Neurology Flashcards
What is myasthenia gravis?
Autoimmune condition that causes muscle weakness that gets progressively worse with activity and improves with rest
Describe the epidemiology of myasthenia gravis
- More commonly affects females under 40 or males over 60
- Association between thymoma and myasthenia gravis (10-20% of patients with myasthenia gravis have a thymoma, 20-40% of patients with a thymoma develop myasthenia gravis)
What are 2 causes of myasthenia gravis?
- Acetylcholine receptor (ACh-R) antibodies (85%)
- Muscle-specific kinase (MuSK) antibodies and low-density lipoprotein receptor-related protein 4 (LRP4) antibodies (15%)
Describe the pathophysiology of myasthenia gravis (due to ACh-R antibodies)?
- Antibodies bind to postsynaptic neuromuscular junction receptors
- This blocks the receptor and prevents acetylcholine from being able to stimulate the receptor and trigger muscle contraction
- During muscle activity, receptors become increasingly blocked up which causes less effective stimulation of muscle with increased activity
- = more muscle weakness the more muscles are used
Antibodies also activate the complement system within the neuromuscular junction which leads to damage to cells at the postsynaptic membrane
Describe the pathophysiology of myasthenia gravis (due to MuSK and LRP4 antibodies)?
- Important proteins for creation and organisation of acetylcholine receptors
- Destruction causes inadequate acetylcholine receptors
What is the characteristic feature of myasthenia gravis?
Weakness that gets worse with muscle use and improves with rest
What are 7 symptoms of myasthenia gravis?
- Diplopia
- Ptosis
- Weakness in facial movements
- Difficulty with swallowing
- Fatigue in jaw when chewing
- Slurred speech
- Progressive weakness with repetitive movements
What are 5 investigations for patients with myasthenia gravis?
- Check fatiguability in muscles
- Check for a thymectomy scar or CT/MRI of thymus gland
- Test forced vital capacity (FVC)
- Antibodies
- Edrophonium test
What are 3 ways of checking fatiguability in muscles?
- Repeated blinking will exacerbate ptosis
- Prolonged upward gazing with exacerbate diplopia
- Repeated abduction of one arm 20 times will result in unilateral weakness when comparing both sides
Which 3 antibodies should you test for in myasthenia gravis?
- Acetylcholine receptor antibodies (85%)
- Muscle-specific kinase antibodies (10%)
- Low-density lipoprotein receptor-related protein antibodies (<5%)
What is the edrophonium test?
- Patient given IV dose of edrophonium chloride
- Acetylcholinesterase enzymes break down acetylcholine in neuromuscular junctions
- Edrophonium blocks enzymes to stop the breakdown of acetylcholine
- Level of acetylcholine increases
- Briefly and temporarily relieves weakness in patients with myasthenia gravis
What is the treatment for myasthenia gravis?
- Reversible acetylcholinesterase inhibitors e.g. pyridostigmine, neostigmine
- Immunosuppression e.g. prednisolone, azathioprine
- Thymectomy
- Monoclonal antibodies e.g. rituximab, eculizumab
What type of drugs are pyridostigmine and neostigmine and how do they work?
Reversible acetylcholinesterase inhibitors - increase the amount of acetylcholine in the neuromuscular junction and improve symptoms
What is rituximab and how does it work?
Monoclonal antibody - targets B cells and reduces the production of antibodies
What is eculizumab and how does it work?
Monoclonal antibody - targets complement protein C5 to reduce inflammation
What is the main complication of myasthenia gravis?
Myasthenia crisis
What does a myasthenia crisis cause?
- Acute worsening of symptoms (often triggered by another illness e.g. respiratory tract infection)
- Can lead to respiratory failure
How is a myasthenia crisis treated?
- Non-invasive ventilation with BiPAP or full intubation and ventilation
- Immunomodulatory therapies e.g. IV immunoglobulins and plasma exchange
What is Parkinson’s disease?
Progressive reduction of dopamine in the basal ganglia leading to disorders of movement
Describe the epidemiology of Parkinson’s disease
- Most common in older men
- 2nd most common neurodegenerative disorder
What are 3 risk factors for Parkinson’s disease?
- Age
- Male
- Pesticide exposure
Describe the pathophysiology of Parkinson’s disease
- Basal ganglia are a group of structure responsible for coordinating habitual movements
- Substantia nigra pars compacta is a part of the basal ganglia that produces dopamine which is essential for the correct functioning of the basal ganglia
- Parkinson’s = gradual fall in the production of dopamine (impaired nigrostriatal pathway)
What is the classic triad for Parkinson’s disease?
- Resting unilateral tremor
- ‘Cogwheel’ rigidity
- Bradykinesia
How does a Parkinson’s tremor differ from a benign essential tremor?
- Asymmetrical
- 4-6 Hz frequency
- ‘Pill rolling’ tremor
- Improves on voluntary movement
- Worsened if patient is distracted
- No change with alcohol
How does bradykinesia present in Parkinson’s patients?
- Handwriting gets smaller
- Can only take small steps when walking
- Difficulty initiating movement
- Difficulty turning around when standing
- Reduced facial movements/expressions (hypomimia)
What are 5 other clinical presentations of Parkinson’s disease?
- Depression
- Sleep disturbance and insomnia
- Loss of sense of smell (anosmia)
- Postural instability
- Cognitive impairment and memory problems
What is the treatment for Parkinson’s disease?
- Synthetic dopamine (levodopa)
- COMT inhibitors (entacapone)
- Dopamine agonists (bromocriptine, pergolide, cabergoline)
- Monoamine oxidase-B inhibitors (selegiline, rasagiline)
What is synthetic dopamine often combined with when treating Parkinson’s disease?
Peripheral decarboxylase inhibitors e.g. carbidopa, benserazide (stop levodopa being broken down in the body before it can reach the brain)
- Co-beneldopa
- Co-careldopa
What do COMT inhibitors do and give an example?
- Inhibit catechol-o-methyltransferase (enzyme that metabolises catecholamine neurotransmitters in the body and brain)
- Extends the effective duration of levodopa
- E.g. Entacapone
What do dopamine agonists do and give 3 examples?
Mimic dopamine in the basal ganglia and stimulate dopamine receptors
1. Bromocriptine
2. Pergolide
3. Cabergoline
What do monoamine oxidase-B inhibitors do and give 2 examples?
Inhibit monoamine oxidase-B (enzyme that breaks down dopamine)
1. Selegiline
2. Rasagiline
What are 3 side effects of excess levodopa (excess dopamine)?
Dyskinesias:
1. Dystonia (abnormal posture or exaggerated movements)
2. Chorea (abnormal involuntary jerking movements)
3. Athetosis (involuntary twisting/writhing movements)
What is a side effect of dopamine agonists?
Pulmonary fibrosis
What is Huntington’s disease?
Autosomal dominant genetic condition that causes a progressive deterioration in the nervous system
Which gene in affected in Huntington’s disease?
- Autosomal dominant condition
- Increase of CAG repeats on the Huntington (HTT) gene on chromosome 4
Describe the epidemiology of Huntington’s disease
Symptoms begin around age 30-50
Describe the pathophysiology of Huntington’s disease
- Caudate nucleus atrophies
- Inhibitory neurones in the corpus striatum degenerate
- Lack of GABA and excessive nigrostriatal pathway activation
Explain the genetics of Huntington’s disease
- Trinucleotide repeat disorder that involves a genetic mutation in the HTT gene on chromosome 4
- Anticipation = successive generations have more repeats in the gene resulting in earlier age of onset and increased severity of disease
What are 4 clinical presentations of Huntington’s disease?
- Chorea (involuntary, abnormal movements)
- Eye movement disorders
- Dysarthria (speech difficulties)
- Dysphagia
What are 2 investigations for patients with Huntington’s disease?
- Genetic test for faulty gene (HTT gene)
- MRI/CT (loss of striatal volume)
What is the treatment for Huntington’s disease?
No treatment
Symptomatic relief:
- Antipsychotics e.g. olanzapine
- Benzodiazepines e.g. diazepam
- Dopamine-depleting agents e.g. tetrabenazine
- Antidepressants
What is the life expectancy of patients with Huntington’s disease?
15-20 years after the onset of symptoms
What are the 2 most common causes of death in patients with Huntington’s disease?
- Respiratory disease e.g. pneumonia
- Suicide
What is Guillain-Barre syndrome?
An acute paralytic polyneuropathy that affects the peripheral nervous system, usually triggered by infection
Describe the epidemiology of Guillain-Barre syndrome
Associated with campylobacter jejuni, cytomegalovirus and Epstein-Barr virus
Describe the pathophysiology of Guillain-Barre syndrome
Molecular mimicry:
- B cells create antibodies against pathogen’s antigens
- These antibodies also match proteins on nerve cells
- Proteins on the myelin sheath of motor nerve cells or nerve axons are targeted (Schwann cells)
What are 8 clinical presentations of Guillain-Barre syndrome?
- Symmetrical ascending weakness (starts at feet and moves up)
- Reduced reflexes
- Peripheral loss of sensation
- Neuropathic pain
- Facial nerve weakness
- Breathing problems
- Urinary retention
- Sweating
What are 2 investigations for patients with Guillain-Barre syndrome?
- Nerve conduction studies = reduced signal through nerves
- Lumbar puncture for CSF = raised protein with normal cell count and glucose
What is the treatment for Guillain-Barre syndrome?
- IV immunoglobulins
- Immunosuppression
- Plasma exchange (alternative to IV Ig)
- Supportive care
- VTE prophylaxis
What 2 complications of Guillain-Barre syndrome?
- Respiratory failure
- Locked in syndrome
What is multiple sclerosis (MS)?
Chronic inflammation of the CNS causing demyelination of myelinated neurones
Describe the epidemiology of MS
- More common in females
- Typically presents in young adults under 50 years
What are 5 causes/associations of MS?
- Genetics (multiple genes)
- Epstein-Barr virus
- Low vitamin D
- Smoking
- Obesity
Describe the pathophysiology of MS
- Typically only affects the CNS (oligodendrocytes)
- Inflammation and infiltration of immune cells causes damage to the myelin
- Lesions vary in location over time
What are 5 clinical presentations of MS?
- Optic neuritis (demyelination of optic nerve)
- Eye movement abnormalities (due to lesions in abducens nerve)
- Focal weakness
- Focal sensory symptoms
- Ataxia (problems with coordinated movement)
Describe the presentation of optic neuritis in patients with MS
- Unilateral reduced vision
- Central scotoma (enlarged blind spot)
- Pain on eye movement
- Impaired coloured vision
- Relative afferent pupillary defect
Describe eye movement abnormalities in patients with MS
- Diplopia
- Internuclear ophthalmoplegia (unilateral lesions - problems with muscles around the eye)
- Conjugate lateral gaze disorder (eye don’t move together to look laterally)
Describe focal weakness in patients with MS
- Bells palsy (sudden weakness in muscles on one side of face)
- Horners syndrome (ptosis, miosis, anhidrosis)
- Limb paralysis
- Incontinence
Describe focal sensory symptoms in patients with MS
- Trigeminal neuralgia
- Numbness
- Paraesthesia (pins and needles)
- Lhermitte’s sign (electric shock sensation)
Describe ataxia in patients with MS
- Sensory ataxia (loss of proprioceptive sense)
- Cerebellar ataxia (problems with cerebellum coordinating movement)
What are the 4 disease patterns of MS?
- Clinically isolated syndrome
- Relapsing-remitting
- Secondary progressive
- Primary progressive
What is clinically isolated syndrome in MS?
- First episode of demyelination and neurological signs and symptoms
- Cannot diagnose with MS (as some patients may never have another episode or develop MS)
What is relapsing-remitting in MS?
- Episodes of disease and neurological symptoms followed by recovery
- Can be further classified as active/not active, progressing/not progressing
What is secondary progressive in MS?
- Relapsing-remitting disease at first but now progressive worsening of symptoms with incomplete remissions
- Can be further classified as active/not active, progressing/not progressing
What is primary progressive in MS?
Worsening of disease and neurological symptoms without initial relapse and remission
What does active/not active, progressing/not progressing mean in MS?
Active = new symptoms/lesions developing
Not active = no new symptoms/lesions developing
Progressing = overall worsening of disabilities/disease over time
Not progressing = no worsening of disabilities/disease over time
What are 4 investigations for patients with MS?
- Exclude other causes for symptoms
- Symptoms must be progressive over a period of 1 year = diagnosis
- MRI for lesions
- Lumbar puncture for CSF = oligoclonal bands
What is the diagnostic criteria for MS?
McDonald’s criteria:
- Dissemination in time (damage that happened at more than 1 point in time)
- Disseminated in space (damage in at least 2 regions of the brain/spinal cord)
What is the treatment for MS?
- Disease modifying drugs and biological therapy (interleukins, inflammatory cytokines, immune cells)
- Steroids e.g. methylprednisolone (for relapse)
- Steroids for optic neuritis
- Symptomatic releief
What symptomatic relief is given for MS?
- Neuropathic pain relief e.g. amitriptyline, gabapentin
- Antidepressants
- Anticholinergic medication for urge incontinence e.g. tolterodine, oxybutynin
- Medication for spasticity e.g. baclofen, gabapentin
What is a side effect of anticholinergic medication?
Can worsen cognitive impairment
What is meningitis?
Inflammation in the meninges
What are 4 causes of bacterial meningitis?
- Neonates = group B strep (s. agalactiae)
- Children <2 = strep pneumoniae
- Up to 50 years = neisseria meningitis (meningococcus), strep pneumoniae
- > 50 = strep pneumoniae, listeria meningitis
What are 2 causes of viral meningitis?
- Enterovirus
- HSV (herpes simplex virus)
What are 2 causes of fungal meningitis?
- Cryptococcus
- Candida
What are 6 risk factors for meningitis?
- Student
- Travel
- Immunocompromised
- Pregnancy
- Extremes of ages
- Unvaccinated
What is characteristic symptom of meningococcal septicaemia?
Non-blanching rash - indicates the infection has caused disseminated intravascular coagulopathy (DIC) and subcutaneous haemorrhage
What are 7 clinical presentations of meningitis?
- Fever
- Neck stiffness
- Vomiting
- Headache
- Photophobia
- Altered consciousness
- Seizures
What are 5 non-specific clinical presentations of meningitis (often in neonates/babies)?
- Hypotonia
- Poor feeding
- Lethargy
- Hypothermia
- Bulging fontanelle
What are 5 investigations for patients with meningitis?
- Lumbar puncture for CSF
- Blood culture
- Bloods (meningococcal PCR)
- Kernig’s test
- Brudzinski’s test
What in the CSF do we look at when investigating meningitis?
- Bacterial culture
- Viral PCR
- Cell count
- Protein
- Glucose
Describe the differences in CSF with bacterial and viral meningitis
- Bacterial = cloudy, viral = clear
- Bacterial = high protein, viral = mildly raised/normal
- Bacterial = low glucose, viral = normal glucose
- High WCC (bacterial = neutrophils, viral = lymphocytes)
- Culture (bacterial = bacteria, viral = negative)
What is Kernig’s test?
- Patient lies on back, flexing one hip and knee to 90 degrees and then slowly straightening the knee whilst keeping the hip flexed at 90 degrees
- Meningitis = spinal pain or resistance to movement
What is Brudzinski’s test?
- Patient lies on back
- Lift their head and neck off the bed and flex their chin to their chest
- Positive = patient involuntarily flexes hip and knees
What is the treatment for bacterial meningitis?
- Meningitis and non-blanching rash = IM/IV benzylpenicillin
- Cefotaxime plus amoxicillin (under 3 months)
- Ceftriaxone
- Vancomycin
- Steroids (dexamethasone)
What other treatment is given for meningitis?
Post exposure prophylaxis = ciprofloxacin
What is the treatment for viral meningitis?
Aciclovir
What are 7 complications of meningitis?
- Hearing loss
- Seizures and epilepsy
- Cognitive impairment and learning disability
- Memory loss
- Cerebral palsy
- Limb weakness
- Spasticity
What is encephalitis?
Inflammation of the brain
What is the most common cause of encephalitis?
Herpes simplex type 1 (HSV-1) from cold sores (95%)
What are 5 other causes of encephalitis?
- Herpes simplex type 2 (HSV-2) from genital herpes (neonates)
- Varicella zoster virus (VZV) associated with chickenpox
- Cytomegalovirus (CMV) associated with immunodeficiency
- Epstein-Barr virus (EBV) associated with infectious mononucleosis, enterovirus, adenovirus and influenza virus
- Viruses from vaccinations (polio, mumps, rubella, measles)
What are 2 risk factors for encephalitis?
- Extremes of ages
- Immunocompromised
What are 8 clinical presentations of encephalitis?
- Fever
- Headache
- Encephalopathy
- Altered consciousness
- Altered cognition
- Unusual behaviour
- Acute onset of focal neurological symptoms
- Acute onset of focal seizures
What are 4 investigations for patients with encephalitis?
- Lumbar puncture for CSF (viral PCR testing, CSF may show uraemia)
- CT/MRI (unilateral temporal encephalitis)
- Swabs
- HIV testing
What is the treatment for encephalitis?
- Aciclovir (for HSV and VZV)
- Ganciclovir (for CMV)
What are 9 complications of encephalitis?
- Lasting fatigue and prolonged recovery
- Change in personality or mood
- Changes to memory and cognition
- Learning disability
- Chronic pain
- Movement disorders
- Sensory disturbance
- Seizures
- Hormonal imbalance
What is dementia?
Irreversible, progressive decline and impairment of more than one aspect of higher brain function (concentration, memory, language, personality, emotion) without impairment of consciousness
Describe the epidemiology of Alzheimer’s disease
- Most common type of dementia
- Most common neurodegenerative disorder
- Commonly affects patients over 65
- More common in females
What are 5 risk factors for Alzheimer’s disease?
- Down’s syndrome
- ApoE E4 allele homozygosity
- Reduced cognitive activity
- Depression/loneliness
- Increasing age
Describe the pathophysiology of Alzheimer’s disease
- Extra-cellular deposition of beta-amyloid plaques
- Tau-containing intracellular neurofibrillary tangles
- Accumulation leads to damaged synapses and atrophy
- Tends to progress steadily over time
What are 5 clinical presentations of Alzheimer’s disease?
- Memory - episodic and semantic
- Language - difficulty understanding or finding words
- Attention and concentration issues
- Psychiatric changes e.g. withdrawal, delusions
- Disorientation e.g. time and surroundings
What are 4 investigations for patients with Alzheimer’s disease?
- MMSE (mini mental state examination)
- Bloods - TFTs, B12
- Memory clinical assessment
- MRI
What is the treatment for Alzheimer’s disease?
- No cure
- Supportive therapy
- Symptomatic management (acetylcholinesterase (AChE) inhibitors e.g. galantamine, donepazil, rivastigmine)
Describe the epidemiology of frontotemporal dementia
- More common dementia in patients under 65
- 5% of dementias
What is a risk factor for frontotemporal dementia?
Family history
Describe the pathophysiology of frontotemporal dementia
- Atrophy of frontal and temporal lobes
- Loss of neurons but no plaque formation
- Tau protein +ve or TDP-43 +VE inclusions
- Onset tends to be insidious and progressive
What are the 3 main symptoms of frontotemporal dementia?
- Behavioural issues
- Progressive aphasia
- Semantic dementia
What are 3 behavioural issues that present in frontotemporal dementia?
- Loss of inhibition/empathy
- Compulsive behaviours
- Difficulty planning
What are 2 progressive aphasia presentations in frontotemporal dementia?
- Slow, difficulty speech
- Grammatical errors
What are 3 semantic dementia presentations in frontotemporal dementia?
- Loss of vocabulary
- Problems understanding
- Inability to recognise objects or familiar faces
What are 4 investigations for patients with frontotemporal dementia?
- Bloods - B12, TFTs, U&Es
- FBC and LFTs (for suspected encephalopathy)
- MMSE (mini mental state examination)
- MRI (frontal/temporal atrophy)
What is the treatment for frontotemporal dementia?
- No cure
- Supportive therapy
- SSRIs
- Levdopa/carbidopa (if Parkinson’s symptoms present)
- Stop exacerbating drugs
Describe the epidemiology of Lewy Body dementia
- Most commonly affects patients over 50
- More common in males
- Most commonly associated with Parkinson’s
Describe the pathophysiology of Lewy Body dementia
- Eosinophilic intracytoplasmic neuronal inclusion bodies (Lewy bodies) in the brainstem and neocortex
- Substantia nigra depigmentation and amyloid deposits
- Rapidly progressive
What are 7 clinical presentations of Lewy Body dementia?
- Loss of cognitive function
- Spatial awareness difficulties
- Visual hallucinations
- Problems multitasking
- Sleep disorders and restless leg syndrome
- Memory loss
- Parkinson-like symptoms (tremor, rigidity, change in gait)
What are 5 investigations for patients with Lewy Body dementia?
- MMSE (mini mental state examination)
- Bloods - B12, TFTs, U&Es
- MRI
- MSU (mid stream specimen of urine - to check for urine infection)
- SPECT/PET scan (low dopamine transported uptake in basal ganglia)
How is Lewy Body dementia diagnosed?
Presence of dementia with 2 of:
- Fluctuating attention and concentration
- Recurrent well-formed visual hallucinations
- Spontaneous Parkinsonism
^ if only 1, diagnosis can be made with SPECT/PET scan
What is the treatment for Lewy Body dementia?
- Supportive therapy
- Cholinesterase inhibitors e.g. rivastigmine (to help with cognitive decline)
- Avoid use of neuroleptic drugs e.g. haloperidol (can produce severe sensitivity reactions)
What is the average prognosis of Lewy Body dementia?
Death most commonly in the first 7 years post-diagnosis
Describe the epidemiology of vascular dementia
- 2nd most common type of dementia
- More common in males
What is the cause of vascular dementia?
Multiple small cerebrovascular infarcts
What are 7 risk factors for vascular dementia?
- Previous stroke/TIA
- Hypertension
- Smoking
- Type 1 diabetes mellitus
- Hyperlipidaemia
- Obesity
- Hypercholesterolaemia
Describe the pathophysiology of vascular dementia
- Most commonly affects white matter of both cerebral hemispheres, grey nuclei, thalamus, striatum
- Progresses in a sudden stepwise fashion (period of stability, acute decline progression, period of stability)
What are 4 clinical presentations of vascular dementia?
- Cognitive impairment
- Mood disturbances and mood disorders
- Visual disturbances
- UMN signs
What are 5 mood disturbances and mood disorders in vascular dementia?
- Psychosis
- Delusions
- Hallucinations
- Paranoia
- Depression
What are 3 UMN signs in vascular dementia?
- Muscle weakness
- Overactive reflexes
- Clonus (involuntary and rhythmic muscle contractions)
What are 3 investigations for patients with vascular dementia?
- MRI (infarcts)
- Patient history (e.g. for previous strokes)
- Cognitive impairment screen (orientation, attention, language, visuospatial functions, motor control)
What is the treatment for vascular dementia?
- Manage predisposing factors
- Supportive therapy
- Symptom control with antidepressants (SSRIs) or anti-psychotics
What are the primary headaches?
Migraine, tension, cluster
What is a migraine?
Recurrent, throbbing headache often preceded by an aura and associated with nausea, vomiting and visual change
Describe the epidemiology of migraines
- Most common cause of episodic headaches
- 3 x more common in females
- 90% have an onset before 40 years
What are the triggers for migraines?
CHOCOLATE
C - chocolate
H - hangovers
O - orgasms
C - cheese
O - oral contraceptives
L - lie-ins
A - alcohol
T - tumult (loud noises)
E - exercise
What are 3 risk factors for migraines?
- Genetics/family history
- Female
- Age (adolescence)
Describe a theory for the pathophysiology of migraines
Irritation of trigeminal nuclei within the brainstem due to changes to arterial blood flow
What are 4 symptoms of migraines?
- Unilateral, throbbing-type pain (moderate to severe intensity)
- Nausea/vomiting
- Motion sensitivity
- Photophobia/phonophobia
What are 3 prodrome symptoms of migraines?
- Yawning
- Cravings
- Mood/sleep changes
What is aura?
- Precedes migraine attacks
- Visual disturbances e.g. lines, dots, zig zags
- Somatosensory disturbances e.g. paraesthesia, pins and needles
What are 2 investigations for patients with migraines?
- CT/MRI
- Lumbar puncture
How are migraines diagnosed?
At least 2 of:
- Unilateral pain (4-72 hours)
- Throbbing-type pain
- Moderate to severe intensity
- Motion sensitivity
Plus at least 1 of:
- Nausea/vomiting
- Photophobia/phonophobia
What is the treatment for migraines?
- Triptans e.g. sumatriptan
- NSAIDs e.g. naproxen
- Anti-emetics e.g. prochlorperazine
- Avoid opioids and ergotamine
What is used to prevent migraines?
- Beta blockers e.g. propranolol
- TCAs e.g. amitriptyline
- Anti-convulsants e.g. topiramate
What is a tension headache?
Mild to moderate pain that is often described as feeling like a tight band around the head
Describe the epidemiology of tension headaches
Most common chronic daily and recurrent headache
What are 9 triggers of tension headaches?
- Stress
- Sleep deprivation
- Bad posture
- Hunger
- Eyestrain
- Anxiety/depression
- Noise
- Dehydration
- Alcohol
What is the difference between episodic and chronic tension headaches?
Episodic <15 days/month
Chronic >15 days/month (for at least 3 months)
Describe the pathophysiology of tension headaches
- Muscle ache in the frontalis, temporalis and occipitalis muscles
- Come on and resolve gradually
What is the main symptom of tension headaches?
‘Pressure behind eyes’ - no aura, vomiting or sensitivity to head movement
What is the treatment for tension headaches?
- Avoidance of triggers and stress relief
- Basic analgesia (aspirin, paracetamol, ibuprofen - avoid opioids)
- Relaxation techniques
- Hot towels to local area
What is a cluster headache?
Excruciating attacks of pain in one side of the head, often felt around the eye
Describe the epidemiology of cluster headaches
- 4 x more common in males
- Much rarer than migraines
- Typically affects adults in 20s-40s
What are 4 risk factors for cluster headaches?
- Male
- Genetics (autosomal dominant gene has a link)
- Smoker
- Alcohol
How long do cluster headaches last?
Episodic headaches, lasting from 7 days up to 1 year with pain-free periods in between that last ~4 weeks
How do cluster headaches present?
- Rapid onset of excruciating pain, classically around the eye (or temples or forehead)
- Pain is strictly unilateral and localised to one area
- Pain rises to a crescendo over a few minutes and lasts for 15-160 minutes, once or twice a day, usually around the same time of day
What are 5 ipsilateral autonomic features of cluster headaches?
- Watery and bloodshot eyes
- Facial flushing
- Rhinorrhoea (runny nose)
- Miosis
- Ptosis
What is the treatment for acute cluster headaches?
- Analgesics unhelpful
- 15L 100% O2 for 15 mins via non-rebreather mask
- Triptans e.g. sumatriptan
What is used to prevent cluster headaches?
- Verapamil (CCB - 1st line)
- Prednisolone
- Reduced alcohol consumption and stop smoking
What is trigeminal neuralgia?
Type of secondary headache causing sudden, severe facial pain
Describe the epidemiology of trigeminal neuralgia
Around 5-10% of people with multiple sclerosis have trigeminal neuralgia
What are 4 triggers for trigeminal neuralgia?
- Cold weather
- Spicy food
- Caffeine
- Citrus fruits
Describe a theory for the pathophysiology of trigeminal neuralgia
Compression of the trigeminal nerve and its branches (ophthalmic, maxillary, mandibular)
How does trigeminal neuralgia present?
- Intense facial pain that comes on spontaneously and lasts anywhere between a few second to hours
- Often described an electricity-like shooting pain
- Attacks often worsen over time
- 90% unilateral, 10% bilateral
What is the treatment for trigeminal neuralgia?
- Carbamazepine
- Surgery to decompress or intentionally damage trigeminal nerve
What is amaurosis fugax?
Temporary blockage of artery to retina resulting in loss of vision in one or both eyes
When does amaurosis fugax happen?
Can happen as a result of strokes
What is epilepsy?
The recurrent tendency to spontaneous, intermittent, abnormal electrical activity in part of the brain, manifesting in seizures
Describe the epidemiology of epilepsy
Onset is most common in the extremes of ages e.g. <20 or >60
What are 6 causes of epilepsy?
- 2/3 idiopathic, often familial
- Cortical scarring e.g. trauma, cerebrovascular disease, infection
- Tumours/space-occupying lesions
- Strokes
- Alzheimer’s
- Alcohol withdrawal
What are 4 risk factors for epilepsy?
- Family history
- Premature babies
- Abnormal cerebral blood vessels
- Drugs e.g. cocaine
Describe the pathophysiology of epilepsy
- Seizures/convulsions are motor signs of abnormal electrical discharges
- Epileptic seizures are convulsions that result directly from epileptic syndromes