List risk factors for stroke
Hypertension
Diabetes
Atrial fibrillation
Smoking
Hyperlipidaemia
Sleep apnoea
Describe the different types of stroke
Ischaemic – blockage of blood vessels (85%)
Haemorrhagic – burst blood vessels (15%)
Describe the clinical presentation of large vessel stroke
- Cortical signs
> Right brain: right gaze preference, neglect
> Left brain: left gaze preference, aphasia - MCA
> Arm > leg weakness
> LMCA: aphasia
> RMCA
> Neglect
> Topographical difficulty
> Apraxia
> Constructional impairment
> Anosognosia (lack of insight - doesnt uderstand or perceive illness)
- ACA
> Leg > arm weakness, grasp
> Muteness, perseveration (stay on same thought), abulia (lack of willpower)
> Personality change - PCA
> Contralateral hemianopia
> Memory loss/confusion
> Ataxia
Describe the clinical presentation of a small vessel stroke
Lenticulostriate perforating arteries supplying deep white matter
No cortical signs
Cause sensory or motor loss, or both
Equally distributed - lacunar syndromes
Describe the clinical presentation of a posterior circulation stroke
Crossed signs
Cranial nerve findings
Headache
Describe brainstem stroke syndromes
Combination of cranial nerve abnormalities and crossed motor/sensory findings e.g.
> Double vision - diplopia
> Facial numbness or weakness (CN V)
> Slurred speech
> Difficulty swallowing
> Ataxia
> Vertigo
> Nausea and vomiting
> Hoarseness
Describe the causes of haemorrhagic strokes
- Uncontrolled hypertension
> Spontaneous rupture of a small artery deep in the brain
Typically in the basal ganglia
- Aneurysm
- Arteriovenous malformation (AVM)
Describe the acute treatment of ischaemic stroke
tPa – tissue plasminogen activator (alteplase)
> Must be used within 4.5 hours of onset
>Reduces disability risk by 30% but an ICH risk
Mechanical clot retrieval - thrombectomy
Aspirin
Double statin dose
What are the contraindications for the use of tPa
Haemorrhage
SBP > 185 or DBP > 110
Recent surgery, trauma or stroke
Coagulopathy
Seizure at onset of symptoms
NIHSS > 21
Age > 80
Glucose < 2.2
Describe the pathophysiology of MS
Idiopathic inflammatory demyelinating disease of the CNS
Acute episodes of inflammation are associated with focal neurological deficits
Demyelination results in loss of neurological function
> Weak leg
Visual loss
Urinary incontinence
Deficits usually develop gradually, last more than 24h and may gradually improve over days to weeks
MS is diagnosed when there is evidence of 2 or more episodes of demyelination disseminated in space and time
Describe the subtypes of MS
- Relapsing remitting Multiple Sclerosis (RRMS)
> Unpredictable attacks which may or may not leave permanent deficits followed by periods of remission - Primary progressive multiple sclerosis (PPMS)
> At least 1 year of disease progression
> Steady increase in disability without attacks - Secondary progressive multiple sclerosis (SPMS)
> Initial relapsing-remitting multiple sclerosis
> Suddenly begins to decline without periods of remission - Benign multiple sclerosis (BMS)
Describe the causes of MS
Genetics
Sunlight / vitamin D exposure
Viral trigger – EBV
Multifactorial – smoking
Which syndromes may develop into MS?
- Optic neuritis
> Painful visual loss that comes on after a few days
> Can resolve after a few weeks
> 30% will develop MS within 5 years, 15% within 15 year - Clinically isolated syndromes
> Single episode of neurological disability due to focal inflammation of brain or spinal cord
> Can be a first attack of MS or be due to infection
> Can include optic neuritis and transverse myelitis - Transverse myelitis
> Inflammation of the spinal cord
> Leg weakness, sensory loss, incontinence, sexual dysfunction
> Causes: MS, viral infections - Radiologically isolated syndromes
> Incidental findings that look like MS; may or may not develop MS
Describe the investigations used in MS
- MRI brain + cervical spine with gadolinium contrast
> Dawson’s finger: radiographic feature of demyelination, reflects perivenular inflammation
> Evidence of demyelination in 2 regions e.g. periventricular and spinal cord - dissemination in space
> If enhancing and non-enhancing areas of demyelination – dissemination in time
- Lumbar puncture
> Oligoclonal bands in CSF - Bloods (exclude other conditions)
> B12/folate
> Serum ACE (sarcoidosis)
> HIV, Lyme and syphilis serology
> ESR/CRP
> ANA/ANCA/RF
> Aquaporin-4 antibodies: if transverse myelitis / optic neuritis
> Calcium (sarcoidosis) - Visual evoked potentials
> Measure conduction of nerve signals in optic nerve to identify subclinical optic neuritis
What is the definition of a relapse and a pseudorelapse in MS?
Relapse
> New neurological deficit lasting >24h in the absence of pyrexia or infection
Pseudo-relapse
> Reemergence of previous neurological symptoms or signs related to an old area of demyelination in the context of heat or infection
What is the steroid regime for an MS relapse?
1g of IV methylprednisolone for 3 days OR
500mg of oral methylprednisolone for 5 days and
PPI for gastroprotection
Describe treatments for MS
RRMS
> Alemtuzumab
> Natalizumab
> Anti-CD20: ocrelizumab, ofatumumab, rituximab
> Fingolimod
> Dimethyl fumarate
> Cladribine
> Stem cell transplants
Progressive MS
> PPMS - ocrelizumab
> SPMS - siponimod
Describe a relative afferent pupillary defect (RAPD) and its causes
Aka Marcus Gunn Pupil
Pupil remains dilated in one eye despite exposure to bright light – swinging light test
Shows unilateral optic nerve or retinal dysfunction
Causes
- Disease of retina
> Retinal detachment
> > Floaters
Flashes of light
Shadow in vision field
> Retinal ischaemia
- Optic nerve disease
> Optic neuritis
> > Pain with eye movement
Loss of vision
> Inflammation from multiple sclerosis
- Severe glaucoma
> Headaches
Nausea/vomiting
Eye redness
Blurred vision
- Trauma
List the different types of primary and secondary headaches
Primary
- Migraine
- Tension headaches
- Trigeminal autonomic cephalgias
Secondary
- Thunderclap headaches
- High pressure headaches
- Low pressure headaches
- Neuralgias
Describe tension type headaches
At least 10 episodes of headache occuring on <1 day/month on average
Lasting from 30 minutes to 7 days
Characteristics
> Bilateral location
> Pressing or tightening (non-pulsating) quality
> Mild or moderate intensity
> Not aggravated by routine physical activity
> No nausea or vomiting
> No more than one of photophobia or phonophobia
Describe the pathophysiology of migraine
Interaction between primary afferent nociceptive neurons / trigeminovascular system / brainstem / thalamus / hypothalamus / cortex
Calcitonin gene related peptide (CGRP)
Not a primary vascular problem
Describe the diagnostic criteria for migraine
At least 5 attacks
Headache attacks lasting 4-72h when untreated
Characteristics
- Unilateral location
- Pulsating quality
- Moderate or severe pain intensity
- Aggravated by routine physical activity
At least one of the following
- Nausea and/or vomiting
- Photophobia and phonophobia
Describe the phases of migraine
Prodrome: hours-days
- Yawning
- Polyuria
- Depression
- Irritability
- Food cravings
- Poor concentration
- Sensitivity to light and sound
- Poor sleep
Aura: 5-60m
- Visual
- Sensory
- Language
- Motor
Headache: 4-72h
- Throbbing headache
- Nausea
- Vomiting
- Photophonophobia
- Worse with activity
Postdrome: 24-48h
- Depression
- Euphoria
- Poor concentration
- Fatigue
Describe the acute treatment of migraine
Avoid opiates
Simple analgesics – aspirin 900mg or ibuprofen 400-600mg
Triptans
> Sumatriptan 50-100mg
> All oral triptans are gastrically absorbed – may not work if patient is vomiting
> Only work once headache starts
Early or persistent vomiting
> Add antiemetic – metoclopramide 10mg or prochlorperazine 10mg
> Consider nasal zolmitriptan or subcutaneous sumatriptan
No response
> Try other triptans OR triptan + NSAID
Describe migraine prophylaxis
Lifestyle advice, triggers
Prophylaxis if >4-5 disabling headaches per month
Use headache diaries
For each medication, determine efficacy at 3 months
> If ineffective, wean medication and try another one
> If effective, continue 6-12 months
Agents
> Propranolol
> Topiramate
> Amitriptyline
> Candesartan
> Flunarazine
Describe the treatment of refractory or chronic migraine
Onabotulinumtoxin A
> Chronic migraine
>15 headache days per month
MOH previously addressed
Failed on at least 3 prophylactics
CGRP inhibitors – monoclonal antibodies
> Erenumab
Describe cluster headaches
At least 5 attacks
Severe or very severe unilateral orbital, supraorbital and/or temporal pain lasting 15-180 minutes when untreated
Signs ipsilateral to the headache
> Conjunctival injection or lacrimation
> Nasal congestion or rhinorrhoea
> Eyelid oedema
> Forehead and facial sweating
> Forehead and facial flushing
> Sensation of fullness in the ear
> Miosis or ptosis
Sense of restlessness or agitation
Occurring with a frequency between one every other day and 8 per day
Describe trigeminal neuralgia including its treatment
One-sided intense, stabbing paroxysmal facial pain
Triggered by wind, chewing, touch
Other symptoms
- Facial muscle spasms
- Autonomic symptoms
> Lacrimation
> Diffuse conjunctival injection
> Rhinorrhoea
Investigations
> MRI
> Trigeminal nerve distorted and compressed by superior cerebellar artery
Treatment
> Carbamazepine
> Surgical microvascular decompression
Describe raised pressure headaches
Characteristics
> Worse on lying flat
> Improve on sitting up
> Worse in the morning
> Persistent nausea/vomiting
> Worse on valsalva e.g. coughing, laughing, straining
> Worse with physical exertion
> Transient visual obscurations with change in posture
Examination findings
> Optic disc swelling – papilloedema
> Impaired visual acuity / colour vision
> Restricted visual fields / enlarged blind spot
> IIIrd nerve palsy
> VIth nerve palsy – false localising sign
> Focal neurological signs
Describe thunderclap headache including causes
First and worst headache – subarachnoid haemorrhage
Severe sudden onset headache
Typically maximum onset within 1 minute, typical duration >1h
Medical emergency, same day specialist assessment
Non-contrast CT scan (NCCT) within 12h onset
> If CT normal, lumbar puncture
> For blood products – oxybilirubin
If CT/LP normal consider other investigations
> MRI
> MR/CT venogram
> MR/CT angiogram
Causes
- Subarachnoid haemorrhage
- Intracerebral haemorrhage
- Aortic dissection – vertebral or carotid
- Cerebral venous sinus thrombosis
- Ischaemic stroke
- Bacterial meningitis
- Spontaneous intracranial hypotension
- Pituitary apoplexy
Describe the course, tract and pathology associated with the olfactory nerve
Smell
Course
> Travels through the ethmoid bone and lays upon the cribriform plate
> Arises from the cerebrum
Tract
> Olfactory cells of nasal mucosa
> Olfactory bulbs
> Pyriform cortex – temporal lobe, near hippocampus
Pathology
> Hyposmia
> Normal ageing
> Viral URTI
> Chronic rhinitis or sinusitis
> Head trauma
> Neurodegenerative disorders – Parkinson’s, Alzheimer’s
Describe the function and tract associated with the optic nerve
Vision
Enter: optic canal
Arises from the cerebrum
Tract
> Retinal ganglion cells
> Optic chiasm
> Thalamus
> Primary visual cortex – occipital lobe
Describe the examination of the optic nerve
Optic discs with ophthalmoscope
> Papilloedema: raised ICP
> Optic atrophy: previous optic neuritis
Pupillary reflexes
> Direct and consensual light reflexes
> Swinging light test for RAPD
> Accommodation reflex
Visual acuity - Snellen chart
Visual fields and blind spot: confrontation
Colour vision: Ishihara colour plates
Describe the physiology of the pupillary light reflex
Light is shone into the the left eye and the travels via the optic tract and synapses at the pretectal nucleus
Interneurones then synapse with both Edinger-Westphal nuclei
Post-ganglionic fibres run with ciliary nerves and terminate on sphincter pupillae
Pupillary constriction in both eyes (direct and indirect) when a light is shone in one
Describe different types of visual field defects
Optic - ipsilateral monocular visual loss
Optic chiasm - bitemporal hemianopia
Optic tract - contralateral homonymous (affecting both visual fields) hemianopia
Parietal upper optic radiation - contralateral homonymous inferior quadrantanopia
Temporal lower optic radiation - contralateral homonymous superior quadrantanopia
Occipital visual cortex - contralateral homonymous hemianopia (macular sparing)
Most common tumours impacting anterior visual pathways
> Pituitary adenoma
> Meningioma
> Craniopharyngioma
Describe eye muscles and movements associated with them, as well as their assessment
Assessment – smooth pursuit – draw H shape in the air
Oculomotor nerve
> Superior rectus
> Elevation of eyeball
> Also adduction and medial rotation
> Inferior rectus
> Depression of eyeball
> Abduction and lateral rotation
> Medial rectus
> Adducts the eyeball
> Lateral rectus
> Abducts the eyeball
> Inferior oblique
> Elevation of the eyeball
> Abduction and lateral rotation
Trochlear nerve
> Superior oblique
> Depression of eyeball
> Abduction and medial rotation
> Abducens nerve
> Lateral rectus
Describe the function and tract of the oculomotor nerve
Eye movements
> Inferior oblique
> Superior, medial and inferior rectus
Levator palpebrae superioris – keeps upper eyelid open
Lens accommodation: ciliary muscles
Pupil constriction - parasympathetic
> Ciliary muscles and sphincter pupillae
Arises from the midbrain-pontine junction
Nucleus
> Motor
> Located in the midbrain at the level of the superior colliculus
> Parasympathetic
> Dorsal midbrain – Edinger Westphal nucleus
Exit: superior orbital fissure
> Exits brainstem from the interpeduncular fossa of the midbrain
> Passes through cavernous sinus
> Enters orbit through superior orbital fissure
Describe complete 3rd nerve palsy
Ptosis
Pupillary dilatation
Eye in a “down and out” position
Due to unopposed actions of lateral rectus and superior oblique
Describe the function and location of the trochlear nerve
Eye movements - superior oblique
Arises from the midbrain
> Level of inferior colliculus
Exit: superior orbital fissure
Describe the function of the trigeminal nerve and its location
Arises from pons
3 branches
- V1 - ophthalmic nerve
> Branches
> Supraorbital nerve
> Nasociliary nerve
> Ciliary branches supply the cornea
> Exit: superior orbital fissure
> Enter: supraorbital foramen
- V2 - maxillary nerve
> Exit: foramen rotundum
Enter: infraorbital foramen
- V3 - mandibular nerve
> Exit: foramen ovale
> V3 meningeal branch exits through foramen spinosum
> Enter: mental foramen
> Muscles of mastication:
> Temporalis
> Masseter
> Pterygoids
> Motor to muscles of mastication and general sensory to face
Describe the function and location of the abducens nerve
Eye movement (abduction - lateral rectus)
Arises from the pontine-medulla junction
Exit: superior orbital fissure
Describe the function and location of the facial nerve
Muscles of facial expression
> Frontalis
> Orbicularis occuli
> Orbicularis oris
Supplies secretory glands
> Sublingual & submandibular glands
> Lacrimal glands
Supplies taste of anterior 2/3 of the tongue
Corneal reflex
> Lightly touch cornea with cotton wool
> Afferent – CN V
> Efferent – CN VII
> Normal response is blinking
> May be lost in pontine lesions
Arises from the pontine-medulla junction
Enter: internal acoustic meatus
Exit: stylomastoid foramen
Describe the location and function of the vestibulocochlear nerve
Arises from the pontine-medulla junction
2 nerves
> Vestibular nerve - balance
> Nerve endings within semicircular canals
> Reach cerebellum and spinal cord
> Cochlear nerve - hearing
Reaches auditory cortex in the temporal lobes
Enter: internal acoustic meatus
Describe the testing of the vestibulocochlear nerve
Rinne’s test
> Tuning fork is held at the mastoid process and then at the external auditory meatus
> Patient is asked which is louder
BC > AC – conductive deafness
AC > BC – normal or sensorineural deafness
Weber’s test
> Tuning fork is held at the vertex
Patient is asked which ear they hear the vibration loudest in
Normal – same in both ears
Conductive hearing loss – deaf ear
Sensorineural hearing loss – good ear
Describe the function and location of the glossopharyngeal nerve
Sensory
> Taste – posterior 1/3 of tongue
> Proprioception for swallowing – pharyngeal wall
> Blood pressure receptors – carotid sinuses
Motor
> Swallow and gag reflex – pharyngeal muscles
> Lacrimation – lacrimal glands
Parasympathetic
> Saliva production – parotid glands
Originates from the medulla, posterior to the olive
Exit: jugular foramen
How is the glossopharyngeal nerve tested?
Motor
Ask patient to open mouth and say “ahh”
Watch for elevation of the soft palate
Unilateral weakness of CN IX – deviation of uvula away from the lesion – glossopharyngeal palsy
Describe the function and location of the vagus nerve
Sensory
> Chemoreceptors
> Blood oxygen concentration
> Carotid bodies
> Pain receptors (dura)
> Respiratory and digestive tracts
> Sensation
> External ear, larynx and pharynx
Motor
> Heart rate and stroke volume
> Pacemaker and ventricular muscles
> Peristalsis
> Smooth muscles of the digestive tract
> Air flow
> Smooth muscles in bronchial tubes
> Speech and swallowing
> Muscles of larynx and pharynx – recurrent laryngeal nerve
Parasympathetic
> Smooth muscles and glands of the same area innervated by the motor component, as well as thoracic and abdominal areas
Exit: jugular foramen
Describe the function and location of the spinal accessory nerve
Exit: jugular foramen
Neck muscles
- Sternocleidomastoid
- Trapezius
Head rotation and shoulder shrugging
Originates from medulla, posterior to the olive
Describe the location and function of the hypoglossal nerve
Motor – speech and swallowing
> Muscles of the tongue
Originates from medulla, anterior to the olive
Exit: hypoglossal canal
Describe a hypoglossal nerve palsy
Observe the tongue at rest and ask patient to stick out their tongue & move it from side to side
Unilateral/bilateral wasting or fasciculations (at rest)
Unilateral XIIth weakness causes the tongue to deviate towards the side of the lesion
Slow and spastic tongue movements suggest pseudobulbar palsy
Describe internuclear ophthalmoplegia
Disorder of conjugate gaze
Failure of adduction of affected eye with nystagmus on lateral gaze in contralateral eye
Can be unilateral or bilateral
Results from lesion of medial longitudinal fasciculus – connects IIIrd and VIth nerve nuclei
Commonly seen in multiple sclerosis (MS)
Describe Horner’s syndrome and its causes
Ipsilateral disruption of cervical / thoracic sympathetic chain
Causes
> Congenital
> Brainstem stroke
> Cluster headache
> Apical lung tumour
> Multiple sclerosis
> Carotid artery dissection
> Cervical rib
> Syringomyelia
Consists of
> Miosis
> Ptosis
> Apparent enophthalmos
> Anhydrosis
Describe herpes zoster ophthalmicus
Pain may precede vesicles
Shingles affects ophthalmic division of trigeminal nerve
> V2/V3 rarely affected
Elderly and immunocompromised at risk
Treated with oral aciclovir
Describe the radiological appearance of different types of brain haemorrhages
Extradural
- Lenticular or “lens” shape - between dura and bone
Subdural
- Scalloped appearance; can have layers depending on freshness of bleed
Subarachnoid
- Blood between sulci
Describe Denis’ 3 columns of spinal injury
To determine spinal stability: if 1 or more affected, unstable
Anterior
> Anterior longitudinal ligament
> Anterior annulus
> Anterior 2/3 vertebral body
Middle column
> Posterior 1/3 vertebral body
> Posterior annulus
> Posterior longitudinal ligament
Posterior column
> Posterior elements: pedicles, facets, laminae, spinous process
> Posterior ligaments
Describe the functions of the different lobes of the brain
Frontal lobe
> Emotions
Mood
Insight
Cognitive and creative function
Primary motor area separated from parietal lobe by central sulcus
Parietal lobe
> Sensation
Coordination of signals from other cortices
Primary sensory area separated from frontal lobe by central sulcus
Occipital lobe
> Vision
Temporal lobe
> Memory
Gustatory function
Smell
Hearing
List the components of the basal ganglia
Basal ganglia
> Caudate nucleus
> Striatum
> Globus pallidus externa and interna
> Substantia nigra pars compacta and pars reticulata
> Subthalamic nucleus
Describe the anatomy of the ventricular system
Lateral two ventricles
> Each one has a
» Frontal horn
» Temporal horn
» Occipital horn
> Come close together in the midline but are separated by the septum pellucidum
> Connect with third ventricle via interventricular foramina of Munro
3rd ventricle
> Narrow space lying in the diencephalon between thalamus and hypothalamus
> Connects to 4th ventricle via aqueduct of Sylvius (midbrain)
4th ventricle
> Lies in the posterior fossa between brainstem and cerebellum
> Communicates with subarachnoid space via lateral foramina of Luschka and median aperture of Magendie
Most CSF produced by choroid plexus in lateral ventricle, some in 4th ventricles
Lis the functions of the CSF
Cushions brain against impact/movement and own weight
Provides stable chemical environment for brain
Nutrient & waste exchange between nervous tissue and blood
Describe the flow of CSF through the ventricular system
Fills lateral ventricles then flows centrally (third ventricle) via the intraventricular foramen of Munro
Then, CSF flows through aqueduct of midbrain and opens up into fourth ventricle
4th ventricle is anterior to the cerebellum and posterior to the pons
Resorbed into venous system via arachnoid granulations
Presence of blood in CSF indicates subarachnoid haemorrhage
Describe the areas if the brain responsible for speech and comprehension
Wernicke’s area – hearing and understanding speech
> Receptive dysphasia
Broca’s area – speech production
> Expressive dysphasia
Connected via the arcuate fasciculus
Describe the anatomy of the spinal cord
- Cervical enlargement
- Lumbosacral enlargement
- Cone-shaped ending of spinal cord - conus medullaris
- End of spinal cord L1/L2 - filum terminale
- Cauda equina - free nerves
List the different sensory and motor tract
Light touch, vibration, proprioception – dorsal column medial lemniscal pathway
Pain, temperature – spinothalamic tract
Corticospinal tract - motor tracts
> Fasciculus gracilis - lower limb
> Fasciculus cuneatus - upper limb
Describe patterns of sensory loss
Generalised peripheral neuropathy – glove and stocking distribution
Specific sensory roots – dermatomal distribution
Single dorsal column lesion – unilateral distribution below level of injury
Transverse thoracic spinal cord lesion – bilateral distribution below level of injury
Unilateral cord lesion (Brown Sequard): ipsilateral loss of light touch and vibration, contralateral loss of pain sensation
Central cord lesion: arm and chest distribution
Mid-brainstem lesion: ipsilateral loss of sensation in face, contralateral loss of sensation in body
Hemisphere (thalamic) lesion: ipsilateral loss of sensation in face and body
Describe the knee jerk reflex
Striking the patellar tendon causes stretching of the quadriceps muscle
Afferent signal sent through sensory neurons up through dorsal root ganglion
Enters dorsal horn, synapse onto motor neuron
Efferent signal causes contraction of quadriceps
Afferent signal also works through interneuron to have an inhibitory effect on motor neuron going to hamstring
Relaxation of hamstrings
Sensory neuron involved in reflex arc also synapses with an inhibitory interneuron
This neuron synapses ipsilaterally with a motor neuron controlling antagonistic muscles
Antagonistic muscles are relaxed, resulting in contraction of other muscle group - reciprocal innervation
Describe the reinforcement of reflexes
Jendrassik manoeuvre - teeth clenching or pulling interlinked fingers in opposite directions
Combination of distraction and cortical inhibition from anterior horn cells
List the root levels for each reflex
Jaw jerk - cranial nerve V
Biceps - C5/6
Tricep C6/7
Supinator C5/6
Knee L3/4
Ankle S1
Describe the differences between upper and lower motor neuron problems
Upper motor neuron
> Increased / “brisk”
> Localises to brain or spinal cord
> Associated with
> Increased tone
> Extensor plantar response
Lower motor neuron
> Decreased or absent
> Localises to peripheral nerve
> Associated with
> Normal or decreased tone
> “Mute” or flexor plantar response
Describe subarachnoid haemorrhage and its causes and predisposing factors
Blood vessels reside in the subarachnoid space
Aneurysms rupture into the subarachnoid space, producing a subarachnoid haemorrhage – acute cerebrovascular event
Other causes
> Arteriovenous malformation (AVM)
> Tumour
Predisposing factors
> Smoking
> Female sex
> Hypertension
> Positive family history
> ADPCK
> Ehlers-Danlos
> Coarctation of the aorta
Describe the diagnosis of subarachnoid haemorrhage
History
> Acute headache
Loss of consciousness
Seizures
Visual, speech and limb disturbance
Sentinel headache
Clinical examination
> Photophobia
Meningism
Subhyaloid haemorrhages
Vitreous haemorrhages – Terson’s syndrome
Speech and limb disturbance
Cardiovascular problems e.g. pulmonary oedema
Describe the grading system used to grade the severity of subarachnoid haemorrhage
Grade I – GCS 15
Grade II – GCS 13-14 without deficit
Grade III – GCS 13-14 with deficit
Grade IV – GCS 7-12
Grade V – GCS 3-6
Describe the investigations used for subarachnoid haemorrhage
CT
> Prognostic: Fisher grade
> Based on the amount of bleeding on CT
LP
> Xanthochromia – yellowing of CSF due to bilirubin (takes 8-12h)
Further investigations
> CTA – eGFR
> MRA – eGFR and gadolinium
> DSA (digital subtraction angiography) – stroke, diabetics
Other
> U&Es – hyponatraemia
> ECG changes
> Elevated troponin
> Echocardiography – Takotsubo cardiomyopathy
Describe the management of subarachnoid haemorrhage
Resuscitation
> Bed rest
> Fluids: 2.5-3.0L normal saline
> Anti-embolic stockings
Nimodipine: calcium channel antagonist
> Prevents delayed ischaemic neurological deficit
Analgesia
Doppler studies
Management
> Endovascular – coils & other devices
> Surgical clipping – early v late
> Conservative
List the complications of subarachnoid haemorrhage
Rehaemorrhage
Delayed ischaemia
Hydrocephalus
Hyponatraemia
> Cerebral salt wasting syndrome (CSW)
> SIADH
Cardiovascular problems
> Stunned myocardium
> Elevation of troponin
> Arrhythmia
> Wall motion abnormalities
> Sudden death
> LVF - Takotsubo cardiomyopathy
Seizures
DVT/PE
LRTI, UTI
Describe cerebral salt wasting syndrome (CSW)
Patients excrete large quantities of sodium and consequently fluid
Intravascular volume depleted
Important to establish volume status
Give hypertonic saline + fludrocortisone
Describe Takotsubo cardiomyopathy
Apical wall hypokinesis – apex of myocardium fails to contract
Associated with development of left ventricular dysfunction and pulmonary oedema
Usually self-resolving
Describe the motor features seen in Parkinson’s disease
Unilateral pill-rolling tremor
> 4-6 Hz rest tremor
> Becomes bilateral as disease progresses
Postural instability
Rigidity – increased tone, “cogwheel rigidity”
Bradykinesia
> Slowness in initiation of voluntary movement
> Progressive reduction in speed and amplitude of repetitive action
List non-motor symptoms of Parkinson’s disease
Dementia
Depression, anxiety
Urinary urgency / nocturia, constipation
Erectile dysfunction
Excessive salivation
Low BP / postural hypotension
Speech difficulties
Hallucinations and delusions
Seborrheoic dermatitis / sweating
REM sleep behaviour disorder
Restless leg syndrome
Reduced olfactory function
Fatigue / daytime somnolence
Pain and sensory symptoms
Describe causes of parkinsonism
Drug-induced
> Dopamine antagonists
Progressive supranuclear palsy (PSP)
> Also cognitive impairment, axial stiffness and difficulty with vertical gaze
Multi systems atrophy (MSA)
> Cerebellar dysfunction & autonomic dysfunction
> Prominent bowel, bladder and BP difficulties
Corticobasal disease (CBD)
> One-sided symptoms and dystonia in affected area
Lewy body dementia
> Visual hallucinations, fluctuations in cognition
Vascular parkinsonism
> Microvascular changes within basal ganglia give rise to lower body parkinsonism
> Leads to gait difficulties, UMN signs
> Does not affect speech, swallowing, upper limbs
List the different drug types used in Parkinson’s disease
- L-dopa
- Dopamine agonists
- MAO-B inhibitors
- COMT inhibitors
- Amantadine
- Anticholinergics
- Botulinum toxin
Describe the use of L-dopa in the management of Parkinson’s disease including adverse effects
L-dopa + carbidopa – Sinemet
L-dopa + benserazide - Madopar
Dosing: 200-1000mg/day across 3-5 doses
Adverse effects
- Peripheral
> Nausea, vomiting
> Postural hypotension - Central
> Confusion
> Hallucinations
Describe the use of dopamine agonists in the management of Parkinson’s disease including side effects
Bind to post-synaptic dopamine receptor
Make patient more sensitive to endogenous dopamine
Ropinirole, pramipexoxle, rotigotine, apomorphine
Longer half-life than L-dopa but less effective
Can be prescribed as monotherapy in early disease or adjunct later
Side-effects
> Fewer motor complications than L-dopa
> Dopaminergic side effects
> Daytime somnolence
> Impulse control disorders – pathological gambling, hypersexuality
Give examples of MAO-B inhibitors
Selegiline, rasagiline
Can be prescribed as monotherapy in early disease or adjunct later
Give examples of COMT inhibitors
Entacapone, opicapone
Results in longer L-dopa half-life / duration of action
Slow breakdown of Levodopa peripherally
Co-prescribed with L-dopa
Side-effects
> Dopaminergic side-effects
> Diarrhoea
Describe the use of amantadine, anticholinergics and botulinum toxin in the management of Parkinson’s disease
Amantadine
> Anti-dyskinetic effects
> Side-effects: confusion and livedo reticularis
Anticholinergics
> Trihexyphenidyl, orphenadrine, procyclidine
> Prescribed for anti-tremor effect
> Side-effects
> Confusion
> Urinary retention
> Blurred vision
> Dry mouth
Botulinum toxin
> Roles in sialorrhoea, blepharospasm / eyelid-opening apraxia, other focal dystonia
Describe problems seen in advanced Parkinson’s disease
Motor
> On/off fluctuations
> L-dopa-induced dyskinesia
Axial
> Gait difficulties – including gait freezing
> Change in posture
> Poor balance / falls
> Speech / swallowing difficulties
Cognitive
> Dementia
> Hallucinations / psychosis
Describe alternative treatments for advanced Parkinson’s disease
Apomorphine pen injection or subcutaneous pump
Intrajejunal duodopa infusion
Deep brain stimulation (DBS) surgery
> Allows electrical stimulation of subthalamic nucleus
> Targeted, adjustable, non-destructive and reversible way of modulating pathological brain circuits
> 3 implantable components
» Brain leads – electrodes at distal end
» Neurostimulator – implantable pulse generator (IPG)
» Extension wires
Describe Parkinson’s disease emergencies
Motor
> Severe OFF periods / severe dyskinesia
> Parkinson-hyperpyrexia syndrome
> High temperature
> Muscle stiffness
> High CK
> Can cause renal failure
> Triggered by sudden reduction in Parkinson’s medications – rare complication
Non-motor
> Acute psychosis
Impulsivity
Dopamine dysregulation (excessive L-dopa)
Dysautonomia
> Postural hypotension
> Dysphagia
> Intestinal pseudo-obstruction
Falls
Device-related - DBS ; apomorphine pump
Outline causes of loss of consciousness
Faints – lack of blood to the brain
Fits – electrical discharge
Other
> Metabolic cause
> Psychiatric / psychological
> Trauma
Describe a seizure including the different phases
A seizure is a sustained and synchronised electrical discharge in the brain causing symptoms or signs
Phases
> PDS – large and prolonged depolarisation with generation of action potential spikes
> At onset of PDS, AMPA channel opens
> Na+ enters cell triggering depolarisation
> NMDA channel then opens
> Allows Na+ and Ca+ entry
> > Following depolarisation, there is opening of the potassium channels and activation of GABA channels with Cl- entering the cell
> > Both influx of Cl- and efflux of K+ lead to hyperpolarisation of the cell
> Tonic phase – very frequent discharges, muscles are stiff
> Clonic phase – discharges come in clusters and reduce in frequency
Describe the excitatory and inhibitory firing of neurons
Excitation
> EAA
> Action on NMDA / AMPA / Kainate
> Na+ / Ca2+ influx
Inhibition
> GABA/glycine
> Action on GABA-R
> Cl- influx
Describe the different types of seizure
Tonic seizure
> Short-lived, <1 minute
> Abrupt
> Generalised muscle stiffening with rapid recovery
Generalised tonic-clonic seizure
> Bilaterally convulsive
> Generalised stiffening
> Subsequent rhythmic jerking of the limbs
> Urinary incontinence
> Tongue biting
Absence seizure
> Behavioural arrest
> Formerly called petit mal seizures
> Brief loss of awareness / responsiveness / blank stare
> Sudden onset / termination - usually no post-ictal state
> Most common in children, 50-100 / day
Atonic seizure
> Sudden onset of loss of muscle tone
Myoclonic seizure
> Brief, ‘shock-like’ involuntary single or multiple jerks
Partial seizures (aka focal seizures)
> With loss of awareness
> With motor phenomena
> With sensory phenomena
> With psychological phenomena
> With cognitive phenomena
Describe the causes and classification of epilepsy
Causes
> Unknown
> Vascular
> Hippocampal sclerosis
> Infection
> Trauma
> Other
> MCD
> Tumour
> Degenerative
Classification
> Focal epilepsy – localised onset
> Genetic generalised – generalised onset
> Uncertain
Describe the management of status epilepticus
If seizure is not self-limiting and carries on
> Initial therapy
> Benzodiazepine
> IV lorazepam
> IV/rectal diazepam
> Buccal midazolam
Treat potential cause
> IV glucose if hypoglycaemia
> IV thiamine if alcohol abuse
If seizure continues for further 5 minutes
> Repeat benzodiazepine dosing
> Administer usual AEDs where necessary
If seizure continues
> IV phenytoin or valproate
If seizure continues
> ITU admission
> Sedation with general anaesthetic
Describe the long-term treatment of epilepsy
Sodium channel blockers
> Reducing pre-synaptic excitability and the ability of action potentials to spread
> Carbamazepine, oxcarbazepine, phenytoin, lamotrigine
SV2A antagonists
> SV2A required for release of neurotransmitter from vesicles
> Inhibited by levetiracetam
N-type calcium channel blocker
> Calcium influx drives neurotransmitter release
> Channel inhibited by pregabalin and gabapentin
> The response of the GABAA receptor to GABA is enhanced by benzodiazepines, barbiturates, felbamate, topiramate
GABA levels are increased by other AEDs
> Tiagabine inhibits the GABA transporter
> Vigabatrin inhibits GABA transaminase (GABAT)
> Felbamate has action on Glu receptors, but its primary mode of action is via inhibition of voltage-gated Na+ channels and some action on GABA transmission
> Topiramate also targets Glu receptors as part of a mixed mode of action, but its primary target is thought to be inhibition of voltage-gated Na+ (and Ca2+)
Describe the structural organisation of a peripheral nerve
Fasciculi
- Each fascicle is a bundle of axons from individual cells
- Surrounded by perineurium
Epineurium
- Surrounds peripheral nerve
- Tough connective tissue
Describe the different types of nerve fibres
Large fibres (myelinated)
> Motor nerves
> Proprioception, light touch and vibration
Thinly myelinated fibres
> Light, touch and temperature
Small fibres (unmyelinated)
> Light touch, pain and temperature
Describe length-dependent axonal neuropathy
Diffuse involvement of peripheral nerves
> Age > 50 years
> Length dependent - starts in toes / feet
> Symmetrical, slowly progressive
> No significant sensory ataxia
> Any weakness is distal and mild
Causes
> Diabetes
> Alcohol
> Nutritional - folate / B12 / thiamine / B6 deficiency
> Immune-mediated: RA, lupus, vasculitis, polyarteritis nodosa
> Metabolic / endocrine
> Renal failure
> Hypothyroidism
> Drugs: isoniazid, cisplatin, amiodarone, gold
> Infectious: HIV, Hep B & C
> Inherited: Charcot-Marie-Tooth, Hereditary neuropathy with liability to pressure palsy (HNPP)
> Neoplastic : myeloma
> Paraneoplastic
> Critical illness
Describe Guillain-Barre syndrome
Acute inflammatory demyelinating neuropathy
Post-infectious autoimmune aetiology
> Campylobacter
> CMV
> EBV
Progressive ascending weakness over days
Flaccid quadriparesis with areflexia
Can have respiratory / bulbar / autonomic involvement
Treatment - IV immunoglobulin or apheresis
CIDP – chronic form
> Steroid and IVIG responsive
Describe nerve conduction studies
Axonal v demyelinating motor studies
Axonal – CMAP is half of the size of a normal curve
Demyelinating
> Normal size but delayed conduction
> OR conduction block with temporal dispersion
» Area under the curve is the same but slower and takes longer to peak
Describe mononeuritis multiplex
Sequential or simultaneous development of neuropathy in 2 or more nerves
Describes a cluster of conditions
Most commonly affects
> Common peroneal
> Weak ankle dorsiflexion
> Sensory disturbance lateral aspect of calf and foot
> Radial
> Wrist / finger drop
> Sensory disturbance – dorsum of hand
> Axillary
> Weakness of shoulder abduction
> Badge of sensory disturbance – inferior deltoid
> Median
> LOAF weakness
> Sensory disturbance
> Femoral
> Weak hip flexion and knee extension
> Sensory disturbance lateral calf and dorsum of foot
Common causes
> Diabetes
Vasculitic – Churg Strauss, polyarteritis nodosa
Rheumatological – RA, lupus, Sjogren’s
Infective – Hep C, HIV
Sarcoidosis
Lymphoma
Investigations
> History and examination
> Nerve conduction studies and EMG
> MRI of plexus with contrast
> LP
Management
> Treat underlying cause
> Symptoms may be irreversible
List muscular dystrophies
- Duchenne and Becker Muscular Dystrophy
- Emery-Dreifus type
- Limb girdle type
- Fascioscapulohumeral type
- Oculopharyngeal type
Describe myasthenia gravis
Pathogenesis
> Autoimmune disorder
> Antibodies to acetylcholine receptor at post-synaptic NMJ
> Association with other autoimmune disorders
> May be associated with thymic hyperplasia or thymoma
Affects young women in 20s and older men in 70s
Signs and symptoms
> Fatiguable weakness of ocular, bulbar, neck, respiratory and/or limb muscles
Investigations
> Antibodies to AChR present in 85%
> Single fibre EMG and repetitive nerve stimulation abnormal
Management
> Pyridostigmine - Anti-acetylcholinesterase
> Immunosuppressive therapies: steroids, IV immunoglobulin
Give examples of cognitive functions which may be affected in dementia
Memory
> Repetitive questions or conversations
> Misplacing personal belongings
> Forgetting events or appointments
> Getting lost on a familiar route
Executive function
> Poor understanding of safety risks
> Inability to manage finances
> Poor decision-making ability
> Inability to plan complex or sequential activities
Visuospatial
> Inability to recognise faces or common objects
> Inability to find objects in direct view despite good acuity
> Inability to operate simple implements or orient clothing to body
Language
> Difficulty thinking of common words while speaking
> Hesitation
> Speech, spelling and writing errors
Give examples of bedside cognitive assessments
Folstein MMSE (30)
Addenbrookes Cognitive Examination (100)
> 4 domains
» Executive function
» Memory
» Language
» Visuospatial
Describe the areas of the brain responsible for executive function
Behaviour
> Orbitofrontal
> Obeying and recognising social cues
> Appropriate behaviour
Attention / working memory
> Dorsolateral prefrontal cortex
Motivation / goal-driven
> Anterior cingulate
Describe the areas of the brain responsible for visual processing and how to test this
Ventral stream
> Object recognition – visual agnosia
> Facial recognition – prosopagnosia
Dorsal stream
> Position of object in space – dyspraxia
Testing ACE-r
> Pentagons
> Cubes
> 3D letters
> Dots counting
Describe attention and how it is tested
Component of consciousness which allows filtering of information to allow one to focus on a particular stimuli
Essential for all aspects of cognition
Pathological process – delirium (or anxiety/depression)
Testing
> ACEr
> Orientation e.g. what is the day/month/year, spell WORLD backwards
> Serial 7s
> Trail making (trails B) - learning and understanding rules
> Proverbs
> Verbal fluency
> Estimates
> Planning
Describe pathological processes associated with episodic memory and how it is tested
Pathological process
> Early Alzheimer’s disease
> Hippocampal atrophy
> Ventricular enlargement
> Limbic encephalitis
Testing ACEr
> Anterograde memory - address learning
> Retrograde memory – historical famous figures
Describe pathological processes associated with semantic memory and how it is tested
Semantic dementia (variant frontotemporal dementia) - anterior temporal atrophy
> Loss of knowledge about the world including words
Testing ACEr
> Marked reduction category verbal fluency e.g. give a list of animals in one minute
> Impairment of irregular words (dyslexia) e.g. pint
Describe the different forms of language, the pathological processes which can arise and how it is tested
3 forms
> Speech – aphasia
> Reading – alexia
> Writing – agraphia
Pathological processes
> Semantic variant – semantic dementia
> Poor confrontation naming e.g. naming common objects
> Impaired single word comprehension
> Poor object/person recognition, surface dyslexia
> Logopenic variant – Alzheimer’s dementia
> Impaired single word retrieval - “thinking of right word”
> Impaired repetition, speech sound errors (phenomic)
> Spared object/person recognition, single word recognition
> Non-fluent variant – progressive non-fluent aphasia (variant FTD)
> Effortful, halting, motor impairment of speech
> Phenomic errors
> Spared object/person recognition, single word recognition
Testing using ACEr
> Naming
> Repetition
> 3 stage command – comprehension
> Reading
Describe the pathophysiology of Alzheimer’s disease
Starts in temporal lobe – impairment of episodic memory
Hippocampal atrophy and ventricular enlargement
Spreads to parietal and frontal lobes – visuospatial dysfunction
Global atrophy including language centres – language disorder
Describe Bell’s palsy and its treatment
Unilateral facial weakness evolves over 48h often preceded by ear pain/distorted sounds
> Decreased tear production – ocular dryness
> Hyperacusis
> Ageusia
Causes
> Unknown
> Viral-associated ischaemia, demyelination
» Herpes zoster, herpes simplex
» EBV
» Lyme disease
Treatment
> Steroids – oral prednisolone
> Artificial tears, eye patching
» Long-term: tarsorrhaphy
> Physical therapy
> May resolve spontaneously within weeks-months
List the main agents which cause CNS infection
Bacterial: meningococcus, pneumococcus, Listeria
Viral: HSV, VZV, enterovirus (D-68), HIV, mumps
Fungal: cryptococcosis
Parasitic: toxoplasmosis
Describe the causative agents of meningitis
Bacterial or viral
> Streptococcus pneumoniae – gram positive diplococci
> > 70% underlying disorder
> Middle ear disease
> Head injury – CSF leak
> Neurosurgery
> Alcohol
> Immunosuppression (HIV)
> > Neurology
> Focal signs
> Seizures
> VIII palsy
> CAP
> ENT
> Endocarditis
> Neisseria meningitidis – gram negative diplococci
Subacute
> Bacterial – Listeria, TB
> > Listeria monocytogenes – gram positive rods
> Immunosuppression
> Pregnancy
Describe the signs and symptoms of meningitis
Inflammation of meninges +/- cerebrum (meningo-encephalitis) - inflammatory CSF
Symptoms and signs
> Headache
> Neck stiffness/rigidity
> Reduced GCS
> Fever
> Confusion indicative of cerebritis / encephalitis
> Rash – purpuric +/- petaechial but macular early on (meningococcal)
Describe LP findings in meningitis
Bacterial
> Low glucose
> High protein
> Neutrophils present
> Lymphocytes in Listeria infection
TB
> Low glucose
> High protein
> Lymphocytes present
Viral
> Normal glucose
> High protein
> Lymphocytes present (also neutrophils early on – esp mumps meningitis)
Fungal
> Low glucose
> High protein
> Lymphocytes present
Describe treatment of suspected bacterial meningitis
Possible bacterial meningitis
> IV ceftriaxone 2g 12 hourly OR benzyl penicillin
> OR if true penicillin allergy: IV chloramphenicol
> If age > 60, immunosuppressed, alcohol excess, liver disease or Listeria meningitis suspected - add IV amoxicillin to ceftriaxone OR if true penicillin allergy> add IV co-trimoxazole
Bacterial meningitis strongly suspected
> Add IV dexamethasone 10mg 6 hourly (4 days)
Duration of antibiotics
> Meningococcal – 5 days
> Listeria – 21 days (IV amoxicillin – stop ceftriaxone)
> Pneumococcal – 10-14 days
> Haemophilus – 10 days
If high likelihood of pneumococcal meningitis add steroids
Describe chemoprophylaxis for meningococcal meningitis
Given to contacts
Ciprofloxacin
Rifampicin
Describe viral encephalitis and its treatment
Confusion, fever +/- seizures
HSV encephalitis
> High mortality rate with neuro sequelae e.g. hearing loss, memory loss
> Lymphocytic CSF
> Normal glucose
> PCR is positive
EEG – temporal lobe changes
Treatment - IV aciclovir 2-3 weeks (HSV, VZV)
Describe intracerebral TB
Subacute – weeks
May be unmasked during TB treatment
CN lesions usually CN III, IV, VI, IX
Sample widely – early morning urines (EMUs), bronchoalveolar lavage (BAL)
CSF may be normal
Treatment for one year
> Rifampicin
> Pyrazinamide
> Isoniazid
> Ethambutol
> Steroids
Describe HIV brain disease
Consequence of unrecognised/untreated infection and marked immunodeficiency
> Encephalitis: responds to antiretroviral therapy
> Dementia: does not respond to antiretroviral therapy
> Neurosyphilis – secondary or tertiary
> Responds to penicillin
> Opportunistic
> TB
> Cryptococcus
> Toxoplasmosis
> JC virus – progressive multifocal leuco-encephalopathy
Describe intracerebral toxoplasmosis
Toxoplasma gondii
Signs and symptoms
> Headache
> Seizures
> Focal CNS signs
> Immunocompromised (HIV)
> Multiple enhancing lesions – basal ganglia
Investigations
> IgG and IgM – blood
> PCR – CSF
Treatment
> Sulphadiazine
> Pyramethamine
> Restore immune function
Describe cryptococcal meningitis
Immunodeficiency usual – HIV
Space occupying lesion (SOL) or meningo-encephalitis (subacute)
Papilloedema usually present
> Will progress to optic atrophy and blindness if untreated
Can cause pulmonary nodules and skin lesions
CSF
> India ink – classic large capsule
> Cryptococcal antigen (also blood)
> Culture
Treatment
> Amphotericin B
> Flucytosine
> Fluconazole, possible steroids
> If raised ICP – shunt
> Paradoxical worsening with ARVs in HIV
Describe the treatment used for acute alcohol intoxication and name complications of chronic alcohol abuse
Chlordiazepoxide PRN and IV Pabrinex (vitamin B1)
Complications: Wernicke’s encephalopathy progressing to Korsakoff’s syndrome
Describe the Oxfordshire Community Stroke Project (OCSP) classification
4 subtypes of ischaemic stroke
1) Lacunar syndrome (LACS)
> pure motor stroke OR pure sensory stroke OR sensorimotor stroke OR ataxic hemiparesis OR clumsy hand-dysarthria
2) Total anterior circulation syndrome (TACS)
> hemiparesis AND higher cortical dysfunction (dysphasia or visuospatial neglect) AND homonymous hemianopia
3) Partial anterior circulation syndrome (PACS)
> Isolated higher cortical dysfunction OR any 2 of hemiparesis, higher cortical dysfunction, hemianopia
4) Posterior circulation infarct (POCS)
> Isolated hemianopia, brainstem or cerebellar syndromes
Describe the CHADS-VASc score and at what score do you anticoagulate and with what?
C – Congestive Heart Failure/ LV Dysfunction
H – Hypertension
A(2) – Age ≥ 75
D – Diabetes Mellitus
S(2) – Stroke/TIA/Thromboembolism
V – Vascular Disease (e.g. PAD, MI)
A – Age (65-74)
Sc – Sex Category (1 point for F)
If CHA2DS-VASc Score ≥ 2:
offer anticoagulation- (Edoxaban/Apixaban).
If patient has a mechanical valve replacement: Warfarin
Discuss management of migraine - acute and prophylactic
Acute (1st line)
- Simple analgesics (Paracetamol, Ibuprofen or Aspirin) UPTO 2 twice a week
- Triptans (e.g. Sumatriptan)
- Avoid if patient has CVD
- Give with anti-emetics if vomiting
- Consider anti-emetics if patient is vomiting (Metoclopramide or Prochlorperazine)
If not working - try other Triptans and NSAIDs (2nd line)
Prophylactic
- Lifestyle: diet and hydration, avoid triggers, relaxation activities, headache diaries
- Medication. Consider if:
>4 disabling headaches per month
Not resolved by acute medication, or risk of Medication overuse headache
Offer EITHER of:
- Propranolol
- Amitriptyline
- Topiramate
- Candesartan
- Flunarazine
If ineffective after 3m, wean and try another
If all failed: refer to neurology specialist
avoid opiates
Summarise peripheral neuropathies - GBS, length dependent, myasthenia gravis
Guillain-Barre Syndrome (medical emergency)
- Ascending weakness (length-dependent) and sensory loss
- Typically after GI infection/ EBV
- Treated with IVIg
- Length dependent axonal neuropathies
- Tend to have a glove-and-stocking distribution, symmetrical
- Multiple causes (B12/B9, Isoniazid, Diabetes, alcohol, Charcot-Marie Tooth) - Neuromuscular Junction Disorders
- Myasthenia Gravis (esp younger women, older men)
- Fatiguable weakness: ptosis, quietening speech, respiratory difficulties
- Ix: Antibodies to post-synaptic ACh receptors at the NMJ, possible mediastinal mass on CT
- Treated with Pyridostigmine (anti-AChE)
Define Pellagra
Pellagra - A deficiency of niacin (vitamin B3). Characterized by the presence of glossitis and “the three Ds”: diarrhea, dermatitis, dementia, and possibly death (the four Ds).
Discuss Bamford Stroke Classification
Describe symtpoms of stroke by location
ACA
- Contralateral leg > arm weakness, sensory loss, urinary incontinence
- Personality changes
MCA
-Arm > leg weakness, sensory loss
- Hemineglect/ aphasia
PCA
- Contralateral hemianopia with macular sparing
- Alexia, prosopagnosia etc
Lacunar strokes
- Pure sensory/motor/mixed (no cortical signs such as neglect, aphasia)
Cerebellar strokes
- Consider if vertigo (vomiting), tremors, slurred speech, ataxia, nystagmus etc
Describe Cushing’s triad
Cushing’s triad refers to signs which indicate increased intracranial pressure (ICP).
These include bradycardia, widened pulse pressure and irregular respirations.
