Peer-Teaching 2 Flashcards
Examples of primary headaches
Migraine
Cluster Headache
Tension-type headache
Trigeminal neuralgia
Examples of secondary headaches
Subarachnoid haemorrhage
Giant cell arteritis
Meningitis
Medication overuse
Patient presents with serious headache, what can neuroimaging (MRI or CT) be used to rule out?
Mass lesions
Describe presentation of a migraine
Unilateral (can be bilateral)
Throbbing / Pulsetile
Can be associated with Aura
Lasts 4-72 hours
Moderate to Severe pain
Can have many triggers
Common migraine triggers
CHOCOLATE: Chocolate Hangovers Orgasms Cheese Oral contraceptive Pill Lie-ins Alcohol Tumult (loud noises) Exercise
Cause of migraine
Changes in brainstem blood flow -> unstable trigeminal nerve nucleus and nuclei in the basal thalamus -> release of vasoactive neuropeptides (CGRP and substance P) -> neurogenic inflammation; vasodilatation and plasma protein extravasation
Types of migraines
Migraine without aura
Migraine with aura
Migraine variant
How is migraine variant characterised
by unilateral motor or sensory symptoms resembling a stroke
*Diagnostic criteria of migraine without aura
A: At least 5 attacks fulfilling B,C&D B: Lasting between 4-72 hours C: ≥2 of the following: Unilateral Pulsating Moderate/Severe pain Aggravation by (or avoidance of) routine physical activity D: ≥1 of the following: Nausea and/or vomiting Photophobia and phonophobia
*Diagnostic criteria of migraine with aura
A: At least 2 attacks fulfilling B&C
B: ≥1 reversible aura symptom
-Visual – zigzags, spots
-Unilateral sensory – tingling, numbness
-Speech – aphasia
-Motor weakness (known as “hemiplegic migraine” so rule out stroke & TIA)
C: ≥2 of the following 4:
- ≥1 aura symptom spreads gradually over ≥5 minutes and/or ≥2 aura symptoms occurring in succession
-Each aura symptom lasts 5-60 minutes
- ≥1 aura symptom is unilateral
-Aura accompanied/followed within 60 minutes by headache
Conservative Treatment of migraine
Avoid triggers
Treatment of migraine: acute attacks
Mild - NSAID +/- anti-emetic
Severe - Oral triptan (e.g. Sumatriptan)
Treatment of migraine: prophylaxis
1st line - Propranolol (Beta-blocker) or Topiramate (Anti-convulsant)
2nd line - Acupuncture
3rd line - Amitriptyline (Tricyclic antidepressant)
1st line prophylaxis for migraine
Propranolol (Beta-blocker)
OR
Topiramate (Anti-convulsant)
Presentation of tension headaches
Typically bilateral (band around the head)
Tight/Pressing
Lasts anywhere from minutes to days
Mild to moderate pain
Can be associated with photophobia or phonophobia
Cause of tension headache
MC SCOLD Missed meals Conflict Stress Clenched jaw Overexertion Lack of sleep Depression
Diagnostic criteria of tension headache
A: Lasts from 30 minutes to 7 days
B: At least 2 of the following 4 characteristics:
Bilateral location
Pressing or tightening (non-pulsating) quality
Mild or moderate intensity
Not aggravated by routine physical activity such as walking or climbing stairs
C: Both of the following
No nausea or vomiting
No more than one of photophobia or phonophobia
Classifications of tension headaches
Infrequent episodic
Frequent episodic
Chronic
Probable
Describe what is meant by each of these classifications of tension headaches: Infrequent episodic Frequent episodic Chronic Probable
Infrequent episodic - <1day/month on average (<12 days/year)
Frequent episodic - 1-14 days/month on average for >3 months (≥12 and <180 days/year)
Chronic - ≥15 days/month on average for >3 months (≥180 days/year)
Probable - Tension type headache missing one of the features required to fulfill all criteria and does not fulfill criteria for another headache disorder
Treatments of tension headaches (in order)
Reassurance
Stress relief
Avoidance of causes
Medication:
Analgesic - NSAIDs (ibuprofen, diclofenac) or aspirin
Tricyclic antidepressants (Amitriptyline)
Presentation of cluster headache
Unilateral orbital, supraorbital or temporal pain
Boring/hot poker characteristic
Lasts between 15-180 minutes
Severe pain
Associated with:
-Ipsilateral eye lacrimation & redness
-Rhinorrhoea (runny nose)
-Miosis and/or ptosis (pupil constriction and drooping of eye-lid)
When do cluster headaches usually occur
Middle of the night
OR
Morning hours
Types of cluster headache
Episodic - ≥2 cluster periods lasting 7 days to 1 year separated by pain free periods lasting ≥1 month.
Chronic - attack occur for ≥1 year without remission or with remission lasting <1 month.
Treatment of cluster headaches (acute attacks and prophylaxis)
Acute attacks - SC Sumatriptan, IM/N Zolmitriptan, 100% Oxygen therapy
Prophylaxis - Verapamil (CCB), Lithium, Corticosteroids
Clinical presentation of trigeminal neuralgia
Unilateral pain confined to one or more divisions of the trigeminal nerve.
Electrifying / Lightning / Stabbing pain
Lasts a few seconds
Very severe pain
Triggers of trigeminal neuralgia
Washing affected area Shaving Eating Dental Prostheses Talking
Aetiology of trigeminal neuralgia
Compression of the trigeminal nerve by intracranial vessels or a tumour, MS, skull base malformation, zoster
Diagnostic criteria of trigeminal neuralgia
A: ≥3 attacks of unilateral facial pain
B: Pain in ≥1 division of the trigeminal nerve with no radiation
C: ≥3 of the following
Paroxysmal attacks lasting from 1-180 seconds
Severe intensity
Electric shock-like / shooting / stabbing / sharp
Precipitated by innocuous stimuli to the affected side of the face
D: No neurological deficit
1st line treatment of trigeminal neuralgia
Carbamazepine (Anti-convulsant)
Medical treatment of trigeminal neuralgia
1st line - Carbamazepine (Anti-convulsant)
2nd line - Phenytoin, gabapentin (Analgesics targeted for neuropathic pain)
Surgical treatment of trigeminal neuralgia
Microvascular decompression - Relieves pressure on the nerve by blood vessels touching the nerve or wrapped around it
Stereotactic Radiotherapy - Concentrated beam of radiotherapy to deliberately damage the trigeminal nerve where it enters the brainstem
Presentation of giant cell arteritis
Usually occurs in people over 50.
Consider Takayashu arteritis if the patient is less than 50
Symptoms of giant cell arteritis
Headache Jaw claudication Amaurosis fugax Temporal artery scalp tenderness Malaise Fever Weight loss Depression
Signs of giant cell arteritis
Palpable, tender and reduced pulsation of the temporal arteries
Gold standard for investigation of giant cell arteritis
temporal artery biopsy
Investigations of giant cell arteritis
Gold standard - temporal artery biopsy
Bloods - raised inflammatory markers (ESR and CRP)
Treatments of giant cell arteritis
40mg Prednisolone (High dose steroid) 75mg low dose aspirin PPI (e.g. omeprazole) as both drugs are associated with gastrointestinal toxicity
Acute glaucoma headache describe
Severe eye pain, red eyes, cloudy cornea, dilated or unresponsive pupil
What headaches are worse when bending over?
Sinusitis
*What medication overused can result in headache
Aspirin Paracetamol NSAIDs Triptans Opioids
What are oligodendrocytes and Schwann cells
Oligodendrocytes - A glial cell that provides myelination of neurons in the CNS
Schwann cells - A glial cell that provides myelination of neurons in the PNS
Most common cause of Parkinsonism
Idiopathic Parkinsons disease
Other causes of Parkinsonism except Parkinsons disease
Vascular parkinsonism
Infections (Encephalitis, CJD)
Toxin induced (Carbon monoxide, drugs)
Aetiology of Parkinsons
NO KNOWN CAUSE!
Thought to be due to abnormal accumulation of alpha-synuclein bound to ubiquitin which forms lewy bodies in the cytoplasm.
Also thought to be some sort of environmental link
Pathophysiology of Parkinsons
Neurodegenerative loss of dopamine secreting cells from the substantia nigra. Lack of dopamine causes alteration in neural circuits within basal ganglia that regulates movement
*Parkinsons Features and explain what each is
Bradykinesia - Problems with daily activities e.g. doing up buttons, micrographia, expressionless face, dysdiadochokinesia
Tremor - Resting, commonly unilateral, Starts in the hands “pill rolling”
Rigidity - Cogwheel like, stooped posture
Gait - Shuffling, reduced arm swing, slow to start
Postural instability - impaired balance, especially when trying to turn
Complications of Parkinsons
Depression
Dementia
Other psychiatric problems (e.g. hallucinations)
Autonomic problems (Constipation, urinary frequency)
Investigations of Parkinsons
CT head or MRI head will show atrophy of the substantia nigra
*Treatment of Parkinsons
- Carbidopa/Levodopa tablets to increase amount ofdopamine
- Dopamine Receptor Agonists to mimic dopamine e.g. Ropinirole, Pramipexole, Rotigotine
- Inhibit enzymatic breakdown of Dopamine
(all these help manage bradykinesia and rigidity, but not affect the tremor) - Tremor management
Why is levodopa given instead of dopamine
Dopamine can’t cross the blood-brain barrier but levodopa can and can be converted to dopamine in the CNS
How is Levodopa converted to dopamine in body (CNS)
Dopa Decarboxylase
Why is levodopa given alongside carbidopa
Dopa decarboxylase also exists outside the CNS
Carbidopa is a Dopa decarboxylase inhibitor.
Carbidopa can’t cross into the CNS so it doesn’t affect dopamine production in the CNS
What enzymes break down dopamine
COMT (Catecholamine-O-Methyltransferase)
MAO-B (Monoamine Oxidase-B)
What drugs can be given to inhibit the breakdown of dopamine
Entacapone and Tolcapone inhibit the action of COMT (Catecholamine-O-Methyltransferase)
Selegiline inhibits the action of MAO-B (Monoamine Oxidase-B)
Describe tremor management in Parkinsons
Amantadine
Anticholinergic
Aetiology of Huntingtons Disease
Autosomal dominant inherited condition.
Caused by CAG trinucleotide repeat in huntingtin gene. CAG triplet codes for Glutamine.
Need ≥36 triplet repeats (hence glutamines) to be diagnostic of Huntington’s
Pathophysiology of Huntingtons disease
Less GABA causes less regulation of dopamine to striatum causing increased dopamine levels and subsequently increased movement
Symptoms of Huntingtons
1st phase - Depression, incoordination, personality changes
2nd phase - Chorea (Purposeless, dance-like movements), dementia & rigidity
Ix of Huntingtons
Genetic testing
MRI - Atrophy of the Striatum (Caudate and Putamen)
Management of Huntingtons
NO CURE!
- Chorea - Antipsychotics (Risperidone) as they are Dopamine Receptor Antagonists. Alternatively, tetrabenazine can be used which depletes dopamine.
- Depression - SSRI (Sertraline)
- Aggressive Behaviour - Antipsychotics (Risperidone)
What is Multiple sclerosis
Chronic autoimmune T-cell mediated demyelination of the CNS
Epidemiology of Multiple Sclerosis
Women:Men = 2:1
More common the further from the equator you go (Possible Vit D link)
Usually diagnosed between 20-40 = Disease of the YOUNG
Diagnostic criteria of Multiple Sclerosis
2 or more attacks of MS with demyelination plaques disseminated in space and time (Old Macdonald Classification)
Types of MS progression
Relapsing-remitting MS
Primary progressive MS
Secondary progressive MS
Progressive-relapsing MS
Describe Relapsing-remitting MS
Unpredictable attacks which may or may not leave permanent deficits followed by periods of remission
Describe Primary progressive MS
Steady increase in disability without attacks
Describe Secondary progressive MS
Initial relapsing-remitting multiple sclerosis that begins to have decline without periods of remission
Describe Progressive-relapsing MS
Steady decline since onset with super-imposed attacks
Signs and symptoms of MS
DEMYELINATION: Diplopia Eye movements painful (Optic Neuritis) Motor weakness nYstagmus Elevated temperature worsens symptoms (Uhthoff’s phenomenon) Lhermitte’s sign (movement of neck causes shocks in neck) Intention tremor Neuropathic pain Ataxia Talking Slurred Impotence Overactive bladder Numbness
Investigations of Multiple sclerosis
MRI with contrast
Lumbar puncture with CSF electrophoresis
Evoked potentials
Define evoked potentials
Electrical activity generated in response to sensory or motor stimulus
What is seen for each of these investigations of MS:
MRI with contrast
Lumbar puncture with CSF electrophoresis
Evoked potentials
MRI with contrast - demyelination plaques
Lumbar puncture with CSF electrophoresis - oligoclonal IgG bands
Evoked potentials - Delayed visual, brainstem, auditory, somatosensory potentials
Symptomatic management of MS
Tremor - Beta blocker
Spacicity - Baclofen
Neuropathic pain - Gabapentin
Management of MS
Acute attacks (RRMS) - IV Methylprednisolone (steroid)
Chronic:
1st line = Beta interferon and glatiramer acetate
2nd line = Alemtuzumab or Natalizumab
Symptom management
Epidemiology of Motor Neurone Disease
More common in men
Most commonly affects people in middle age
Most die within 3 years of diagnosis
Aetiology of Motor Neurone Disease
Unknown cause but believed to be associated with SOD-1 gene mutation
What results from degeneration or destruction of motor neurones in:
Motor cortex
Anterior horn cells
Cranial nerve nuclei
Motor cortex = UMN signs
Anterior horn cells = LMN signs
Cranial nerve nuclei = Mixed UMN & LMN signs
How are upper limbs affected by MND
Reduced dexterity
Stiffness
Wasting of intrinsic muscles of hand
How are lower limbs affected by MND
Tripping
Strumbling gait
Foot drop
MND of Bulbar (Cranial nerve 9-12) symptoms
Slurred speach
Hoarseness of voice
Dysphagia
Overall symptoms of MND
Muscle atrophy
Spasiticity
Types of MND
Amyotrophic Lateral Sclerosis (ALS)
Primary Lateral Sclerosis (PLS)
Progressive muscular atrophy (PMA)
Progressive Bulbar Palsy (PBP)
What is most common type of motor neurone disease
Amyotrophic Lateral Sclerosis (ALS)
Signs of Amyotrophic Lateral Sclerosis (ALS)
UMN+LMN signs
Describe Amyotrophic Lateral Sclerosis (ALS)
Progressive focal wasting, weakness and fasciculation spreading to other limbs, Cramps, Spasticity and brisk reflexes
Signs of Primary Lateral Sclerosis (PLS)
UMN signs only
Describe Primary Lateral Sclerosis (PLS)
Slow progressive tetraparesis and pseudobulbar palsy
Signs of Progressive muscular atrophy (PMA) MS
LMN signs only
Describe Progressive muscular atrophy (PMA)
Weakness and fasiculations starting in one limb and progressing to adjacent spinal segments
Signs of Progressive Bulbar Palsy (PBP)
UMN + LMN + Cranial Nerve IX,X,XI,XII signs
Describe Progressive Bulbar Palsy (PBP)
Lower cranial nerve nuclei affected causing dysarthria, dysphagia, nasal regurgitation of fluids, choking
UMN lesion: Weakness Atrophy Reflexes Plantars Tone Fasciculation
Weakness - Yes Atrophy - NO Reflexes - UP Plantars - UPgoing Tone - UP Fasciculation - NO
LMN lesion: Weakness Atrophy Reflexes Plantars Tone Fasciculation
Weakness - Yes Atrophy - YES Reflexes - DOWN Plantars - DOWNgoing Tone - DOWN Fasciculation - YES
Investigations of MND
Largely a clinical diagnosis Electromyography - Denervation of muscles Bloods - Raised Creatinine Kinase Nerve Conduction studies Lumbar puncture MRI
Why is there raised Creatinine kinase in MND
Muscle destruction
Ix of MND - What is purpose of:
Nerve Conduction studies
Lumbar puncture
MRI
Nerve conduction studies - To rule out motor neuropathies
Lumbar puncture - To exclude inflammatory causes
MRI - To rule out lesions
Differential diagnosis if no sensory loss
Multiple sclerosis
Myelopathy
Differential diagnosis if no disturbances in eye movements
Myasthentia gravis
Multiple Sclerosis
Differential diagnosis if no sphincter disturbances
Multiple sclerosis
Management of Motor Neurone Disease
Riluzole - Anti-glutaminergic sodium channel blocker
Refer to MDT
Symptomatic Management
Symptomatic management of MND
Dysphagia - NG/PEG tube
Spasticity - Baclofen
Joint pain - Analgesic ladder
General features of brain tumours
Progressive focal neurological deficit (symptoms vary depending on location of the tumour)
Raised intracranial pressure
Epilepsy (generalised or focal seizures)
General cancer symptoms (weight loss, malaise, night sweats etc)
Symptoms resulting from raised intracranial pressure
Headaches worse on couching/leaning forward
Vomiting
Papilledema
