Neurology AS Flashcards
Gross anatomy of the spinal cord?
- From Foramen magnum to L1
- Terminates as conus medullaris
- Spinal nerves continue inferiorly as corda equina
- Denticulate ligament and filum terminale are pial extensions that suspend cord in subarachnoid space.
What is the blood supply of the spinal cord?
3 longitudinal vessels.
- 2 posterior spinal arteries supply the dorsal 1/3
- 1 anterior spinal artery supplies 2/3
- Reinforced by segmental feeder arteries (artery of Adamkiewicz)
- Longitudinal veins drain into extradural vertebral plexus.
What are the tracts of the spinal cord?
Dorsal Columns
Lateral spinothalamic tract
lateral corticiospinal tract
Thalamic nuclei
Where are the dorsal columns organised in the spinal cord?
Most posteriorly.
- Composed of the fasciculus gracilis and cuneate fasciculus.
- Cuneate is cervical + thoracic and is positioned less posteriorly than gracile (sacral and lumbar).
- Sensory tracts moving info upwards.
What mode of information do the dorsal columns carry?
- Fine touch
- Vibration
- Proprioception
Cell body in the dorsal root ganglion
Where is the decussation of the dorsal columns?
In the medulla forming medial lemniscus
Where is the lateral spinothalamic tract situated in the spinal cord?
- Organised anterolaterally
Cervical is medial, whilst sacral is lateral. - Also known as the anterior white commisure
What mode of information does the lateral spinothalamic tract carry?
- Pain and temperature
- Cell body in the DRG
Carrying information upwards
Where is the decussation of the lateral spinothalamic tract
In the cord, at the entry level.
Where is the lateral corticospinal tract situated in the spinal cord?
Motor Pyramidal tracts
These are the pyramidal tracts
- posterio-laterally but also anterior.
What mode of information does the lateral corticospinal tract carry?
- Motor information
- Cell body in the primary motor cortex.
Where is the decussation of the lateral corticospinal tract?
Pyramidal decussation in the ventral medulla
Other motor tracts of the spinal cord?
Rubrospinal
Reticulospinal
Vestibulospinal
Olivospinal
Other sensory tracts?
Spinocerebellar
What are the thalamic nuclei?
VPL: Ventral posteriolateral nucleus
VPM: Ventral posteriomedial nucleus
LGN: Lateral Geniculate Nucleus
MGN: Medial Geniculate Nucleus
What is the role of the ventral posteriolateral nucleus?
Somatosensory body - Touch
What is the role of the ventral posteriomedial nucleus?
Somatosensory head - Touch
What is the role of the lateral geniculate nucleus?
Visual
What is the role of the medial geniculate nucleus?
Auditory
Role of the cerebellum and basal ganglia?
- Output to cortex via thalamus
- Regulation of posture, locomotion, coordination and movement.
Role of internal capsule?
White matter carrying axonal fibres from motor cortex to pyramids of medulla
An infarction here –> Contralateral hemiparesis
Role of the frontal lobe?
- Cognition and memory
- Executive function
- Motor cortex
- Dominant hemisphere: motor speech (Broca’s Area).
Role of the parietal lobe?
What will a defect in this present as?
Sensory cortex
- sensory inattention
- apraxias
- astereognosis (tactile agnosia)
- inferior homonymous quadrantanopia
- Gerstmann’s syndrome (lesion of dominant parietal): alexia, acalculia, finger agnosia and right-left disorientation
Apraxia is a disorder of the brain and nervous system in which a person is unable to perform tasks or movements when asked, even though: The request or command is understood. They are willing to perform the task.
Astereognosis is used to describe both the inability to discriminate shape and size by touch and the inability to recognize objects by touch. These are apperceptive and associative types of agnosia.
Body orientation - Visuospatial processing
Role of temporal lobe
Memory
Dominant hemisphere: receptive language (Wernicke’s - language comprehension).
Homunculus structure?
Medially, the feet, legs, then head.
Laterally, hand, nose, upper lip.
Anterior cerebral circulation?
Medial top band of brain.
Therefore occlusion = paralysis or weakness of foot and lef on the opposite side.
Cortical sensory loss in opposite foot and leg
Middle cerebral
- Bulk of lateral surface of hemisphere
- Superior division of Broca’s area = language expression (resulting aphasia) (anterior branch of MCA)
- INferior devision supplies lateral temporal lobe (location of Wernicke’s areas - Language comprehension
(posterior branch of MCA)
Lesion is located in the superior temporal gyrus.
Posterior cerebral artery
Supplies occipital lobe, cerebellum and brainstem.
Vertebral arteries
- Basilar artery splits
- Can get PICA (posterior inferior cerebellar artery) = Lateral medullary syndrome
- Anterior inferior cerebellar artery
Long tracts of the motor pathway?
Descending motor pathway (UMN)
- From motor cortex
V
- internal capsule
V
- Midbrain
V
- Pons
V
- Medulla
V
- Decussation of pyramids (cross over)
V
- Cervical cord
- Thoracic cord
etcLong tracts of the dorsal column pathway? Sensory (proprioception, fine touch, vibration)
- Post-central gyrus
V
- Thalamus (VPL)
V
- Midbrain
V
- Pons (becoming the medial lemniscus)
V
- Medulla (cross over of medial lemniscus (becomes nucleus gracilis, nucleus cuneate)
V
- Decussation of pyramids (cross over)
V
- Cervical cord
- Thoracic cord
etcLong tracts of the spinothalamic pathway? Sensory (pain + temperature)
- Post-central gyrus
V
- Thalamus (VPL)
V
- Midbrain
V
- Pons (becoming the medial lemniscus)
V
- Medulla
V
- Cervical cord
- Thoracic cord
etc
- Lumbar
V
- CROSS OVER THEN12 cranial nerves?
I - Olfactory II - Optic III - Oculomotor IV - Trochlear V - Trigeminal VI - Abducens VII - Facial VIII - Vestibulocochlear IX - Glossopharyngeal X - Vagus XI - Accessory XII - Hypoglossal
Nuclei of the cranial nerves?
All cranial nerves have a nucleus that are present in the brainstem EXCEPT the optic and olfactory (I + II).
Mid-brain contains nuclei of which cranial nerves?
Mid- brain houses oculomotor nerve (III) and trochlear nerve (IV).
Pons contains nuclei of which cranial nerve?
Trigeminal (V) (M+S)
Abducens (VI)
Facial nerve (VII)
Vestibulocochlear (VIII)
Medulla contains nuclei of which cranial nerve?
Glossopharyngeal (XI)
Vagus (X)
Accessory (XI)
Hypoglossal (XII)
Rule of S + M
What is special about Trigeminal (V)
Sensory and motor nerve fibres from 4 nuclei
What is the structure of the NMJ + Stages of synaptic conduction?
- Presynaptic voltage-gated Ca2+ channels open –> Ca influx
- ACh vesicles released from presynaptic terminal
- Ach diffuses across cleft
- Ach binds to NICOTINIC receptors on post-synaptic terminal
- –> Na+ influx –> Depolarisation –> Ca2+ release from SR –> Muscle contraction
- Ach is degraded by acetylcholinesterase and choline is taken up into presynaptic terminal
What drug is used to block presynaptic choline uptake?
Hemicholinium
What drug blocks ACh vesicle fusion?
Botulinum
Lambert-Eaton Myasthenic Syndrome
Which drugs block nicotinic ACh receptors?
Antimuscarinic blocks muscarinic Ach
Antinicotonic block nicotonic receptors.
Non-depolarising: Atracurium, vecuronium
Depolarising: suxamethonium - paralysis therefore short-term paralysis as part of GA.
Antimuscarinic agents?
Antipsychotics (clozapine) Atropine Tropicamide Scopolamine Atropine
Antinicotinic agents?
Bupropion
Hexamethonium
What are the dopamine pathways of the CNS?
Mesocorticolimbic
Nigrostriatal
Tuberoinfundibular
Role of Mesocorticolimbic in disease?
Schizophrenia
Role of Nigrostriatal in disease?
Parkinson
Role of tuberoinfundibular?
Hyperprolactinaemia
Sympathetic Nervous System structure?
- Autonomic nervous system
- Cell Bodies from T1-L2.
Response to fight-flight or freeze. - Supplied form the spinal cord, to the left + right ganglia.
Where do general visceral efferent fibres synapes to in the sympathetic nervous system?
- Paravertebral ganglia
- Prevertebral ganglia
- Chromaffin cells of adrenal medulla
How are preganglionic fibres different to postganglionic fibres?
Pre = Myelinated + release ACh @ nicotinic receptors Post = Unmyelinated + release noradrenaline @ adrenergic receptors (except @ sweat glands where they reelase ACh for muscarinic receptor)
What are the parasympathetic nerve system cranial nerves?
Rest and digest/ Feed and Breed. Arousal, salivation, lacrimation, urination, digestion, defectation.
3 - Ciliary Ganglion for eye
7 -
- Pterygopalatine: mucus membranes of nose, palate + lacrimal gland
- Submandibular: submandibular and sublingual glands
9 - Otic: Parotid gland
10 - Vagus (thoracic and abdo viscera)
Sacral: Pelvic splanchnic nerves (S2-4) innervate pelvic viscera.
What is the difference between preganglionic and post ganglion parasympathetic fibres?
Pregang = ACh @ nicotinic receptors Postgang = ACh @ muscarinic receptors
All nuclei except 4 in Cranial nerves?
All except 4 innervate ipsilateral side.
Fibres from trochlear nucleus decussate in medulla + supply contralateral superior oblique muscle.
Vestibulo-ocular pathways?
Vestibulo-ocular reflex (VOR)
- Axons from vestibular neurons project via MLF to abducens and oculomotor nuclei.
- Head turns L –> Eyes turn R
Absent Doll’s Eye Sign
Brainstem death
Caloric Test physiology?
Warm –> Increasing firing of vestibular nerve –> eye turn to contralateral side with nystagmus to ipsilateral side.
- Fast direction of nystagmus COWS
Cold: opposite
Warm: Same
Absence = brainstem damage on side being tested
Visual Field Defects? Central Scotoma?
Blind Spot or due to MS
Visual Field Defects? Monocular vision loss?
Damage of the optic nerve
Bitemporal hemianopia?
Damage at the optic chiasm
Upper quadrant defect > lower quadrant defect = inferior chiasmal compression, from pituitary tumour
Lower quadrant defect > upper quadrant defect = superior chiasmal compression, commonly a craniopharyngioma. This may cause a diabetic insipidus.
Contralateral homonymous hemianopia
Therefore a left contralateral homonymous hemianopia means there is damage to the right hand side. Defect is on the left.
Due to damage at the optic tract. = Incongruous defect
Also due to damage at the whole of the optic radiation. = congrous defect.
Also due to damage of the entire calcarine fissure.
Contralateral superior quadrantanopia?
- Damage at the right Meyer’s Loop in the right temporal radiation.
- Temporal = Superior
Superior TEMPO
Contralateral inferior quadrantanopia
- Damage at the calcarine fissure at the parietal lobe
Inferior quadrantanopia - Remember left inferior quadrantanopia = right parietal lobe lesion.
Homonymous hemianopia with central macular sparing?
Lesion at occipital pole - Contralateral. Lesion of the occipital cortex
Pupillary light reflex? Optic nerve damage to left?
Left direct reflex is lost. When left eye is stimulated, neither pupil constrict.
Right consensual reflex is lost. When left eye is stimulated, right does not constrict.
Right direct reflex is intact. Right constricts when signs.
Left consensual is intact as it relies on the oculomotor nerve.
Schematic diagram for pupillary light reflex?
- Retina on left and right
- Travels down optic nerve either side.
- Cross overs at retectal N to contralateral and ipsilateral Edinger-Westphal nuclei.
- Then travels down CN3 (oculomotor) to the ciliary sphincter.
Oculomotor nerve damage on left?
- Left direct is lost
- Right consensual reflex is intact
- Right direct reflex is intact.
- Left consensual reflex is lost.
What is a Marcus Gunn Pupil
- Person with abnormal left direct + abnormal right consensual reflex
- Afferent pupillary defect.
Pattern of Motor Deficits
- Cortical Lesions?
Hyperreflexia proximally in arm or leg
Pattern of Motor Deficits
- Internal capsule and corticospinal lesions?
- Contralateral hemiparesis with pyramidal distribution
- Lesions with epilepsy, decrease cognition of homonymous hemianopia = In cerebral hemisphere
- Lesion with contralateral CN palsy = brainstem lesion on the side of the palsy (e.g Milliard-Gubler syn)
Pattern of Motor Deficits
- Cord Lesions?
Quadriparesis/paraparesis
Motor and reflex level: LMN signs at level of lesion and UMN sign below
Pattern of Motor Deficits
- Peripheral Neuropathies?
- Usually distal weakness
- GBS weakness is proximal (root involvement)
- Single nerve = Mononeuropathy: trauma or entrapment
- Several nerves = mononeuritis multiplex: Vasculitis or DM.
Asymmetrical involvement of individual non-contiguous nerve trunks.
What is the UMN lesion pattern?
- increased tone ± clonus
- Hyperreflexia
- Up-going plantars
- pyramidal weakness:
extensors in UL (weak extensor)
flexors in LL (weak flexor) - No wasting
Motor cells in pre-central gyrus to anterior horn cells in the cord.
What is the LMN lesion pattern
- Decreased tone/flaccidity
- Hyporeflexia
- Down-going plantars (normal
- Wasting
- Fasciculations
Anterior horn cells to peripheral nerves
Pattern of Motor Deficits
- Primary Muscle Lesions?
- Symmetrical loss
- reflexes lost later vs neuropathies
- No sensory loss
- Fatiguability in myasthenia
Patterns of sensory deficits
- Where do sensations travels in the cord?
- Pain + temp travel along spinothalamic tracts
- Touch, joint and vibration travel in large fibres peripherally + dorsal column centrally.
Patterns of sensory deficits
- Distal sensory loss?
Neuropathy
Sensory level?
Hallmark of cord lesion
- Hemi-cord lesion –> Brown-Sequard Syndrome
- Ipsilateral loss of proprioception + vibration and UMN weakness with contralateral loss of pain + temp
Dissociated sensory loss cause?
- Selective loss of pain and temp with conservation of proprioception and vibration
- Occurs in cervical cord lesions e.g syringomyelia
What are the specific signs of cerebellar syndrome?
DANISH
- Dydiadochokinesia
- Dysmetria: past-pointing
- Ataxia
- Nystagmus
- Intention Tremor
- Speech: slurred, staccato, scanning dysarthria
- Hypotonia
Head: head tremor (titubation) eye nystagmus and dysarthria (Speech - British Constitution)
Arms: rebound pehomenon, intention tremor, past pointing.
LEgs: heel-shin, ataxic gait, Romberg’s negative.
Cerebellar hemisphere - finger-nose ataxia.
Cerebellar vermis - Gait ataxia.
What are the common causes of cerebellar syndrome?
PASTRIES
- Paraneoplastic: e.g from bronchial Ca
- Alcohol: thiamine
- Sclerosis
- Tumour: e.g CPA lesion
- Rare: MSA, Friedrich’s, Ataxia Telangiectasia
- Iatrogenic: phenytoin
- Endo: hypothyroidism
- Stroke: vertebrobasilar
Anterior Cerebral Artery stroke?
- Supplies frontal and medial part of cerebrum
- Contralateral motor/sensory loss in the legs >arms
- Face is spared
- Abulia (pathological laziness)
Middle Cerebral Artery?
- Supplies lateral and external part of hemisphere
- Contralateral motor/sensory loss in face and arms > legs
- Contralateral homonymous hemianopia due to involvement of optic radiation.
- Cognitive changes
Dominant (L): aphasia (Broca’s)
Non-dominant (R): neglect, apraxia.
Broca's = inferior frontal gyrus. expressive. Comprehension is normal, but speech is non-lfuent, laboured and halting. Wernicke's = receptive aphasia - superior temporal gyrus. Sentences make no sense, speech remains fluient and comprehension is impaired.
Dominant is normally left. Therefore the middle cerebral artery supplies both Wernicke’s and Broca’s area.
Posterior cerebral artery?
Supplies occipital lobe
Contralateral homonymous hemianopia with macula sparing
Vertebrobasilar Circulation
- Supplies cerebellum, brainstem and occipital lobes.
- Combination of symptoms
: Visual: hemianopia, cortical blindness - Cerebellar: DANISH
- CN Lesions
- Hemi-/quadriplegia
- Uni/bilateral sensory symptoms.
What is lateral medullary syndrome/Wallenberg’s syndrome?
PICA: Ipsilateral: facial pain and temperature loss
Contralateral: limb/torso pain and temperature loss
Ataxia, nystagmus
AICA: Symptoms are similar to Wallenberg’s (see above), but:
Ipsilateral: facial paralysis and deafness
It is an important syndrome to be aware of as it is most often due to a stroke affecting the posterior inferior cerebellar artery (PICA). It is the most commonly survived stroke that affects the brainstem and is commonly used as an exam question scenario. Given her symptoms, this would be in keeping with a right-sided posterior inferior cerebellar artery infarct.
An anterior inferior cerebellar artery infarct would present in the same way but with the additional symptoms of a same-sided facial weakness and loss of hearing. A basilar artery infarct would result in a locked-in syndrome where the patient is unable to move or communicate but is fully conscious. Both of these are more likely to affect the autonomic centres in the medulla and are associated with a higher mortality.
Millard-Gubler Syndrome: Crossed hemiplegia
Pontine lesions (e.g infarc) Effects: 6th (can't look laterally) and 7th CN palsy + contralateral hemiplegia.
Locked in syndrome?
- Pt is aware + cognitively intact but completely paralysed except for eye muscle
Causes
- Ventral pons infarction: basilar artery. Secondary to hypertension. Reduced GCS, quadriplegia, miosis, absent horizontal eye movement. Pinpoint pupils point to pons.
- Central pontine myelinolysis: rapid correction of hyponatreamia
Cerebellopontine Angle Syndrome?
Causes: Acoustic neuroma, meningioma, cerebellar astrocytoma, metastasis
Leads to a ipsilateral CN5,6,7,8 + cerebellar signs
Subclavian Steal Syndrome?
Subclavian A stenossi proximal to origin of vertebral A may_-> blood being stolen from this vertebral artery by retrograde flow
- Syncope/presyncope or focal neurology using the arm
- BP difference of >20mmHg between arms.
What is anterior spinal artery/ Beck’s Syndrome
- Infarction of spinal cord in distribution of anterior spinal artery: ventral 2/3 of cord.
- Causes: Aortic Aneurysm dissection or repair
- Effects
Para/Quadriparesis
Impaired pain and temperature sensation
Preserved touch and proprioception
What are the differentials for muscle weakness? Causes in the CNS?
Cerebrum
- Vascular: infarct, haemorrhage
- Inflammation: MS
- SOL
- Infection: Encephalitis, abscess
Cord
- Vascular: Anterior spinal artery infarction
- Inflammation: MS
- Injury
Anterior Horn
- MND, polio
What are the differentials for muscle weakness? Causes in the PNS?
- Motor Nerves Mononeuropathy: compression Polyneuropathy: GBS, CMT - NMJ GB, LEMS, Botulism - Muscle Toxins: steroids Poly/dermatomyositis Inherited: DMD, BMD, FSH
Gait Disturbance Differential (Motor) - Basal Ganglia: Shuffling gait
Basal:
- PD
- Parkinsonism: MSA, PSP, Lewy Body Dementia, CBD
Hypokinetic (parkinsons)
Hyperkinetic (Huntington’s)
Gait Disturbance Differential (Motor)
UMN Bilateral: Spastic, scissoring
Cord: Compression, trauma, hereditary spastic paraparesis, syringomyelia, transverse myelitis
Bihemispheric: CP, MS
Gait Disturbance Differential (Motor)
UMN Unilateral: Spastic circumducting
Hemisphere lesion: CVS, MS, SOL
Hemicord: MS, tumour
Gait Disturbance Differential (Motor)
LMN bilateral: bilateral foot drop
Polyneuropathy: CMT (charcot-marie tooth), GBS
Corda equina
Gait disturbance differential: (Motor) LMN Unilateral: foot drop –> high stepping gait.
Ant horn: Polio
Radicular: L5 root lesion
Sciatic/common peroneal nerve: trauma, DM.
Weakness of hip abduction is L5 radiculopathy.
Mixed UMN and LMN: MAST ?
- Motor Neuron Disease
- Friedrich’s ataxia - Same as SCD but with cerebellar ataxia.
- Subacute combined degeneration of the cord =
First to go is the dorsal column with joint position and vibration.
bilateral spastic paresis (damage to lateral columns) bilateral loss of proprioception and vibration sensation (damage to posterior columns) leading to sensory ataxia and positive romberg’s test. Bilateral limb ataxia (damage to peripheral nerve) - absent ankle and knee jerk.
What are the differentials for hand wasting?
Cord
- Anterior Horn: MND, polio
- Syringomyelia
Roots
- Compression: spondylosis, neurofibroma
Brachial Plexus - Compression Cervical rib Tumour: Pancoast's, breast - Avulsion: Klumpke's palsy
Neuropathy - Generalised: Charcot Marie Tooth - Mononeuritis multiplex: DM - Compressive mononeuropathy Median: thenar wasting Ulnar: hypothenar and interossei wasting
Muscle
- Disuse: RA
- Compartment syndrome: Volkman’s ischaemia
- Distal myopathy: myotonic dystrophy
- Cachexia
Gait disturbance due to sensory impairment? Vestibular causes?
(all Romberg’s +ve)
Meniere’s
Viral Labyrinthitis
Brainstem Lesion
Gait disturbance due to sensory impairment? Cerebellar causes?
Ataxic
- ETOH
- Infarct
Wide-based gait, loss of heel to toe pattern and instability.
Gait disturbance due to sensory impairment? Proprioceptive loss (Romberg’ +ve)
Dorsal columns: B12 deficiency
Peripheral Neuropathy: DM, ETOH, Uraemia
Visual Loss
What are the cardiac causes of LOC?
Stokes-Adams Attack = collapse without warning and loss of consciousness.
- Bradycardia: heart block, sick sinus, Long QT
- Tachycardia: SVT, VT
- Structural
Weak heart: LVF, tamponade
Block: AS, HOCM, PE, ACS
What are the reflex causes of LOC?
Vagal overactivity
- Vasovagal syncope
- Situational: cough, effort, micturition
- Carotid sinus syncope
Sympathetic underactivity= postural hypotension
- Salt deficiency: hypovolaemia, Addison’s
- Toxins
Cardiac: ACEi, diuretics, nitrates, a-B
Neuro: TCAs, benzos, antipsychotics, L-DOPA
- Autonomic neuropathy: DM, Parkinson’s, GBS
Dialysis
Unwell: chronic bed-rest
Pooling, venous: varicose veins, prolonged standing (orthostatic hypotension) .
What are the arterial causes of LOC?
Vertebrobasilar insufficiency: migraine, TIA, CVA, Subclavian steal
Shock
HTN: phaeochromocytoma
What are the systemic causes of LOC?
Metabolic: decreased glucos
Resp: hypoxia, hypercapnoea
Blood: anaemia, hypervisocity
What are the head causes of LOC?
Epilepsy
Drop Attacks
Examination of LOC?
- Postural HTN: difference of >20/10 after standing for 3 mins vs lying down - Orthostatic hypotension
- Cardiovascular assessment
- Neurological assessment
Investigations of LOC?
- ECG ± 24hr ECG
- U+E, FBC, Glucose
- Tilt table (confirms dysautomomia for neuro)
- EEG, Sleep EEG
- Echo, CT, MRI brain
Presentation of cardiogenic syncope?
Trigger: Exertion, drug, unknown
Before: Palpitations, chest pain, dyspnoea
During: pale, slow/absent
pulse, clonic jerks may occur
After: Rapid recovery
IX: ECG, 24hr ECG, Echo
Presentation of vasovagal syncope?
Trigger: prolonged standing, heat, fatigue, stress, emotional upset
Before
- Gradual onset: sec–> mins
- Nausea, pallor, sweating, tunnel vision, tinnitus.
- Cannot occur lying down
During
- Pale, grey, clammy, brady
- Clonic jerks and incontinence can occur, but no tongue biting
After: rapid recovery
Ix: Tilt-table testing
Reflex: Postural hypotension presentation?
Prodrome of sweating, pallor and N+V before a transient LOC are suggestive of a reflex syncope.
Most common cause.
Defined as SBP fall of at least 20mmHg within 3 mins of standing.
Trigger: standing up
Before, during and after same as vagal above
Ix: Tilt-table testing
Presentations of Arterial causes of LOC?
Trigger: Arm elevation (Subclavian steal), migraine
Before, during and after same as vasovagal ± brainstem signs (diplopia, nausea, dysarthria
Ix: MRA, duplex vertebrobasilar circulation
Presentation of systemic causes of LOC?
Hypoglycaemia: tremor, hunger, sweating, light-headedness –> LOC
Epileptic presentation of LOC?
Trigger: flashing lights, fatigue, fasting
Before: aura in complex partial seizures - feeling strange, epigastric rising, deja/jamais vu, smells, lights, automatisms
During: tongue biting, incontinence, stiffness –> Jerking, eyes open, cyanosis, Decreased SpO2.
After: headache, confusion, sleeps, Todd’s palsy.
Ix: EEG, increased SE prolactin at 10-20mins (greater than 2x baseline indicates generalise tonic clonic seizure). Check glucose, WBC, electrolytes.
Drop attack? Distinct from syncope?
No trigger. No warning.
During: Sudden weakness of legs causes older woman to fall to ground.
No post-ictal phase.
What is the definition of vertigo?
- The illusion of movement: usually rotatory
- Of patients or surrounding
- Worse on movement
What is not classified as vertigo?
Faintness
Light-headedness
Lost awareness
What is dizziness?
With impaired consciousness = blackout
Without impaired consciousness:
- Vertigo: Vestibular in nature
- Imbalance: vestibular, cerebellar, extrapyramidal
What are the causes of Vertigo? Infection?
IMBALANCE
Infection/Injury
- Labyrinthitis: post-viral severe vertigo, n/v, hearing loss
- Ramsay Hunt (shingles of facial nerve)
- Trauma: to petrous temporal bone
Investigation with audiogram, Rinne’s and Weber’s test. Will show a sensorineural hearing loss. Previous viral infection.
What are the causes of Vertigo? Meniere’s
- Recurrent vertigo (~20mins) ± n/v
- Fluctuating SNHL (sensorineural hearing loss)
- Tinnitis
- Aural fullness (ear feeling full)
What are the causes of Vertigo? BPPV?
Sudden vertigo proved by head rotation. Short lived experience. Free-floating endolymph particles otoconia).
- Episodic vertigo.
Other causes of vertigo?
Aminoglycosides/Frusemide
Lymph, peri, fistula
Path: Connection between inner and middle ears
Causes: congenital, truama
PC: vertigo, SNHL
O/E: tulio’s phenomenon - nystagmus evoked by loud sound
Arterial
- Migraine
- TIA/Stroke
Nerve
- Acoustic Neuroma/Vestibular schwannoma
Central lesions
- Demyelination, tumour, infarction
Epilepsy
- Complex partial
Causes of hearing loss - Conductive?
WIDENING
- Wax or foreign body
- Infection: Otitis media, OME
- Drum perforation
- Extra: ossicle discntinuity - otosclerosis, trauma
- Neoplasia: carcinoma
- Injury: Barotrauma
- Granulomatous: Wegener’s, Sarcoid
Causes of hearing loss: sensorineural? DIVINITY
Development
- Genetic: Alport’s
- Congenital: TORCH
- Perinatal: Anoxia
Degenerative
- Presbyacusis
Infection
- VZV, Measles, Mumps, Influenza
- Meningitis
Vascular
- Ischaemia: Interal Auditory Artery - sudden hearing loss and vertigo
- Stroke
Inflammation
- Vasculitis
- Sarcoidosis
Neoplasia
- CPA tumours: acoustic neuroma (commonest cause of unilateral SNHL)
Injury
- Noise
- head trauma
Toxins
- Gentamicin
- Frusemide
- Aspirin
Lymph
- Endolymphatic hydrops = Meniere’s (abnormal fluctuation of the fluid in the ear).
- Perilymphatic fistula: ruptured round window.
Abnormal Involuntary Movements - Dyskinesias.
Define Tremor
Regular, rhythmic oscillation
Asterixis = rhythmic myoclonus - tremor of the hand when stretched out
Types of Tremor? RAPID?
Resting
Action/Postural
Intention
Dystonic
What is a resting tremor?
Features
- 4-6 Hz, pill rolling
- Abolished on voluntary movement
- increased with distraction (counting backwards)
Causes: Parkinsonism
Management: Dopamine agonists (levodopa, cabergoline, bromocriptine), antimuscarinic (procyclidine)
What is a postural/action tremor?
Features
- 6-12Hz
- Absent at rest
- Worse with outstretched hands or movement (part of the essential tremors)
- Equally bad at all stages of movement
- Can also affect the vocal cords.
Cause
- Benign essential tremor
- Endo: thyrotoxicosis, decreased glucose, phaeo
- Alcohol withdrawal (caffeine, opioids)
- toxins, valproate, theophylline
- Sympathetic: physiological tremor may be enhanced e.g in anxiety
What is an intention tremor?
Features
- > 6Hz, irregular, large amplitude
- worse at the end of movement
- E.g past-pointing
Causes: cerebellar damage
What is a dystonic tremor
Variable presentations
Mostly idiopathic, as for dystonia
What is a benign essential tremor?
- Autosomal dominant
- Occurs with action and worse with anxiety, emotion, caffeine
- Arms, neck, voice
- Doesn’t occur during sleep
- Better with ETOH.
Management: Propranolol
Primidone
What is myoclonus?
Sudden, involuntary jerks
What is myoclonus caused by?
Metabolic = asterixis (L, R, increased CO2)
Neurodegenerative disease
CJD
Myoclonic epilepsies (infantile spasms)
What is benign essential myoclonus?
- AD
- Childhood onset frequency generalised myoclonus without progression
- May respond to valproate
What is dystonia?
Prolonged muscle contractures –> Unusual joint posture or repetitive movement
What is idiopathic generalised dystonia?
AD
Childhood onset: starts in one leg, spreads on that side of the body over 5-10 years.
What is idiopathic focal dystonia
- Commonest form of dystonia
- Confined to one part of the body
- worsened by stress
- Involves rigidity and writhing movements rather than twitching.
Types
- Spasmodic torticolis
- Blepharospasm (eyelids)
- Oromandibular
What is acute dystonia?
- Torticollis, trismus and or occulogyric crisis
- Typically a drug reaction:
Antipsychotics
Metoclopramide
L-Dopa
Rx: Procyclidine (antimuscarinics).
Chorea?
- Non-rhythmic, purposeless, jerky, flitting movements
- Facial grimacing, extending the fingers
- Huntington’s
- Sydenham’s
- Wilson’s
- L-Dopa
Athetosis?
Slow, sinuous, writhing movements
- Causes
Cerebral palsy
Kernicterus
Tardive Syndromes?
Delayed onset following chronic exposure to Da agonists (antipsychotics, antiemetics, L-DOPA).
- Dyskinesia: orobuccolingual, truncal
- Dystonia: Sustained, sterotyped muscle spasms of twitching or turning
- Akathisia: unpleasant sense of inner restlessness ± repetitive movements
Manage: Change to atypical or slowly withdraw drug
Dyskinesia: Da antagonist
Akathisia: B-Blockers.
Define Dementia?
Chronically impaired cognition that affects multiple domains: memory, attention, language
- No impairment of consciousness
- Acquired and progressive
What are the most common types of dementia?
Alzheimer’s
Vascular
Lewy Body
Frontotemporal Dementia (Pick’s)
Summary of Alzheimer’s?
Epi: 50%
Path: neurofibrillary tangles and B amyloid plaques
PC: Progressive, global cognitive decline. Memory loss, loss of recent memory first. Misplacing items, apathy, decline in activities, personality change. IADLs.
RF: ApoE4, presenillin 1/2 mutation, Down’s
Ix: MRI - medial temporal lobe atrophy. MMSE, metabolic panel
Rx: cholinesterase inhibitor (Donepezil, rivastigmine) if MMSE is 10-20.
Summary of Vascular Dementia?
Epi: 20%
Path: multiple infarcts
PC: sudden onset, stepwise deterioration, patchy deficits, vascular RFs.
Ix: MRI - extensive infarcts or small vessel disease
Rx: Manage predisposing factors
Summary of Lewy Body Dementia
Epi: 20%
Path: Lewy body in occipito-parital cortex.
PC: Fluctuating cognitive dysfunction, recurrent visual hallucinations, REM sleep behaviour disorder. MAy have a symptom of parkinson’s. Distinguished from parkinson’s in the onset of dementia first.
Rx: Minise antipsychotics, use cholinesterase inhibitors - donepezil/rivastigmine.
Summary of Frontotemporal Dementia (Pick’s)
<5%
- Path: Pick bodies
- PC: Disinhibition, personality change, early memory preservation, progressive aphasia
- Ix: MRI - frontal or temporal atrophy
What are the ameliorable causes of dementia?
Infection
- viral: HIV, HSV, PML
- Helminth: cysticercosis, toxi
Vascular
- Chronic subdural haematoma
Inflammation
- SLE
- Sarcoid
Neoplasia
Nutrition
- Thiamine deficiency
- B12 and folate deficiency
- Pellagra (B3/niacin deficiency)
Endocrinology
- hypothyroidism
- Hypoadrenalism
- Hypocalcaemia
- Hypocephalus (normal pressure)
What is the definition of delirium?
Globally impaired cognition and impaired consciousness
Features of delirium?
- Disorientation of person, time and place
- Reversal of sleep-wake cycle (hyperactive at night)
- Labile mood
- illusions, delusions and hallucinations
- Cognitive impairment: memory, language, concentration
What are the causes of Delirium?
DELIRIUMS
- Drugs : opiods, sedatives, L-DOPA
- Eyes, ears and other sensory deficit
- Low O2 states: MI, stroke, PE
- Infection: UTI
- Retention: stool or urine
- Ictal
- under-hydration/nutrition
- Metabolic: DM, post-op, sodium, uraemia
- Subdural haemorrhage or other intracranial pathology
Investigations for delirium
- Bloods: FBC, U+E, LFTs, glucose, ABG
- Urine Dip
- Septic Screen
- ECG, LP
Confusion screen = B12/folate, macrocytic anaemia and deficiencies worsen confusion.
Management of delirium
ID and Rx underlying cause
Surround with familiar people
Nurse in moderately lit, quiet room
Find glasses, hearing aids
Avoid sedatives if possible, but if disruptive:
- Haloperidol 0.5-2mg
- Chlorpromazine 50-100mg PO/IM (avoid in elderly)
What are the differentials for an acute headache?
Common
- Acute sinusitis
- Otitis media
- Menstrual headache
- Medication withdrawal/overuse
- Migraine
- Tension headache
- Cerebrovascular incident
ACUTE: Vicious - Vascular Haemorrhage: SAH, intracranial, intracerebral, intraventricular Infarction: esp. posterior circulation Venous: Sinus/cortical thrombosis
- Infection/Inflammation Meningitis Encephalitis Abscess trigeminal neuralgia
- Compression
Obstructive hydrocephalus:tumour
Pituitary enlargement: apoplexy
ICP
- Spontaneous intracranial hypotension
Acute dural CSF leak
Worse on standing initially
Ophthalmic
- Acute Glaucoma
Unknown
- Situational: cough, exertion, coitus.
- medication overuse/withdrawal
- Dental caries/wisdom tooth
Systemic
- HTN: Phaeo, PET
- Infection: sinusitis, tonsillitis, atypical pneumonia
- Toxins: CO
Chronic headache?
MCD TINGS - Migraine - Cluster Headache - Drugs Analgesics Caffeine Vasodilators: Ca2+ antagonists, nitrates
Tension headaches
ICP increased/decreased
- Increased: tumour, aneurysm, AVM, benign intracranial HTn
- Decreased: Spontaneous intracranial hypotension
Trigeminal Neuralgia
GCA
Systemic
- HTN
- Organ failure e.g uraemia
What are the investigations for headache?
- Bloods
- Urine
- Micro
Blood cultures
Serology: enterovirus (common cause if viral meningitis), HSV, HIV, Syphilis, crypto - CSF
- Radiology
- Non-contrast CT
SAH: blood in sulci, cisterns (white). 90% sensitivity in first 24hr - MRI: MRA - aneurysm
- MRV: sinus thrombosis
CSF opening pressure for headaches?
Opening pressure (normal = 5-20cm H20):
- increased: SAH, meningitis
- decreased: spontaneous intracranial hypotension
What is xanthochromia?
Yellow appearance of CSF due to bilirubin. Detected by spectrophotometry. Can show evidence of a subarachnoid haemorrhage.
If no answer here then cerebral angiography.
Bacteria on CSF?
Appearance - Turbid Cells - PMN Count - 100-1000 Glucose - decreased (<1/2 plasma) Protein - Increased x2 (>1.5)
TB on CSF?
Appearance - fibrin web Cells - lympho/mononuc Count - 10-1000 Glucose - Decreased (<1/2 plasma) Protein - Very very high (X3)
Viral of CSF?
Appearance - Clear Cells - Lympho-mononuclear Count - 50-1000 Glucose - >1/2 plasma Protein - mild increased (<1)
Summary of subarachnoid headache?
- Sudden onset, worse ever, occipital headache
- Meningism, focal signs, decreased consciousness
Summary of Venous sinus thrombosis?
Rapid onset of symptoms
Unilateral.
Can be septic or aseptic (trauma, prothrombotic feature)
Can have fever, ptosis, reduced corneal reflex, retinal-vein dilatation.
Sagittal: headache, vomiting, seizures, decreased vision, papilloedema
Transverse: headache ± mastoid pain, focal CNS signs, seizure, papilloedema
Need a contrast enhanced high res CT of head.
Contrast-enhanced MRI of head
Blood cultures
Factor V Leiden
Summary of Meningitis
- Fever, photophobia, neck stiffness, Kernig’s +ve
- Purpuric rash
- Decreased consciousness
Summary of Encephalitis?
- Fever
- Odd behaviour/confused
- fits
- focal neurology (complicated by temporal lobe may give motionless stare or confusion)
- Decreased consciousness
Investigation
CSF: lymphocytosis, elevated protein
PCR for HSV
CT: medial temporal and inferior frontal changes (e.g. petechial haemorrhages) - normal in one-third of patients
MRI is better
EEG pattern: lateralised periodic discharges at 2 Hz
Summary of acute glaucoma?
- Constant unilateral eye pain, radiating to forehead
- Decreased acuity, haloes, n/v
- Red eye, cloudy cornea
- Dilated non-responsive pupil
Summary of tension headache?
- Bilateral/vertex-bitemporal
- Non-pulsatile, bandlike headache.
What is a cortical vein thrombosis?
- Thunderclap headache
- Stroke-like focal symptoms over days
- Focal seizures are common
Migraine headache?
Prodrome –> aura –> headache
- Unilateral, throbbing
- n/v phono/photophobia
Cluster headache?
Alcohol may trigger an attack. Occurs in smokers.
- Rapid onset very severe pain around/behind eye
- Red, watery eye, nasal congestion
- Miosis, ptosis
- Attacks last 15mins -3hrs, 1-2x a day.
- Mostly nocturnal
- Clusters last 4-12 weeks, remission lasts 3months - 3yrs.
Management: 100% O2 via non-rebreathe mask, sumitriptan
Prevention: verapamil, topiramate, Li.
What is miosis?
Constriction of eye
What is ptosis
Dropping of eyelid
What is mydriasis
Dilation of the pupil of eye
What is trigeminal neuralgia?
Paroxysms of unilateral intense stabbing pain in trigeminal distribution (usually V2/V3).
- triggers: washing area, shaving, eating ,talking
- Male >50yrs (refer if less than 50)
- 2ndry in 14%: compression of CNV, MS, Zoster, Chiari malformation
- Exclude 2nd cause by MRI
Management: carbamazepine, lamotrigine, gabapentin
Management surgery: microvascular decompression
Analgesia overuse?
- Episodic headache becomes daily chronic headache
- Use OTC analgesia on 6 days/month max
ICP headache?
Increased ICP: worse in AM, stooping, visual problems (papilloedema), obese women
decreased ICP: worse sitting or standing
Red flags for headache?
- Worse on lying down
- Pain wakes patient up
- Present when waking up
- Unexplained weight loss
- Focal neurological deficit
- N/V
- Seizures
- Vomiting more than once with no cause
- New neurological deficit
- Reduction in conscious level
- Valsalva (coughing or sneezing headache)
- Progressive headache with fever)
2 or more red flag are present an urgent CT should be performed as the likelihood of a serious intracranial pathology is high.
TMJ dysfunction headache?
Preauricular pain on chewing
Associated with crepitus
Earache, headache
Giant Cell arteritis (>60 yrs, ESR >60, pred 60mg)
- Unilateral temple/scalp pain and tenderness
- Thickened, pulseless temporal artery
- Jaw claudication
- amaurosis fugax,
- sudden blindness
- Associated with PMR in 50%
Ix: ESR very high, platelets raised, ALP raised, HB reduced, temporal artery biopsy
Management
- High dose prednisolone (60mg) for 5-7 days
- guideed by symptoms and ESR
- Give PPI + bisphosphonates
- Prognosis: 2yr course then complete remission
What are the risk factors for migraine?
Family history High caffeine intake Obesity Female Stress life event Lack of sleep
What is the pathophysiology of migraine?
Vascular: cerebrovascular constriction –> aura, dilatation –> headache
Brain: spreading cortical depression
Inflammation: activation of CN V nerve terminals in meninges and cerebral vessels
What are the triggers for migraines?
Chocolate Cheese OCP - contraindicated due to increased risk of stroke. Caffeine Alcohol Anxiety Travel Exercise
Symptoms of a migraine?
Headache- Aura lasting 15-30 mins then unilateral, throbbing headache
- Phono/photophobia
- N/V
- Allodynia (pain in response to touch etc)
- Often premenstrual
- Prodrome: precedes migraine by hrs - days
Yawning
Food cravings
Changes in sleep, appetite, mood. - Aura: precedes migraine by mins + may persist
Visual: distortion, lines, dots, zig-zags, scotoma. Hemianiopic disturbance - spreading scintillating scotoma.
Are fully reversible, develop over at least 5 mins, lasts 5-60 minutes.
hemianopia
Sensory: Paraesthesia (Fingers –> Face)
Motor: dysarthria, ataxia, ophthalmoplegia. May have a hemiplegia.
Speech: Dysphasia, paraphasia
How do you classify migraine?
Migraine with aura (classical migraine) - 25% of patients
Migraine without aura (common migraine)
What is the diagnostic criteria for migraine?
- Typical aura + headache or
- > 5 headaches lasting 4-72hrs with either N/v or photo/phonophobia + >2:
- Unilateral
- Pulsating
- Interferes with normal life
- Worsened by routine activity
During headache at least one of the following:
- nausea and/or vomiting
- photophobia and phonophobia
What is the differential for a migraine?
- Cluster/tension headache
- Cervical spondylosis
- HTN
- Intracranial pathology
- Epilepsy
Acute Management of migraine?
Acute episode
NICE = oral triptan + NSAID/paracetamol
(diclofenac/aspirin) + M/D
2nd: Paracetamol + metoclopramide/domperidone
(metoclopramide can cause extrapyramidal SE)
3rd: Rizatriptan (CI: IHD, Uncontrolled HTN, SSRI)
Prophylactic management of migraine?
Avoid triggers
1st line: Propranolol, topiramate. Propranolol instead of topiramate in child bearing age.
2ns line: Valproate, pizotifen (increased weight) gabapentin
Causes of subarachnoid haemorrhage?
- Rupture of saccular aneurysms (80%)
- AVMs
- Anticoagulants
Risk factors for SAH?
- Smoking
- HTN
- ETOH
- Bleeding diathesis
- Mycotic aneurysms (SBE)
- FH (close relatives have 3-5x isk)
What are the sites of berry aneurysms?
- Junction of the posterior communicating with internal carotid artery
- Anterior communicating with anterior cerebral artery
- Middle cerebral artery bifurcation
Associations of berry aneurysms with other diseases?
Adult Polycystic kidneys
CoA
Ehler’s Danlos
Symptoms of SAH?
- Sudden, severe occipital headache
- Collapse
- Meningism: neck stiffness, n/v, photophobia
- Seizures
- Drowsiness –> coma
Signs of a SAH?
- Kernig’s +ve (flex hips, and knee at 90 degree, extension of knee causes back pain)
- Retinal or subhyaloid haemorrhage
- Focal neuro
@presentation suggests aneurysm location
Later deficits suggests complications
Sentinal headache
Around 6% of patients experience sentinel headache from a small warning bleed
Differential for SAH?
In primary care, 25% of those with thunderclap headache have SAH
- 50-60% no cause found
- Rest: Meningitis, intracerebral bleed, cortical vein thrombosis
Investigations for SAH?
Hyponatraemia is very common in these patients and sodium levels are usually closely monitored in the acute period.
CT
- Detects >90% of SAH within first 48hrs
Hyperdense areas in the basal cisterns, sulci + major fissures.
50% of patients have an abnormal ECG
LP
- If CT -ve and no CIs >12hr after start of headache.
- Xanthochromia due to breakdown of bilirubin
- May have normal or raised opening pressure.
On LP = straw coloured, protein.
Refer to Neurosurg as soon as SAH is confirmed
Then confirm SAH with intracranial angiogram +/- digital subtraction angiogram
What is the management of an SAH?
- Frequent neuro obs: pupils, GCS, BP
- Maintain CPP: Keep SBP >160
- CCB vasospasm prophylaxis: Nimodipine 60mg orally every 4hrs for 21 days.
- Endovascular coiling (preferable to surgical clipping)
If young unruptured aneurysms >7mm, young patients benefit from surgery.
Complications of SAH?
- Rebleeding in 20%
- Cerebral ischaemia - Due to vasospasm
- Hydrocephalus
Due to blockage of arachnoid granulations. Suddenly become unresponsive.
May require ventricular or lumbar drain
- hyponatraemia: common and don’t manage with fluid restriction SIADH
Define stroke?
Rapid onset, focal neurological deficit due to a vascular lesion lasting >24hr
Pathogenesis for a stroke?
Infarction due to ischaemia (80%) or intracerebral haemorrhage (20%)
Causes of an ischaemic stroke?
Atheroma (80%)
- Large (MCA
- Small vessel perforators (lacunar)
Embolism
- Cardiac (30%) of strokes: AF, endocarditis, MI
- Atherothromboembolism: from carotids
Causes of a haemorrhagic stroke?
- Increased BP
- Trauma
- Aneurysm rupture
- Anticoagulation
- Thrombolysis
What are the rarer causes of stroke?
- Watershed stroke: sudden decreased in BP (e.g sepsis)
- Carotid artery dissection
- Vasculitis: PAN, HIV
- Cerebral vasospasm: 2ndry to SAH
- Venous sinus thrombosis
- Antiphospholipid syndrome, thrombophilia
Risk factors for stroke?
Hypertension!!! Smoking DM Increased lipids FH Cardiac: AF, valve disease Peripheral vascular disease Previous histroy Ethnicity: Increased in blacks and asians Increased PCV/Hct OCP
Investigations for HTN induced stroke?
retinopathy
nephropathy
Big heart of CXR
Investigations for cardiac emboli
- ECG± 24hr tape: AF
- Echo: mural thrombus,
- hypokinesis, valve lesions, ASD, VSD (paradoxical emboli)
Investigations for carotid artery stenosis?
Doppler US ± Angio
Endarterectomy beneficial if >70% symptomatic stenosis
Bleeding and thrombotic tendency investigations?
‘Young’ Stroke blood test include thrombophilia and autoimmune screening - performed in those under 55
- ANA, APL, ACL, Lupus anticoagulant, coagulation factors, ESR, homocysteine, syphilis.
Thrombophilia screen
Autoimmune
Thrombocytopenia
What is the classification of Stroke?
Oxford/Bamford Classification
- Based on clinical localisation of infarct
S = Syndrome: prior to imaging
I = Infarct: after imaging when atheroembolic infarct confirmed
In the Oxford/Bamford classification - what is a TACS?
Total Anterior Circulation Stroke (TACS)
- Highest mortality + poor independence
- Large infarct in carotid/MCa, ACA territory.
Has all 3 of
1) Hemiparesis (contralateral) and or sensory deficit (>2 of face, arm and leg)
2) Homonyzmous hemianopia (contralateral)
3) Higher cortical dysfunction
(dysphagia)
- Dominant (L usually) dysphasia
- Non-dominant: hemispatial neglect
In the Oxford/Bamford classification - what is a PACS?
Partial Anterior Circulation Stroke (PACS)
- Carotid, MCA and ACA territory. Smaller arteries of anterior circulation (upper/lower division of middle cerebral artery)
- 2/3 TACS criteria, usually:
1) Hemiparesis (contralateral) and/or sensory deficit (>2 of face, arm and leg)
2) Higher cortical dysfunction - Dominant: dysphasia
- Non-dom: neglect, constructional apraxia
Deficit is less dense or incomplete.
In the Oxford/Bamford classification - what is a Posterior Circulation Stroke?
- Infarct in the vertebrobasilar territory?
- Any of
1. Cerebellar syndrome
2. Brainstem syndrome
3. Contralateral homonymous hemianopia (to the damage). Therefore homonymous hemianopia is on the same side as the paresis.
Lesion in the superior cerebellar artery, PICA or AICA.
Presetns with vertical nystagmus, and ataxia.
In the Oxford/Bamford classification - what is a LACS (lacunar infarct stroke)
Presents with
- Unilateral weakness of face and arm, arm and leg or all three
- pure sensory stroke
- ataxic hemiparesis
- Unilateral weakness of face and arm, arm and leg or all three
Small infarct around the basal ganglia, internal capsule, thalamus and pons. - Absence of Higher cortical dysfunction Homonymous hemianopia Drowsiness Brainstem signs
What are the 5 syndromes of a LACS?
- Pure motor: Post. limb of internal capsule (commonest)
- Pure sensory: Posterior thalamus (VPL)
- Mix sensorimotor: internal capsule
- Dysarthria/clumsy hand
- Ataxic hemiparesis: ant. limb of internal capsule - weakness + dysmetria
Other signs of ischaemic stroke?
Carotid bruit
AF
Past TIA
IHD
Other signs of haemorrhagic stroke?
Meningism
Severe headache
Coma
Brainstem infarcts - what are the signs for a corticospinal tract damage?
Hemi/quadrparesis
Brainstem infarcts - what are the signs for oculomotor system damage
Conjugate gaze palsy (difficulty in moving eyes in the same direction)
Brainstem infarcts - what are the signs for a Sympathetic fibres?
Horner’s
Brainstem infarcts - what are the signs for a CN7 infarct?
Facial weakness
Brainstem infarcts - what are the signs for a CN8 infarct?
Nystagmus, Vertigo
Brainstem infarcts - what are the signs for CN 9 and 10 infarct?
Dysphagia, dysarthria
Brainstem infarcts - what are the signs for cerebellar damage?
Dysarthria, ataxia
What is the acute management of a stroke? Step 1 = Resuscitate
Assessment - ROSIER. Exclude hypoglycaemia.
LOC = -1
Seizure activity = -1
New acute onset
- Asymmetric facial weakness
- Asymmetric arm weakness
- Asymmetric leg weakness
- Speech disturbance
- Visual field defect
Investigations = Non-contrast CT head scan is first line.
ABCDE
Ensure patent airway: consider NGT
NBM until swallowing assessment by SALT
Don’t overhydrate: risk of cerebral oedema
What is the acute management of a stroke? Step 2 = Monitor
- Glucose: 4-11mM: sliding scale if DM
- BP: <185/110 (for thrombolysis)
- Rx of HTN can –> decreased cerebral perfusion
- Neuro obs
What is the acute management of a stroke? Imaging Step 3
Urgent CT/MRI
Diffusion-weight MRI is most sensitive for acute infarct. T2 weighted
CT will exclude primary haemorrhage (contraindicatons = seizure at onset of stroke, cancer, GI haemorrhage, active bleeding, pregnancy, oesophageal varicies, uncontrolled HTN >200)
Carotid Dopplers (>70% stenosis) - don't treat it because it's done. ECG and ECho
24hr tape to identify AF.
What is the acute management of a stroke? Step 4 = Medical Management
- Consider thrombolysis if 18-80 yr and <4.5hr since onset of symptoms
- Alteplase (tPA)
Thrombectomy - pre-stroke status of <3 on Rankin scale. >5 on NIHSS.
OFfer thrombectomy within 6hrs + IV thrombolysis IF acute ischaemic stroke + occlusion of the proximal anterior circulation on CTA.
Offer thrombectomy ASAP between 6-24hr if confirmed occlusion of proximal anterior circulation and if there is a potential to salvage brain tissue shown on DW MRI.
Consider thrombectomy + IV thrombolysis as soon as possible for people last known to be well up to 24hrs.
+ CT 24hr post-thromboylsis to look for haemorrhage
+ ASAP Aspirin 24hr (300mg) once haemorrhagic stroke excluded ± PPI. If outside of the window give aspirin (Clopi is a more chronic drug).
Clopidogrel if aspirin sensitive.
VTE prophylaxis - heparin 5000 units every 12hrs.
What is the acute management of a stroke? Step 5 = Neurosurgical opinion if intracranial haemorrhage
May coil bleeding aneurysm
Decompressive hemicraniectomy for some forms of MCA infarction.
Stroke Unit
- Specialist nursing and physio
- Early mobilisation
- DVT prophylaxis
Secondary prevention
Rehab
What is the primary prevention management of stroke?
- Control RFs: HTN, increased lipids, DM, smoking, cardiac disease. Consider statin is cholesterol >3.5.
- Consider life-long anticoagulation in AF (use CHADS2)
- Carotid endarterectomy if symptomatic 70% stenosis
- Exercise
What is the secondary prevention management of stroke?
Risk factor control as above - Start on a statin
- Aspirin/Clopi 300mg for 2 weeks after stroke then either
- Clopi 75 OD (preferred)
- Aspirin 75mg OD
Warfarin instead of aspirin/clopi if
Cardioembolic stroke or chronic AF
- Starts 2 weeks post-stroke (INR 2-3)
- Don’t use aspirin and warfarin together. Switch to NOAC.
Carotid endarterecotmy if good recovery + ipsilateral stenosis >70%
What is the rehabilitation for stroke patients?
MDT: Physio, SALT, Dietician, OT, specialist nurses, neurologist, family
Eating
- Screen swallowing: refer to specialist (consider PEG/NG)
- Screen for malnutrition
Neurorehab: physio and speech therapy (Botulinum can help)
DVT prophylaxis
Sores must be avoided.
Occupational therapy
- Impairment
- Disability
- Handicap
Chronic Risk management
- AF start anticoagulation 10-14 days after stroke
- HTN
- Diabetes
- Smoking
Carotid artery stenosis> Don’t forget carotid dopplers in investigations.
What is a TIA?
- Sudden onset focal neurology lasting <24hr due to temporary occlusion of part of the cerebral circulation
~15% of 1st strokes are preceded by a TIA.
Symptoms of TIA?
- Symptoms usually brief
- Global events (syncope, dizziness) are not typical
- Signs mimic those of CVA in the same arterial territory
Signs of Causes of TIA?
- Carotid bruits
- Increased BP
- Heart murmur
- AF
Causes of TIA?
Atherothromboembolism from carotids is main cause
Cardioembolism: post-MI, AF, Valve disease
Hyperviscosity: poylcythaemia, SCD, myeloma
Differentials for a TIA
Vascular: CVA, migraine, GCA
Epilepsy
Hyperventilation
Hypoglycaemia
Investigations for a TIA?
Blood glucose: <3.3 = hypo U+E - Na, K, High Ca FBC: usually normal ECG: look for AF CXR Carotid doppler ± angiography Consider diffusion weight MRI
Management of TIA - Antiplatelet?
In last 7 days = Make urgent assessment within 24hrs by stroke physician.
More than a week = refer to specialist assessment as soon as possible within 7 days.
Time to intervention is crucial
- Avoid driving for 1 month
ACAS
- Antiplatelet therapy =
Aspirin/clopi 300mg/d for 2 weeks then 75mg/d
Add dipyridamole MR to aspirin
- Warfarin if cardiac emboli: AF, MI, MS
After 2 weeks
The Royal College of Physicians have published National Clinical Guidelines for Stroke that recommend Carotid endarterectomy for carotid stenosis 50-99% by NASCET criteria, for patients with TIA. The most appropriate initial treatment would therefore be antiplatelet therapy, and a statin would also be indicated.
The National Stroke Guidelines suggest patients with suspected TIA who are at high risk of stroke (e.g. an ABCD2 score of 4 or above) should receive aspirin or clopidogrel (each as a 300 mg loading dose and 75 mg thereafter) and a statin, e.g. simvastatin 40 mg started immediately after specialist assessment and investigation within 24 hours of onset of symptoms.
Therefore she could be given either aspirin or clopidogrel 300mg (as a one-off dose) then to continue on either aspirin or clopidogrel long-term.
Give clopidogrel as first line (aspirin acutely), then aspirin and dipyridamole for patients who cannot tolerate clopidogrel. Give it lifelong.
Don’t give aspirin if patient has bleeding disorder, taking an anticoagulant, patient is already taking low-dose aspirin regularly. Aspirin is contraindicated.
A single TIA patients can start driving if symptom free for 1 month and there is no need for them to inform the DVLA.
If multiple TIA 3 months off driving and inform DVLA.
Management TIA - Cardiac Risk factor control
BP, lipids, DM Smoking
Exercise
Diet: decreased salt
Management TIA - Assess risk of subsequent stroke
ABCD2
Specialist referral to TIA clinic in how long if ABCD >4?
Within 24hr
Specialist referral to TIA clinic in how long if ABCD <4?
Within 1 week
What does ABCD2 Score stand for?
- Age >60
- BP >140/90
- Clinical Features
1. Unilateral weakness (2 points)
2. Speech distubances w/o weakness - Duration
>1hr = 2 points
10-59 mins - DM
NB: 7 points max
What is a subdural haemorrhage?
- Bleeding from bridging veins between cortex and sinuses
- Haematoma between dura and arachnoid
- Often due to minor trauma that occured a long time previously - especially deceleration injuries.
Acute subdural
- Collection of fresh blood within the subdural space and is most commonly caused by high-impact trauma.
- CT shows cresentic collection, not limited by suture lines. Appear hyperdense in comparison to brain.
Chronic subdural haematoma
- Collection of blood in the subdural space that has been present for weeks to months.
- Elderly and alcoholic patients are particularly at risk. Taught bridging veins.
Risk factors for a subdural haemorrhage?
Elderly: brain atrophy
Falls: Epileptics, alcoholics
Anticoagulation
Symptoms for subdural haemorrhage?
- Headache
- Fluctuating GCS, sleepiness that can last for days.
- Nausea/Vomiting
- Gradual physical or mental slowing
- Unsteadiness
SUBDURAL cannot cause meningeal irritation.
