3a Neurology Flashcards
Define stroke
Rapid onset of focal / global neurological dysfunction where Sx last ≥ 24hrs / lead to death
Causes of a stroke…
Cardiac:
AFib
Infective endocarditis
Paradoxical emboli - (Embolus from DVT enters left circulation through heart defect)
Vascular:
Vasculitis
Aortic dissection
Haematological:
Atherosclerosis
Polycythaemia
Sickle cell
Risk factors for stroke…
Increased age
FHx
HTN
Smoking
Diabetes
Hypercholesteronaemia
Similar to Atherosclerosis R.F
Carotid artery stenosis
Arteries inc. in anterior circulation of the brain
Anterior cerebral artery (ACA)
Middle cerebral artery (MCA)
Arteries inc. in posterior circulation of brain
Posterior cerebral artery (PCA)
Basilar arteries
Vertebral arteries
What part of the body is affected if ACA is affected
Lower extremities > upper extremities
What part of the body is affected if MCA is affected
Upper extremities > lower extremities
How can you tell what part of the body is affected when there is a disruption to the ACA/MCA?
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!
Describe stroke signs when ACA is affected
Contralateral hemiparesis +/ hemisensory loss in
Lower extremities > upper
Describe stroke signs when MCA is affected
Contralateral Hemiparesis +/ hemisensory loss in
Upper extremities > lower
Contralateral homonymous hemianopia
Aphasia (if dominant hemisphere affected)
Hemispatial neglect (if non-dominant hemisphere affected)
Why is contralateral homonymous hemianopia a stroke sign in MCA infarct?
MCA supplies region where optic tracts lie.
Left hemisphere processes the right visual field
Right hemisphere processes the left visual field
Why is Aphasia a stroke sign in MCA infarct?
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!
What is hemispatial neglect
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
Why is hemispatial neglect a stroke sign for MCA infarcts?
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)
Give an associated effect in a stroke when there’s a PCA infarct
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…)
Why is Contralateral homonymous hemianopia with macular sparing a stroke sign of PCA infarct
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
Give 3 associated signs of a stroke when vertebrobasilar arteries are affected
Cerebellar signs; D.A.N.I.S.H
Quadriplegia or Hemiplegia
Dysdiadokinesia / dysmetria.
Ataxia.
Nystagmus.
Intention tremor.
Slurred speech
Hypotonia.
If basilar artery supply to the pons is interrupted, what condition could you get
Locked-in syndrome
Describe what locked-in syndrome is…
Px is completely conscious (cortex is intact)
But…
Complete paralysis with only eye movement (motor tracts in pons disrupted)
What artery supplies the pons
Mainly pontine arteries which are branches of the basilar arteries
What is a ROSIER score and what’s it used for
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)
What tool is used to identify stroke in the community
Face
Arms
Speech
Time (act fast, call 999)
What tool is used to identify stroke in the emergency department
ROSIER
What are the types of stroke
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
Stroke classification system
Oxford’s stroke classification
AKA
Bamford’s classification.
Classifies strokes according to area affected
What does oxford’s stroke classification state?
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
State 4 Sx you more likely to see in haemorrhagic > Ischaemic
Reduced levels of consciousness
Headaches
N & V
Seizures
Vessels affected in lacunar stroke
Perforating arteries
surrounding thalamus, basal ganglia, internal capsule.
Lesion to what part of brain causes locked-in syndrome
Basilar artery infarct
Lesion to what part of the brain causes amaurosis fugax
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.
Lesion to what part of the brain can lead to Wellenberg’s syndrome
Posterior inferiorly cerebellar artery
Define wellenberg’s syndrome
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
Define Weber’s syndrome
Essentially stroke of the midbrain
Ipsilateral CNIII Palsy
Out and Down,
Ptosis (droopy eyelid)
Pupil mydriasis (pupil dilation)
+
Contralateral Hemiparesis
Lesion to which part of the brain causes lateral pontine syndrome
Anterior inferior cerebellar artery = lateral pontine syndrome
_____________________________________________________________________
Remember; Posterior inferior cerebellar artery infarct = Wellenberg’s syndrome
Define lateral pontine syndrome
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
Lesion in what part of the brain can cause Amaurosis fugax
Retinal ophthalmic artery
_______________________________________________________________________
”transient darkening” - temporary vision loss through one eye!
Describe symptoms of cerebellar syndrome
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
What investigations are done for suspected stroke?
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
What is 1st line investigation for stroke
Non-contract CT head
Imaging be done within 1hr of hospital admission
What presents in non-contrast CT head for ischaemic stroke
hypodensity in affected region with hyperdense vessels
What presents on non-contrast CT head in haemorrhagic stroke
Typically hyperdensity (blood) surrounded by hypodensity (oedema)
Px comes in with a stroke… how are you managing it?
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
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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
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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
What is the long-term management of an ischaemic stroke
Clopidogrel 75mg lifelong
MoA for thrombolysis + its risk/ contraindication
MoA:
plasminogen —> plasmin
Promotes the breakdown of fibrin clots
Risk
Haemorrhage
Contraindication
Haemorrhagic stroke,
Active internal bleeding,
Recent surgeries,
Active cancer
Give 2 examples of a thrombolytic agent
Alteplase
Streptokinase
Stroke Px is allergic to 1st line long-term management… what is given alternatively?
1st line longterm:
Clopidogrel 75mg
Alternative:
Aspirin + Dipyramidol (given together, not individually)
Tx for haemorrhagic stroke
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
2º prevention for stroke
Clopidogrel 75mg once daily (or Aspirin + Dipyramidole)
Atorvastatin 80mg - delay giving for at least 48hrs
Address modifiable risk factors - smoking, obesity, diabetes, HTN
What key risk factors need further investigation for stroke
Carotid artery stenosis
Carotid imaging(carotid ultrasound, or CT/MRI angiogram)
AFib
ECG
Px has a stroke most likely due to their AFib… how are you going to manage it?
Start Dx & Tx for stroke…
Plus…
Anticoagulation for AFib - Rivaroxaban
What surgical interventions are there for carotids artery stenosis {stroke risk factor}
Carotid endarterectomy
Angioplasty and stenting
What advice do you give to a stroke Px regarding driving
No driving for 1 month
HGV drivers cannot drive for 1year
Summarise TIA info into 5 points…
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
Tool used to assess risk of Px with aFib developing a stroke
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)______________[+]
What is the immediate management of TIA
Aspirin 300mg
If Px already taking low dose aspirin regular;y, advise them to continue - do not off them Aspirin 300mg.
What is the management of a TIA in a suspected TIA after aspirin has been given..?
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.
Define Multiple Sclerosis
Chronic, autoimmune demylination of the CNS.
Immune systemattacks themyelin sheathof themyelinated neurones
What type of hypersensitivity reaction occurs in multiple sclerosis
Type 4 Hypersensitivity
Epidaemiology of multiple sclerosis
F > M
20-40yr olds
Risk factors of multiple sclerosis
Female
20-40yrs old
Other autoimmune conditions
Vitamin D deficiency
EBV
Aetiology of multiple sclerosis
Environmental
Idiopathic
Genetic predisposition
Pathophysiology of multiple sclerosis
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
Where would demyelinating plaques/lesions be seen in multiple sclerosis
Periventricular
Perpendicular to ventricles
Give three main features of a multiple sclerosis plaque
Inflammation
Demyelination
Loss of axons
What cells are affected in multiple sclerosis
Oligodendrocytes
Myelin is provided by cells that wrap themselves around the axons:
٠Oligodendrocytes in the central nervous system
٠ Schwann cellsin theperipheral nervous system
What types of patterns in multiple sclerosis are there?
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
Signs and Sx of multiple sclerosis
_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.
What is the first episode of demyelination with neurological signs also known as?
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
What the management of multiple sclerosis
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
How do you manage a relapse in multiple sclerosis
PO Methylprednisolone 500mg OD
IV if oral fails/not tolerated
How do you maintain remission in multiple sclerosis
Monoclonal antibodies
Natalizumab // Ofatumimab
Immunomodulators
Siponimod // beta-interferon // Glatiramer acetate
Tx of fatigue in multiple sclerosis
Amantadine
Tx of neuropathic pain in multiple sclerosis
Amitryptaline
Gabapentin
Tx of spasticity in multiple sclerosis
Beclofen
Gabapentin
Tx of oscillopia in multiple sclerosis
Gabapentin
What type of investigations can be done in multiple sclerosis
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
What is the diagnostic criteria for multiple sclerosis
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
How are the lesions in multiple sclerosis described
Lesions are disseminated in space (clinically or on MRI) and time (>1 month apart).
What is the most common presentation of multiple sclerosis
Optic neuritis
Demyelination of optic nerve —> unilateral reduced vision
How does optic neuritis present
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
Define RAPD
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.
Tx for optic neuritis
High dose Methylprednisolone
Aim of steroid therapy in an acute relapse of MS is what…
Aim is to shorten length of recovery NOT degree of recovery
Aim of DMT in maintaining remission for MS is what…
To slow progression of MS and reduce rate of relapses
Does DVLA need to be notified about MS
Yes
Legal obligation to notify DVLA
Mention 4 complications of multiple sclerosis
UTI
Osteoporosis
Depression
Visual impairment
Give 4 differential Dx for multiple sclerosis…
Fibromyalgia
Vit B12 deficiency
Peripheral neuropathy
Ischaemic stroke
What types of headaches are there…
1º headaches
Non-specific cause as typically no underlying pathology
2º headaches
cayuse is more specific because of *Underlying pathology
Give examples of a 1º headache
Migraine
Tension
Cluster
Trigeminal Neuralgia
Give examples of 2º headaches
Giant cell arthritis
SAH
Meningitis
CO poisoning
Give red flags for headaches
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
Describe pain of a migraine
Unilateral…
Throbbing
Moderate —> Severe
Worsened on exercise
+/-
Photophobia/Phonophobia
N&V
Types of migraines
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
Describe migraine auras..?
Visual phenomena / disturbance…
ZIGZAG lines
Blurry / loss of different visual fields
Sparks / lines in vision
Can last up to 60mins
What can trigger migraines
CHOCOLATE
Chocolate
Oral cpontraceptive
Cheese
AlcohOL
Anxiety
**Travel
Exercise
How long do migraines last?
Have different stages…
Prodrome - stages before the headache (mood ∆)
+/- Aura - Part of the attack; minutes before headache
Throbbing headache - 4 - 72hrs
Women comes omplaining of migraines and is on oral contraceptive… what would you do as her dr?
Stop Oral contraceptive;
Offer alternatives; as it acts as a trigger, increases stroke risk, decreases Triptan efficacy
What is the criteria for a migraine…
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
Tx for migraine
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
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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
What drug class are triptans
5-HT receptor agonist
MoA of triptans
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
When are triptans ContraIndicated
HTN
IHD
TIA
Previous Stroke
When is topiramate contraindicated and its side effect
Can be given as a prophylaxis in migraines
C.I in Preganancy because it is teratogenic
+
Reduces contraceptive efficacy
Side-effect; Cleft lip/palate
What is defined by a chronic migraine
Headaches > 15 days /month…
8 of which have migraine features
Most common type of 1º headache is…
Tension headache
Describe pain/features of a tension headache
Bilateral
Generalised pain; Pressing/tight
Mild —> Moderate
Not-exercise induced
Pain in Frontalis, temporalis and occipitalis muscles
Rubber band, tight around head
Duration of a tension headache
30 mins —> 7 days
Excluding the generalised pain in tension headaches, are there any other sx…
No
No motion sickness
No aura
No photophobia / phonophobia
Which muscles are involved in tension headaches
Frontalis
Temporalis
Occipitalis
Treatment of tension headache
Basic Analgesia
Paracetamol // Aspirin
Hot towel across head
Relaxation techniques
Describe the pain of a cluster headache
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”
What is a cluster headache a type of?
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
How long do cluster headaches last for
15mins —> 3hrs
What type of 1º headache is the most debilitating
Cluster headaches
Risk factor for cluster headaches
Male
Smoking
Genetics
Signs and Sx of a cluster headache
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)
Tx for cluster headaches
Acute
High flow 02 - for 15-20mins
Triptans - Sumotriptan subcutaneously
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Prophylaxis
1st line: Verapamil [CCB]
Lithium //
Prednisolone… taper off
Alongside cluster headaches… what other types of Trigeminal Autonomic Cephalgia
[TAC] are there?
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
What is the most common type of Trigeminal Autonomic Cephalgia [TAC]
Cluster headaches
Investigations and Dx of cluster headaches
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!
What syndrome can present 2º to cluster headaches
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
Give differential Dx for cluster headaches
Migraines
Other TACs; Paroxysmal hemicrania, unilateral neurologiform headache, hemicrania continua
Giant cell arteritis
SAH
Idiopathic intracranial hypertension
Define a subarachnoid haemorrhage
Bleeding into the subarachnoid space
What can cause a subarachnoid haemorrhage
Trauma
Ruptured berry [/ saccular] aneurysms - M.C cause… usually arise at bifurcation points in circle of Willis
Arteriovenous malformation
Where are berry aneurysms commonly located
junction between the anterior communicating and anterior cerebral arteries
What are the Sx of subarachnoid haemorrhage
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
What type of headache precedes a berry aneurysm rupture
Sentinel headache
throbbing occipital pain
What are the 2 signs of meningism
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
What investigations are done for suspected Subarachnoid haemorrhage
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
What is the management/Tx of SAH
1st line:
Neurosurgery referral endovascular coiling
+
Nifedipine - CCB; decrease vasospasms + BP
What is the management of raised ICP
For raised ICP; IV mannitol
Give 4 risk factors for subarachnoid haemorrhage
HTN
Autosomal dominant Polycystic kidney disease (ADPKD)
Smoking
FHx
Increased age
Marfans/EDS
Give 3 differential Dx for SAH
Migraine
Cluster headache
Meningitis
Give 5 complications of SAH
Re-bleeding
Vasospasms
Hydrocephalus
Seizures
Hyponatraemia 2º to SIADH
Give 1 predictive factor in SAH and how it can be monitored
Conscious level on admission
Monitored using GCS
What is GCS referring to…
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 **
Define sub subdural haemorrhages
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
Risk factors for subdural haemorrhage
Shaken baby syndrome - child abuse
Trauma
Increased age -cortical atrophy e.g. in dementia
Signs and Sx of subdural haemorrhages
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
Investigations and Dx of a subdural haemorrhage
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
Tx for subdural haemorrhage
Refer to neurosurgery; burr hole + craniotomy
To reduce ICP: IV mannitol
Give 2 complications of subdural haemorrhage
Brain stem herniation
Respiratory distress
Define extradural haemorrhage
Accumulation of blood within the duration of mata space and the skull
What is the main cause of extradural haemorrhages
Trauma
Mainly Middle meningeal artery bleed.
In the temporoparietal region (pterion; thinnest part of skull)
Give risk factors for developing an extradural haemorrhage
M.C seen in 20-30y/o
Increased age actually has decreased likelihood of EDH
M>F
Anticoagulation use
Signs and symptoms of extradural haemorrhage
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
What causes the rapid deterioration in in extradural haemorrhages
Increased ICP
Blood clots become haemolysed and take up water (i.e. they’re osmotically active) so they increase in volume, increasing the pressure.
Complication of extradural haemorrhage
Death by respiratory arrest;
Due to unTx raised ICP…
herniation + coning of the brain —> compressed respiratory centres
Investigation and Dx of extradural haemorrhage
Non-contrast CT head
Lentiform-shaped hyperdense bleed
Confined by suture line
Midline shift
Which investigation is contraindicated in extradural haemorrhage
Lumbar puncture;
The sudden drop in pressure of the CSF in the spinal column —> herniation // brain stem compression + respiratory arrest
What is the management of extradural haemorrhage
Urgent surgical intervention; Craniotomy // Burr holes
IV mannitol to decreased ICP
Define trigeminal neuralgia
Facial pain syndrome caused by compression of the trigeminal nerve ≥1 division
What are the branches of the trigeminal nerve
Ophthalmic (VI)
Maxillary (V2)
Mandibular (V3)
Are trigeminal neuralgia cases unilateral / bilateral
90% of cases; Unilateral
Which branch of the trigeminal nerve is most affected in trigeminal neuralgia
Mandibular
Give 4 possible aetiologies for trigeminal neuralgia
1º: Idiopathic
2º: MS // Tumour // Sarcoidosis
What key disease is trigeminal neuralgia associated with
Multiple sclerosis
Give triggers for trigeminal neuralgia
Cold weather
Shaving
Brushing teeth
Eating (spicy foods / citrus fruits)
Talking
Dental prostheses
Signs and Sx of trigeminal neuralgia
Unilateral electric shock pain across the face
Very severe
Duration of trigeminal neuralgic pain
A few seconds
Secs —> 2 Mins
Give 3 risk factors for trigeminal neuralgia
Multiple sclerosis
Increased age
F>M
Investigation & Dx for trigeminal neuralgia
Clinical Dx:
≥ 3 attacks of Sx
Can do MRI/CT to rule out 2º causes
Tx for trigeminal neuralgia
Carbamazepine
(Anti-convulsant)
Surgery if persistent
Give 2 complications of trigeminal neuralgia
Jaw weakness
Diplopia
Define hydrocephalus
Excessive build up of CSF within the ventricular system lead by an imbalance in production and absorption
What is CSF produced by
Choroid plexus
network of blood vessels in each ventricle of the brain
What absorbs CSF
Arachnoid granulations
projections of the arachnoid membrane (villi) into the dural sinuses that allow CSF to pass into the venous system
What is the flow of CSF
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.
Give 3 functions of CSF
Protects brain and spinal cord by providing cushioning
Provides nutrients to the brain
Removal of waste products from cerebral metabolism
What aetiologies are there for hydrocephalus
Obstructive - structural pathology blocks the flow of CSF
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Non-obstructive - mismatch in production:absorption of the CSF
Subtype; Normal pressure hydrocephalus (enlarged ventricles with increased CSF but normal pressure)
What can cause obstructive hydrocephalus
Malignancy (tumour)
Haemorrhage
Congenital defect
What can cause non-obstructive hydrocephalus
Meningitis - reduced absorption
Choroid plexus tumour - increased production
Signs and Sx of hydrocephalus
Signs of raised ICP
Headache - worse on waking up / lying down
N&V
Papilloedema
Blurred vision
Investigation and Dx for hydrocephalus
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
Tx of hydrocephalus
Ventriculoperitoneal shunt; surgical implantation that help remove CSF via GI system
Complication; infection // blockage // intraventricular haemorrhage during surgery
Define normal pressure hydrocephalus and how it presents
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
Define syncope
Transient loss of consciousness
Aetiology of syncope
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
Types of Sx experienced in prodromal phase of syncope
Headaches
Vertigo
Blurry vision
Light headedness
Sweating
Hot / clammy
Give 5 signs that a transient loss of conciousness is due to syncope
Situational
5-30s in duration
Sweating
Nausea
Pallor
Dehydration
Give 5 causes of transient loss of conciousness
Syncope
Epileptic seizures
Non-epileptic seizures
Intoxication; alcohol
Hypoglycaemia//Ketoacidosis
Define epilepsy
Neurological disorder characterised by recurrent seizures
Define a seizure
Paroxysmal alteration of neurological function leading to hypersynchronous discharge of electrical activity at neurons
(I.E. sudden uncontrollable burst of electrical activity)
What are the types of seizures
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
