogrel 75mg once daily (or Aspirin + Dipyramidole)

Atorvastatin 80mg - delay giving for at least 48hrs

Address modifiable risk factors - smoking, obesity, diabetes, HTN

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49
Q

What key risk factors need further investigation for stroke

A

Carotid artery stenosis
Carotid imaging(carotid ultrasound, or CT/MRI angiogram)

AFib
ECG

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50
Q

Px has a stroke most likely due to their AFib… how are you going to manage it?

A

Start Dx & Tx for stroke…

Plus…

Anticoagulation for AFib - Rivaroxaban

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51
Q

What surgical interventions are there for carotids artery stenosis {stroke risk factor}

A

Carotid endarterectomy

Angioplasty and stenting

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52
Q

What advice do you give to a stroke Px regarding driving

A

No driving for 1 month

HGV drivers cannot drive for 1year

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53
Q

Summarise TIA info into 5 points…

A

Transient episode of neurological dysfunction 2º to the focal brain/spinal cord/ retinal ischaemia with no sign of infarction

٠ 1st line: Aspirin 300mg

٠ _Prophylaxis: Lifelong Clopidogrel 75mg_ // Atorvastatin 80mg

٠ Review Px in TIA clinic within 24hrs if… Sx < 1 week
OR… Sx > 1 week, review within 7 days

٠ No need for CT imaging, routinely —> but need to check if its a stroke due to infarction

٠ ABCD 2 is NO longer used to assess the risk of a TIA patient having a stroke in the next 48 hours

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54
Q

Tool used to assess risk of Px with aFib developing a stroke

A

CHA2DS2 Vasc

Congestive H.F____________________________[+1]

Hypertension _____________________________[+1]

Age ≥ 75yrs _______________________________[+2]

Diabetes __________________________________[+1]

Previous Stroke/TIA ____________________[+2]

Vascular disease __________________________[+1]

Age ≥ 65 __________________________________[+1]

Sex category (Female)______________[+]

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55
Q

What is the immediate management of TIA

A

Aspirin 300mg

If Px already taking low dose aspirin regular;y, advise them to continue - do not off them Aspirin 300mg.

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56
Q

What is the management of a TIA in a suspected TIA after aspirin has been given..?

A

For people who have had a suspected TIA less than 7 days ago:
- Specialist assessment within 24 hours

For people who have had a suspected TIA more than 7 days ago:
- Specialist assessment as soon as possible within 7 days.

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57
Q

Define Multiple Sclerosis

A

Chronic, autoimmune demylination of the CNS.

Immune systemattacks themyelin sheathof themyelinated neurones

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58
Q

What type of hypersensitivity reaction occurs in multiple sclerosis

A

Type 4 Hypersensitivity

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59
Q

Epidaemiology of multiple sclerosis

A

F > M

20-40yr olds

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60
Q

Risk factors of multiple sclerosis

A

Female

20-40yrs old

Other autoimmune conditions

Vitamin D deficiency

EBV

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61
Q

Aetiology of multiple sclerosis

A

Environmental

Idiopathic

Genetic predisposition

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62
Q

Pathophysiology of multiple sclerosis

A

Genetic + environmental triggers —> T cell activation —> B cell and macrophages activation —> Inflammation of myelin sheath and damage causes demyelination and Loss of axons

In early disease,re-myelination can happen, but much thinner myelin… resolving Sx.

In the later stages, re-myelination is incomplete. Sx become more permanent - inefficient nerve conduction

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63
Q

Where would demyelinating plaques/lesions be seen in multiple sclerosis

A

Periventricular

Perpendicular to ventricles

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64
Q

Give three main features of a multiple sclerosis plaque

A

Inflammation

Demyelination

Loss of axons

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65
Q

What cells are affected in multiple sclerosis

A

Oligodendrocytes

Myelin is provided by cells that wrap themselves around the axons:

٠Oligodendrocytes in the central nervous system
٠ Schwann cellsin theperipheral nervous system

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66
Q

What types of patterns in multiple sclerosis are there?

A

Relapsing-remitting
Episodic flare-ups (lasting days/weeks/months) with periods of no Sx in-between (periods of remission)

2º progressive
Starts off as relapsing-remitting… but…
Sx get progressively worse with no periods of remission

1º progressive
Sx get progressively worse from disease onset with no periods of remission

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67
Q

Signs and Sx of multiple sclerosis

A

_Remember as D.E.M.Y.E.L.I.N.A.T.I.O.N_
Disturbance to the…
Eyes (Optic neuritis // Interocular ophthalmoplegia // Conjugate lateral gaze disorder)
Motor weakness; Pyramidal pattern - Upper; weaker extensors > flexors // Lower; weaker flexors > extensors
Nystagmus
Elevated temperature makes Sx worse (Uhtoff’s phenomenon)
Lhermittes phenomenon - electric pain on neck flexion
Intention tremor
Neuropathic pain
Ataxia
Talking slurred (Dysarthria)
Impotence (sexual dysfunction)
Overactive bladder
Numbness (Sensory disturbance)
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Optic neuritis - *pale optic disk; can’t see red —> 1st presenting Sx

Interocular opthalmoplegia - demyelination of medial longitudinal fasciculus (affected eye CANNOT move medially.

Conjugate lateral gaze disorder - Affected eye CANNOT move laterally.

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68
Q

What is the first episode of demyelination with neurological signs also known as?

A

Clinically isolated multiple sclerosis

NOT diagnostic as Px with clinically isolated syndrome may never have another episode OR may go on to develop MS
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Radiologically isolated syndrome;
The presence of MRI activity in the absence of clinical activity

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69
Q

What the management of multiple sclerosis

A

Managing Relapse
PO Methylprednisolone - 500mg OD for 5 days
IV Methylprednisolone - 1g OD … if oral fails/not tolerated
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Maintaining Remission: Disease-Modifying Therapies
Monoclonal antibodies - Natlizumab // Ofatumimab

Immunomodulators; - Siponimod // Beta Interferon // Glatiramer Acetate
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Controlling Sx
Fatigue - Amantadine
Spasticity - Baclofen // Gabapentin
Oscillopia - Gabapentin
Neuropathic pain - Amitryptiline // Gabapentin
Urge Incontinence - Anticholinergics; Oxybutynin

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70
Q

How do you manage a relapse in multiple sclerosis

A

PO Methylprednisolone 500mg OD

IV if oral fails/not tolerated

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71
Q

How do you maintain remission in multiple sclerosis

A

Monoclonal antibodies
Natalizumab // Ofatumimab

Immunomodulators
Siponimod // beta-interferon // Glatiramer acetate

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72
Q

Tx of fatigue in multiple sclerosis

A

Amantadine

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73
Q

Tx of neuropathic pain in multiple sclerosis

A

Amitryptaline

Gabapentin

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74
Q

Tx of spasticity in multiple sclerosis

A

Beclofen

Gabapentin

75
Q

Tx of oscillopia in multiple sclerosis

A

Gabapentin

76
Q

What type of investigations can be done in multiple sclerosis

A

MRI brain and spine
٠ Periventricular demyelinating plaques
٠ High signal T2 lesions

Lumbar puncture
٠ Oligoclonal bands (+ve in CSF -ve in serum —> i.e. Unmatched)
٠ Increased IgG

77
Q

What is the diagnostic criteria for multiple sclerosis

A

McDonalds criteria
≥ 2 relapses

& either…

Clinical evidence of ≥ 2 lesions OR 1 lesion + Hx of previous relapse
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Clinical evidence = abnormal neuro exam / MRI / L.P, for example.
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Relapse = Sx ≥ 24hrs experience with ≥ 1 month apart

78
Q

How are the lesions in multiple sclerosis described

A

Lesions are disseminated in space (clinically or on MRI) and time (>1 month apart).

79
Q

What is the most common presentation of multiple sclerosis

A

Optic neuritis

Demyelination of optic nerve —> unilateral reduced vision

80
Q

How does optic neuritis present

A

Impaired colour vision - Struggle to see red

Pain - with eye movement

Central scotoma - enlarged central blind spot

Relative Afferent Pupillary Defect (RAPD) - Affected eye; reduced direct light response, normal consensual pupillary reflex

81
Q

Define RAPD

A

Affected eye; reduced direct light response, normal consensual pupillary reflex

Where the pupil in theaffected eyeconstricts when shining a light in thecontralateral eye
BUT NOT when shining it in theaffected eye.

82
Q

Tx for optic neuritis

A

High dose Methylprednisolone

83
Q

Aim of steroid therapy in an acute relapse of MS is what…

A

Aim is to shorten length of recovery NOT degree of recovery

84
Q

Aim of DMT in maintaining remission for MS is what…

A

To slow progression of MS and reduce rate of relapses

85
Q

Does DVLA need to be notified about MS

A

Yes
Legal obligation to notify DVLA

86
Q

Mention 4 complications of multiple sclerosis

A

UTI
Osteoporosis
Depression
Visual impairment

87
Q

Give 4 differential Dx for multiple sclerosis…

A

Fibromyalgia

Vit B12 deficiency

Peripheral neuropathy

Ischaemic stroke

88
Q

What types of headaches are there…

A

1º headaches
Non-specific cause as typically no underlying pathology

2º headaches
cayuse is more specific because of *Underlying pathology

89
Q

Give examples of a 1º headache

A

Migraine

Tension

Cluster

Trigeminal Neuralgia

90
Q

Give examples of 2º headaches

A

Giant cell arthritis

SAH

Meningitis

CO poisoning

91
Q

Give red flags for headaches

A

Rapid new onset occipital headaches subarachnoid haem

Fever + neck stiffness meningitis

Dizziness stroke

Worsening on cough / strain raised ICP

Confusion / altered state of consciousness

Postural raised ICP

Visual disturbance G.C arteritis / glaucoma

Papilloedema raised ICP;brain tumour, HTN, bleed

92
Q

Describe pain of a migraine

A

Unilateral…
Throbbing
Moderate —> Severe
Worsened on exercise

+/-

Photophobia/Phonophobia
N&V

93
Q

Types of migraines

A

Episodic
With Aura (1/3)
Without Aura (2/3)

Chronic

Silent
Px have aura but without headaches

Hemiplegic
Mimics a stroke; Px has Sx of migraine + unilateral weakness in limbs

94
Q

Describe migraine auras..?

A

Visual phenomena / disturbance…
ZIGZAG lines

Blurry / loss of different visual fields
Sparks / lines in vision

Can last up to 60mins

95
Q

What can trigger migraines

A

CHOCOLATE

Chocolate
Oral cpontraceptive
Cheese
AlcohOL
Anxiety
**Travel
Exercise

96
Q

How long do migraines last?

A

Have different stages…

Prodrome - stages before the headache (mood ∆)
+/- Aura - Part of the attack; minutes before headache

Throbbing headache - 4 - 72hrs

97
Q

Women comes omplaining of migraines and is on oral contraceptive… what would you do as her dr?

A

Stop Oral contraceptive;

Offer alternatives; as it acts as a trigger, increases stroke risk, decreases Triptan efficacy

98
Q

What is the criteria for a migraine…

A

Criteria is with / without aura dependant… but… general Dx criteria is…

Atleast 2 of…
Unilateral pain
Throbbing in nature
Moderate—>severe
Motion sensitivity

Plus, atleast 1 of…
N+/V
Photophobia+/Phonophobia

99
Q

Tx for migraine

A

Acute
Analgesia; Aspirin 900mg // NSAIDs [Ibuprofen/Naproxen] // Paracetamol

Triptans; Sumotriptan 50mg

± Anti-emetics; Metoclopramide // Prochlorperazine for N&V
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Chronic
Headache diary
ــــــــــــــــــــــــــــــــــــــــــــــــــــــــــــــــــــــــــــــــــــــــــــــــــــــــــــــــــــــــــــــــــــــــــــــــــــــــــ
Prophylaxis [Pharmacological]
Beta-Blocker; Propanolol - If Asthmatic give…
Anti-convulsant; Topiramate

Anti-depressant; Amitriptyline
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Prophylaxis [Non-pharmacological]
Acupuncture
Vitamin B supplements; Riboflavin
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Avoid Opiates

100
Q

What drug class are triptans

A

5-HT receptor agonist

101
Q

MoA of triptans

A

They cause Vasoconstriction of cerebral blood vessels - Alleviates pain as vessels are painfully dilated in migraines

The act on peripheral pain receptors to inhibit activation of the pain receptors - Alleviating pain

ٍReduce neuronal activity in CNS

102
Q

When are triptans ContraIndicated

A

HTN

IHD

TIA

Previous Stroke

103
Q

When is topiramate contraindicated and its side effect

A

Can be given as a prophylaxis in migraines

C.I in Preganancy because it is teratogenic
+
Reduces contraceptive efficacy

Side-effect; Cleft lip/palate

104
Q

What is defined by a chronic migraine

A

Headaches > 15 days /month…
8 of which have migraine features

105
Q

Most common type of 1º headache is…

A

Tension headache

106
Q

Describe pain/features of a tension headache

A

Bilateral
Generalised pain; Pressing/tight
Mild —> Moderate
Not-exercise induced

Pain in Frontalis, temporalis and occipitalis muscles
Rubber band, tight around head

107
Q

Duration of a tension headache

A

30 mins —> 7 days

108
Q

Excluding the generalised pain in tension headaches, are there any other sx…

A

No
No motion sickness
No aura
No photophobia / phonophobia

109
Q

Which muscles are involved in tension headaches

A

Frontalis
Temporalis
Occipitalis

110
Q

Treatment of tension headache

A

Basic Analgesia
Paracetamol // Aspirin

Hot towel across head

Relaxation techniques

111
Q

Describe the pain of a cluster headache

A

Unilateral
Sharp stabbing pain around eye // temporal region
Severe —> very severe
Headache is accompanied by cranial autonomic features

٠ AKA “Suicide Headache; due to severity”

112
Q

What is a cluster headache a type of?

A

Type of Trigeminal Autonomic Cephalgia
[TAC]

Hypersensitivity of the trigeminal autonomic reflex arc (vascular dilation + nerve simulation + increased histamine release from mast cells) —> all adding to the symptoms of a cluster headache

113
Q

How long do cluster headaches last for

A

15mins —> 3hrs

114
Q

What type of 1º headache is the most debilitating

A

Cluster headaches

115
Q

Risk factor for cluster headaches

A

Male

Smoking

Genetics

116
Q

Signs and Sx of a cluster headache

A

Crescendo unilateral periorbital pain - a sharp stabbing pain around an eye // temporal region
Severe —> very severe

With Ipsilateral autonomic features;
Ptosis (droopy eye)
Miosis (constricted unilateral pupil)
Lacrimation (watery blood shot eyes)
Rhinorrhoea (runny nose)

117
Q

Tx for cluster headaches

A

Acute
High flow 02 - for 15-20mins
Triptans - Sumotriptan subcutaneously
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Prophylaxis
1st line: Verapamil [CCB]
Lithium //
Prednisolone… taper off

118
Q

Alongside cluster headaches… what other types of Trigeminal Autonomic Cephalgia
[TAC] are there?

A

Remember they are… A collection of 1º headache disorders characterised by unilateral pain with ipsilateral cranial autonomic features

Cluster headaches
Paroxysmal hemicrania
Unilateral neuralgiform headache
Hemicrania continua

119
Q

What is the most common type of Trigeminal Autonomic Cephalgia [TAC]

A

Cluster headaches

120
Q

Investigations and Dx of cluster headaches

A

Clinical Dx; ≥ 5 similar attacks confirms Dx

But remember these headaches come in clusters and so they may experience Sx for like a week — month but then not experience them for years before the next cluster.

Rule out differentials like ESR; for giant cell arteritis!

121
Q

What syndrome can present 2º to cluster headaches

A

Horner’s syndrome;

**Pain and inflammation from headache —> compression/damage of post-ganglion nerves —> Horner’s syndrome … **
Sympathetic nerves running alongside the internal carotid artery!

Triad of Sx: Ptosis, miosis, anhidrosis

122
Q

Give differential Dx for cluster headaches

A

Migraines

Other TACs; Paroxysmal hemicrania, unilateral neurologiform headache, hemicrania continua

Giant cell arteritis

SAH

Idiopathic intracranial hypertension

123
Q

Define a subarachnoid haemorrhage

A

Bleeding into the subarachnoid space

124
Q

What can cause a subarachnoid haemorrhage

A

Trauma

Ruptured berry [/ saccular] aneurysms - M.C cause… usually arise at bifurcation points in circle of Willis

Arteriovenous malformation

125
Q

Where are berry aneurysms commonly located

A

junction between the anterior communicating and anterior cerebral arteries

126
Q

What are the Sx of subarachnoid haemorrhage

A

Occipital Thunderclap headache; ”Worse headache ever experienced”

Meningism (photophobia + neck stiffness)
Kernig sign - when hip and knee are flexed, hard to extend knee again
Brudzinski sign - automatic knee flexion when neck is flexed - Severe neck stiffness causes Px hips and knees to flex when the neck is flexed

N&V // Confusion // Photophobia; non-specific signs of raised ICP

Seizures

127
Q

What type of headache precedes a berry aneurysm rupture

A

Sentinel headache

throbbing occipital pain

128
Q

What are the 2 signs of meningism

A

Kernig’s sign
When hip and knee are flexed 90º, inability to then further straighten at the knee - causes pain and irritation

Brudzinski’s sign
Flexing the Px neck causes flexion of the knee and hip - due to severe neck stiffness

129
Q

What investigations are done for suspected Subarachnoid haemorrhage

A

1st line/diagnostic:
Non-contrast CT head - star-shaped

If +ve:
CT angiogram - extent of rupture

If -ve:
Lumbar puncture - ≥12 hrs post Sx onset is when test is most sensitive.
~ Xanthochromia; yellowish CSF —> RBC haemolysis; for SAH

130
Q

What is the management/Tx of SAH

A

1st line:
Neurosurgery referral endovascular coiling
+
Nifedipine - CCB; decrease vasospasms + BP

131
Q

What is the management of raised ICP

A

For raised ICP; IV mannitol

132
Q

Give 4 risk factors for subarachnoid haemorrhage

A

HTN

Autosomal dominant Polycystic kidney disease (ADPKD)

Smoking

FHx

Increased age

Marfans/EDS

133
Q

Give 3 differential Dx for SAH

A

Migraine
Cluster headache
Meningitis

134
Q

Give 5 complications of SAH

A

Re-bleeding

Vasospasms

Hydrocephalus

Seizures

Hyponatraemia 2º to SIADH

135
Q

Give 1 predictive factor in SAH and how it can be monitored

A

Conscious level on admission

Monitored using GCS

136
Q

What is GCS referring to…

A

Best Motor Response
6. Obeys commands
5. Localises to pain
4. Flexes to pain
3. Abnormal flexion
2. Extends to pain
1. None

Best Verbal Response
5. Orientated in time, place, and person
4. Confused
3. Inappropriate words
2. Incomprehensible sounds
1. None

Best Eye Opening Response
4. Eyes open spontaneously
3. Eyes open to speech
2. Eyes open to pain
1. None

**15: best response… ≤ 8: comatose… ≤ 3: totally unresponsive **

137
Q

Define sub subdural haemorrhages

A

Blood accumulates between the dura mata and the arachnoid mata.
[subdural space]

Bridging veins found in this space… can rupture due to ‘shearing injury’ - pressure separating the 2 layers

138
Q

Risk factors for subdural haemorrhage

A

Shaken baby syndrome - child abuse
Trauma
Increased age -cortical atrophy e.g. in dementia

139
Q

Signs and Sx of subdural haemorrhages

A

Acute - within 3 days of incident
Cushings triad/reflex - Widened pulse pressure, Bradycardia, Reduced resp rate SIGNS OF RAISED ICP
+
Papilloedema // Reduced consciousness // headaches & vomiting

Chronic
Focal neurological deficits -CNIII Palsy

140
Q

Investigations and Dx of a subdural haemorrhage

A

Non-contast CT head
- banana/crescent shaped haematoma; not confined to suture lines; midline shift

Acute
Hyperdense -bright

Subacute
Isodense

Chronic
Hypodense - darker than brain image

141
Q

Tx for subdural haemorrhage

A

Refer to neurosurgery; burr hole + craniotomy

To reduce ICP: IV mannitol

142
Q

Give 2 complications of subdural haemorrhage

A

Brain stem herniation

Respiratory distress

143
Q

Define extradural haemorrhage

A

Accumulation of blood within the duration of mata space and the skull

144
Q

What is the main cause of extradural haemorrhages

A

Trauma

Mainly Middle meningeal artery bleed.
In the temporoparietal region (pterion; thinnest part of skull)

145
Q

Give risk factors for developing an extradural haemorrhage

A

M.C seen in 20-30y/o
Increased age actually has decreased likelihood of EDH

M>F

Anticoagulation use

146
Q

Signs and symptoms of extradural haemorrhage

A

Acute
Lucid intervals
Initial loss of consciousness; Intervals of feeling okay // rapid deterioration because of ICP

cushing’s triad
Bradycardia, Widened pulse pressure, irregular resp rate

Reduced GCS
+ papilloedema

147
Q

What causes the rapid deterioration in in extradural haemorrhages

A

Increased ICP

Blood clots become haemolysed and take up water (i.e. they’re osmotically active) so they increase in volume, increasing the pressure.

148
Q

Complication of extradural haemorrhage

A

Death by respiratory arrest;

Due to unTx raised ICP…
herniation + coning of the brain —> compressed respiratory centres

149
Q

Investigation and Dx of extradural haemorrhage

A

Non-contrast CT head
Lentiform-shaped hyperdense bleed
Confined by suture line
Midline shift

150
Q

Which investigation is contraindicated in extradural haemorrhage

A

Lumbar puncture;

The sudden drop in pressure of the CSF in the spinal column —> herniation // brain stem compression + respiratory arrest

151
Q

What is the management of extradural haemorrhage

A

Urgent surgical intervention; Craniotomy // Burr holes

IV mannitol to decreased ICP

152
Q

Define trigeminal neuralgia

A

Facial pain syndrome caused by compression of the trigeminal nerve ≥1 division

153
Q

What are the branches of the trigeminal nerve

A

Ophthalmic (VI)

Maxillary (V2)

Mandibular (V3)

154
Q

Are trigeminal neuralgia cases unilateral / bilateral

A

90% of cases; Unilateral

155
Q

Which branch of the trigeminal nerve is most affected in trigeminal neuralgia

A

Mandibular

156
Q

Give 4 possible aetiologies for trigeminal neuralgia

A

1º: Idiopathic

2º: MS // Tumour // Sarcoidosis

157
Q

What key disease is trigeminal neuralgia associated with

A

Multiple sclerosis

158
Q

Give triggers for trigeminal neuralgia

A

Cold weather

Shaving

Brushing teeth

Eating (spicy foods / citrus fruits)

Talking

Dental prostheses

159
Q

Signs and Sx of trigeminal neuralgia

A

Unilateral electric shock pain across the face

Very severe

160
Q

Duration of trigeminal neuralgic pain

A

A few seconds

Secs —> 2 Mins

161
Q

Give 3 risk factors for trigeminal neuralgia

A

Multiple sclerosis

Increased age

F>M

162
Q

Investigation & Dx for trigeminal neuralgia

A

Clinical Dx:
≥ 3 attacks of Sx

Can do MRI/CT to rule out 2º causes

163
Q

Tx for trigeminal neuralgia

A

Carbamazepine
(Anti-convulsant)

Surgery if persistent

164
Q

Give 2 complications of trigeminal neuralgia

A

Jaw weakness

Diplopia

165
Q

Define hydrocephalus

A

Excessive build up of CSF within the ventricular system lead by an imbalance in production and absorption

166
Q

What is CSF produced by

A

Choroid plexus

network of blood vessels in each ventricle of the brain

167
Q

What absorbs CSF

A

Arachnoid granulations

projections of the arachnoid membrane (villi) into the dural sinuses that allow CSF to pass into the venous system

168
Q

What is the flow of CSF

A

lateral ventricles ———> foramen of Munro ———> 3rd ventricle ———> cerebral aqueduct ———> 4th ventricle ———> subarachnoid space (Medially by foramen of Magendie, Lateral by Luschka) ———> dural sinus via arachnoid granulations.

169
Q

Give 3 functions of CSF

A

Protects brain and spinal cord by providing cushioning

Provides nutrients to the brain

Removal of waste products from cerebral metabolism

170
Q

What aetiologies are there for hydrocephalus

A

Obstructive - structural pathology blocks the flow of CSF
ــــــــــــــــــــــــــــــــــــــــــــــــــــــــــــــــــــــــــــــــــــــــــــــــــــ
Non-obstructive - mismatch in production:absorption of the CSF
Subtype; Normal pressure hydrocephalus (enlarged ventricles with increased CSF but normal pressure)

171
Q

What can cause obstructive hydrocephalus

A

Malignancy (tumour)
Haemorrhage
Congenital defect

172
Q

What can cause non-obstructive hydrocephalus

A

Meningitis - reduced absorption

Choroid plexus tumour - increased production

173
Q

Signs and Sx of hydrocephalus

A

Signs of raised ICP

Headache - worse on waking up / lying down

N&V

Papilloedema

Blurred vision

174
Q

Investigation and Dx for hydrocephalus

A

1st line: CT head

Lumbar puncture; diagnostic and therapeutic allows sampling, measuring opening pressure and can drain CSF to reduce pressure
Contraindicated in obstructive hydrocephalus - ∆ in cranial:spinal CSF pressure —> herniation

175
Q

Tx of hydrocephalus

A

Ventriculoperitoneal shunt; surgical implantation that help remove CSF via GI system

Complication; infection // blockage // intraventricular haemorrhage during surgery

176
Q

Define normal pressure hydrocephalus and how it presents

A

Increased CSF and enlarged ventricles without increased pressure

Triad of Sx
dementia
urinary incontinence
abnormal gait
To remember the Sx think… very very old person

177
Q

Define syncope

A

Transient loss of consciousness

178
Q

Aetiology of syncope

A

1º syncope
Dehydration
Missed meals
Vasovagal response; vagus nerve —> parasympathetic nervous system —> vasodilation —> reduced blood pressure in cerebral circulation —> hypoperfusion of brain tissue —> leads to survival mechanism to preserve brain by losing consciousness
Prolonged standing in a warm environment

2º causes
Anaemia
Hypoglycaemia
Cardiac; Arrythmias // hypertrophic obstructive cardiomyopathy // valvular heart disease

179
Q

Types of Sx experienced in prodromal phase of syncope

A

Headaches
Vertigo
Blurry vision
Light headedness
Sweating
Hot / clammy

180
Q

Give 5 signs that a transient loss of conciousness is due to syncope

A

Situational

5-30s in duration

Sweating

Nausea

Pallor

Dehydration

181
Q

Give 5 causes of transient loss of conciousness

A

Syncope

Epileptic seizures

Non-epileptic seizures

Intoxication; alcohol

Hypoglycaemia//Ketoacidosis

182
Q

Define epilepsy

A

Neurological disorder characterised by recurrent seizures

183
Q

Define a seizure

A

Paroxysmal alteration of neurological function leading to hypersynchronous discharge of electrical activity at neurons

(I.E. sudden uncontrollable burst of electrical activity)

184
Q

What are the types of seizures

A

Generally, in adults…
Generalised tonic-clonic - typical epileptic seizure; tonic-stiffening of the arms/legs/trunk… clonic-jerking of arms/legs on one/both sides of the body
Partial // focal
**
Myoclonic
Tonic
Atonic

Generally, in children…
Absence
Infantile spasm
Febrile convulsions

phase 3a (4 decks)

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