Epilepsy, MS and lesions Flashcards
Tonsilitis Centor criteria
To see if antibiotics are needed
History of fever
Tonsillar exudates
No cough
Tender anterior cervical lymphadenopathy
Whats important to know in a headache
History
How rapid was the headache
Postural component
TVOs
Risk factors for sinister headaches e.g pregnancy, CVST (cavernous sinus thrombosis) risk – COCP, infection, malignancy, anaemia etc
Examination
BP
Pupils, discs, fields, EOM,
?horner’s
STAs (superficial temporal artery) – if elderly
Headache- raised intracranial pressure
- Worse in the morning, lying flat. Daily and progressive
- Papilloedema is usually associated but may be mild and missed, not invariable
Headache- idiopathic intracranial hypertension (secondary)
More common in women and usually in context of raised BMI
Typically present to opticians
Need CT and CTV, if normal, LP (lumbar puncture)
Weight loss is key to remission, about 10% of body weight
Temporary measures; Acetazolamide, topiramate, repeated LP, LP shunts (ideally avoid)
Headache- spontaneous intracranial hypotension
- Worse standing/sitting, relieved lying flat
- CSF pressure can be low (but dont need LP to diagnse)
- MRI with contrast: brain sagging (cerebellar tonsillar descent, pituitary hyperaemia, Pachymeningeal enhancement (dura and arachnoid mater)
- Usually improves on its own- bed rest, lie flat, fluids, simple analgesics. If conservative measures fail use an epidural blood patch
Headaches- Reversible Cerebral Vasoconstriction syndrome (RCVS)
Mean age ~40, female>male
Transient dysregulation of cerebral vascular tone
Multiple segments of cerebral vasoconstriction; can cause non-aneurysmal bleeds
Recurrent, thunderclap headaches
Risk factors: Post partum, cocaine, cannabis, amphetamines, nasal decongestants
Monophasic illness
Horners syndrome
Epilepsy mimic- vasovagal syncope
- Prodrome- appears pale, disorientated, tunnelling of vision, muffling of sounds, feeling faint
- Pulse may be abnormal, eyes open during event
- Seconds to minute duration
- May be incontinent of urine or have anterior tongue bight or the buccal mucosa
- Brief jerky movement
- May sweat beforehand
Vasovagal syncope causes and management
Causes- pain, unpleasant sensation, orthostatic, prolonged recumbency
Mangement- Lie flat, reassurance
Epilepsy symptoms
Tonic-clonic movement
Biting the lateral sides of the tongue
Fecal and urine incontinence
Tends to be symmetrical
Epilepsy mimics- Cardiogenic syncope
- No prodrome, sudden collapse
- Abnormal pulse
- Rapid recovery to normal consciousness without significant confusion
- Causes: arrhythmias, cardiac outflow obstruction (aortic stenosis), pulmonary hypertension
Epileptic mimics- Dissociative non epileptic attacks
- Forced eye closure, breath movement
- Bizarre movement, asynchronous.
- Changing movements during event, retained awareness
- Psychological causes
- Quite common
- Management: drug treatment isn’t helpful, psychological treatment
Seizure
Electrical discharge within the brain in the cortically based Epilepilogenic zone
Types of seizures- generalised, focal, unknown
Focal seizure
Can be aware or impaired awareness
May be motor or non-motor onset
Focal to bilateral tonic clonic
70% of focal epilepsies are from the temporal lobe, 15% are frontal
Epilepsy exams
EEG- doesnt exclude epilepsy, helps assess risk of reoccurence
ECG- in case its an arrhyhtmia (check QTc)
Observation
Basic bloods including glucose
Neurological and cardiovascular exam
Consider brain imaging i.e. head injury, neurological abnormality, Todds paresis
Epilpsy- driving and when to treat
After their first seizure, the patient cant drive for 6 months
The patient isnt scanned after one seizure but after 2 or more you scan and treat (depends on the time interval)
Risk factors for recurrent seizures
Remote symptomatic seizure
Neurological defecit
Seizure whilst asleep
Abnormal EEG
Abnormal MRI
Management of status epilepticus
Early onset 5-10 mins- Lorazepam (Benzo diazepam)
Established status 10-30mins- Valproate/ Phenytoin/ Levetiracetam
Refractory status >30 mins- Propofol/ Midazolam/ Thiopentone
Lots of epipilepsy medication is teratogenic (valproate) and shouldnt be given to anyone of child bearing age
SUDEP
Sudden unexplained death in epilepsy with no clear cause
Risk factors- male, poor compliance, generalised seizures, nocturnal seizures, LD, pregnancy
Management mainly around managing epilepsy and education/awareness
Causes of seizures
- Generalised seizures are due to global problems with the brain i.e. probably genetic
- Focal seizures are due to local problems i.e. stroke, tumour, encephalomalacia secondary to trauma
- Provoked seizures i.e. metabolic (glucose, sodium), head injuries, drugs, alcohol withdrawal
Epilepsy- definition
Predisposition to seizures
In a practical sense: > 2 seizures occurring > 24 hours apart
Status epilepticus (convulsive)-stages
Early 5-10mins of continuous seizures or recurrent seizures without recovery in between
Established 10-30mins
Refractory >30mins
Causes of recurrent seizures in epilepsy
Drug resistant epilepsy (1/3 all patients)
Non compliance
Alcohol/drugs
Sleep deprivation
Changes in AED levels e.g. pregnancy, enzyme inducing meds
Infection
Wrong diagnosis
Development of another diagnosis e.g. syncope
Medications for epilepsy
Generalised seizures- Sodium valproate, Lamotrigine, Levetiracetam
Focal seizure- Lamotrigine, Carbamazepine, Levetiracetam
Major congenital malformation and epilepsy
Major congenital malformations in normal population rate of 2%
In epilepsy without medication 2.5%
Heart defects, neural tube defects, facial clefts, hypospadias, limb disorders
Valproate= 6-30%
Lamotrigine and Levetiracetam 2.5% so safe in pregnancy
Frontal lobe lesions
Frontal lobe = responsible for motor skills, language, intellect, memory and behaviour
Lesion symptoms:
- speech impairment (Broca’s damage in the inferior frontal)
- loss of motor activity
- behavioural changes
- absence of sense of smell
Temporal lobe lesions
Temporal lobe = responsible for hearing, memory and speech
Lesion symptoms:
- memory problems
- disruption in the senses
- speech and language disorders
- behavioural changes (Wernicke’s damage in the superior temporal)
Parietal lobe lesions
Parietal lobe = responsible for somatosensory detection, pressure and pain
Lesion symptoms:
- loss of somatosensory perception
- asterognosis
- poor language development
Occipital lobe lesion
Responsible for vision
Lesion symptoms- visual changes
Dorsal column lesions
Ipsilateral loss of fine touch, vibration, and proprioception sensation (fibres decussate in the medulla oblongata)
Anterolateral system lesion
Consists of the anterior and lateral spinothalamic tract
Anterior = crude touch and pressure
Lateral= pain and temperature
Lesion therefore results in impaired pain and temperature sensation on the side contralateral to the lesion (fibres decussate within the spinal cord)
Brown-sequard syndrome
Hemisection of the spinal cord i.e. one sided lesion
Involving both the DCML and the anterolateral system
DCLM = ipsilateral loss of touch, vibration and proprioception
Anteriolateral system = contralateral loss of pain and temperature sensation
Spinocerebellar lesion
Ipsilateral loss of muscle coordination - leading to ataxia
This is because the spinocerebellar system feeds back to the cerebellum on proprioceptive information in order to aid balance and fine movement
Multiple sclerosis
An autoimmune disorder of the myelin on neurones in the CNS
Symptoms:
- tends to present in 50 year old women
- optic neuritis
- abducens nerve problems leading to internuclear opthtalmoplegia and conjugate lateral gaze disorder i.e. problems moving the eye
- focal weakness
- focal sensory problems- numbness
- ataxia
- urinary and fecal incontinence
Multiple sclerosis diagnosis and treatment
Diagnosis:
- MRI scans contributes to Mcdonalds criteria
- Lumbar puncture to see oligoclonal bands in the CSF
- Needs to fit fundamental criteria: dissemination in time (DIT) and space (DIS)
Treatment:
- methylprednisiolne in relapses
- symptomatic treatment with depression / anticholinergics / gabapentin
- ranitidine or omerazole
Huntingtons disease
Autosomal dominant condition of the nervous system due to TAG repeat i.e. a genetic mutation on the HTT gene on chromosome 4
Symptoms:
- progressive worsening cognitive, psychiatric and mood problems
- movement e.g. chorea / slow eye movement / difficulty speech and swallowing
- cognitive e.g. memory loss / learning difficulty / lack of impulse control
- psychiatric e.g. depression / fatigue / suicide / insomnia
Huntingtons diagnosis and management
Diagnosis:
- genetic testing
- MRI shows atrophy of the caudate nucleus and putamen
Management:
- no treatment
- supportive care
- medications to help manage symptoms may be antipsychotics, benzodiazepines
- life expectancy is around 15-20 yers after symptom onset
Anticipation and huntingtons disease
The disease displays ‘genetic anticipation’
This is where successive generations have more repeats in the gene
Therefore resulting in an earlier age of onset and increased severity of the disease
Motor neurone disease
Progressive and ultimately fatal condition of both upper and lower motor neurone deterioration - ALS is the most common type
Symptoms:
- middle aged man most likely
- mixed upper and lower motor neurone signs
- progressive weakness of the limbs / trunk / face
- speech problems
- increased fatigue
- foot drop
- increased clumsiness
- patients usually die of respiratory failure
Motor neurone disease- diagnosis and management
Diagnosis:
- purely clinical
Management:
- no treatment
- riluzole can slow down progression by a few months (NMDA receptor inhibitor)
- non invasive ventilation improves prognosis
ALS
Amyotrophic lateral sclerosis - most common type of motor neurone disease
Spinal = classical MND presentation
Bulbar = early tongue and bulbar insolence t
Associated with the SOD1 gene / FUS gene / C9ORF72
90% of cases are sporadic however
Other types of MND
Progressive muscular atrophy = lower motor neurone features only
Primary lateral sclerosis = upper motor neurone features only
MS classification
Primary progressive: steady progression in symptoms from onset, presents late
Relapse remitting: relapses (neurological dysfunction) with improvements (remissions)
Secondary progressive: most patients with RRMS will progress to this stage after 15 years where they are primary progressive
Clinically isolated syndrome: almost like the prequal to MS (one attack of MS). May not develop MS
Radiologically isolated syndrome: the prequal to the prequal, appears on scans. Has no symptoms of MS, may develop MS
Different types of lesions
Brainstem lesions- cause issues with cranial nerves
Spinal cord lesions- loss of pain, temperature and sphincter issues. UMN signs in their legs
Root or plexus issues= extreme pain, pins and needles
Muscle issues- no change in sensation, just muscle weakness
MS presentation
- Optic neuritis
- Brainstem events
- Spinal cord syndrome
MS presentation- brainstem events
- Diplopia, Oscillopsia (jumping images), vertigo, nausea/vomiting. Diagnosed with internuclear opthalmoplegia (INO)
- Trigeminal neuralgia (5)- pain along the face
- 6th CN palsy +/- 7th cant move eye to the side
Cause of MS
Risk factors: 30/40, female
Multifocal areas of myelin loss with axonal loss over time. Loss of myelin, axons, surrounding oedema and inflammation all lead to disability
CT
- Emits lots of x-rays (ionising radiation)
- Good bone detail
- Quick, relatively inexpensive
- Rules out major abnormalities
- Contraindications: Pregnancy, children, other recent CT or x-ray
- Contraindications for iodinated contrast: Allergy, poor renal function
MRI
- Uses magnets and radiofrequency pulses
- No ionising radiation
- Good anatomical detail, poor bone detail
- Long acquisition time (patient has to sit still for a while), expensive
- Contraindications: pacemakers, implanted defibrillators, metal implants, first trimester of pregnancy
- Gadolinium based contrast: allergy, poor renal function
Imaging in stroke: subarachnoid haemorrhage
Shortly afterwards there is a hypodense area with oedema and midline shift
Directions in CT and MRI
The left and rights are opposite
Imaging in stroke: Ischaemic stoke
- Dark (hyperdense) area
- Stroke on the right side of the brain causes left sided symptoms
- Plain CT head is first investigation in stroke
- Can take time for ischaemic stroke to appear on CT
- The blocked vessel may appear bright and wont fill with dye
Stroke- MRI
- Use diffusion weighted imaging in acute stroke
- May use MRI if unsure about diagnosis i.e. young person or woke up with stroke symptoms
- Rules in or out definitively
- Appear bright where is a strok
Types of intracranial haemorrhage
- Parenchymal: stroke
- Subarachnoid: stroke
- Subdural
- Extradural
Subarachnoid haemorrhage imaging
- In the ventricles looks grey
- Causes: burst aneurysm in the circle of willis
- Give contrast to look at vessels
- Outpouching is created with aneurysm
Imaging: subdural and extradural haemorrhage
Subdural haemorrhage: crescent (banana) shape, torn veins
Extradural haemorrhage: Rounded (egg shaped), torn middle meningeal artery
MS- imaging
MRI: for diagnosis
Flare MRI is used to darken the CSF
White fluffy areas appear around the edge of the ventricles
Seizures and visual disturbances- imaging
- CT head to rule out tumours (non-contrast)
- Give contrast if on plain CT, you see something wrong like a tumour
For visual disturbances you do a plain CT
