Neurology Flashcards
Describe the cranial nerves and their functions
I - olfactory (sensory) - olfaction
II - optic (sensory) - vision
III - oculomotor (motor) - innervates pupil + lens, upper eyelid, majority of extraocular muscles
IV - trochlear (motor) - rotates down and in
V - trigeminal (both) - sensory in ophthalmic, maxilllary, mandibular; mandibular also muscles of mastication and some neck muscles
VI - abducens (motor) - rotates outwards
VII - facial (both) - muscles of facial expression, taste in anterior 2/3, lacrimal + saliva glands
VIII - vestibulocochlear (sensory) - hearing and balance
IX - glossopharyngeal (both) - muscles of swallowing, parasympathetic of parotid, taste of posterior 1/3 (assess with cough and soft palate - ah)
X - vagus (both) - parasympathetic control and sensory of thoracic / abdominal organs, motor control of pharynx + larynx
XI - accessory (motor) - sternocleidomastoid and trapezius
XII - hypoglossal (motor) - muscles of tongue, speech, swallowing
What are the affects of brain lesions in different sections
Frontal lobes lesions: disinhibition, perseveration, anosmia, inability to generate a list
Broca’s aphasia: located on the posterior aspect of the frontal lobe, in the inferior frontal gyrus. Speech is non-fluent, laboured, and halting
Parietal lobe lesions: sensory inattention, apraxias, astereognosis (tactile agnosia), inferior homonymous quadrantanopia. Gerstmann’s syndrome (lesion of dominant parietal): alexia (read), acalculia (arithmetic), agraphia (writing), finger agnosia and right-left disorientation
Temporal lobe lesion: superior homonymous quadrantanopia, auditory agnosia, prosopagnosia, (difficulty recognising faces)
Wernicke’s aphasia: this area ‘forms’ the speech before ‘sending it’ to Broca’s area. Lesions result in word substitution, neologisms but speech remains fluent
Occipital lobe lesions: homonymous hemianopia (with macular sparing), cortical blindness, visual agnosia
Cerebellum lesions: midline lesions: gait and truncal ataxia; hemisphere lesions: intention tremor, past pointing, dysdiadokinesis, nystagmus
How do upper and lower motor neuron lesions present
Upper (faulty input): weakness, hyperreflexive, increased tone, spasticity + rigidity, minimal paralysis, tremor, chorea + dystonia (twisting)
Lower (less): atrophy, loss of tone, flaccidity, weak reflexes, fasciculations
Describe the presentations of strokes in different circulations
Anterior cerebral: leg weakness, gait apraxia, incontinence, drowsiness
Middle cerebral: contralateral arm + leg weakness, contralateral sensory loss, hemianopia, aphasia + dysphasia
Posterior cerebral: contralateral homonymous hemianopia, cortical blindness, other visual
Ventral midbrain (Weber’s): ipsilateral CN III palsy, contralateral weakness of limbs
Posterior circulation: motor deficits, dysarthria, vertigo, altered consciousness
Anterior inferior cerebellar: Nystagmus, vertigo, sudden hearing loss, facial weakness. (A for audio)
Posterior inferior cerebellar (Wallenberg / LMS): Nystagmus, vertigo, Horner’s, dysarthria + dysphagia, ipsilateral hemiataxia. (P for poor balance)
Basilar: locked in syndrome
Pontine haemorrhage: reduced GCS (collapse), paralysis, bilateral pinpoint pupils
Supplies motor tracts (bilateral paralysis), cranial nerves V-IX, haemorrhage causes stimulation of parasympathetic - pinpoint pupils
Describe the bamford classification of stroke
Anterior (anterior and middle cerebral). Total = all 3 of: unilateral weakness of arm + leg + face, homonymous hemianopia, higher cerebral dysfunction (dysphasia, visuospatial)
Partial = 2 out of 3. Also: amaurosis fugax, dysarthria (speech defect due to muscles), dysphagia (receptive, expressive), higher cortical dysfunction
Posterior = one of: cranial nerve palsy + contralateral motor / sensory deficit, conjugate eye movement disorder (won’t move together), cerebellar dysfunction, isolated homonymous hemianopia
Cerebellar: vertigo, nystagmus, ataxia, dysarthria. Also aphasia, dysphasia
Lacunar = one of: pure motor, pure hemisensory, ataxic hemiparesis, mixed sensorimotor, clumsy hand dysarthria
One deep penetrating artery, subcortical so no cortical features
How are strokes investigated and what scores are used
Acute - CT (rule out haemorrhagic), next day MRI to confirm
ROSIER score: exclude hypoglycaemia; -1 for loss of consciousness, seizure activity; +1 for acute asymmetric facial weakness, arm weakness, leg weakness, visual field defect. Stroke > 0
BP, ECG (AF), FBC
NIHSS score used for severity / prognosis / thrombolysis decision, the higher the score also the higher the certainty of diagnosis. >20 severe, >16 moderate to severe, >5 moderate, >1 minor. Max 42
How are ischaemic strokes managed
Maximise reversible ischaemic tissue - hydration, sats > 95%
Ischaemic: thrombolysis only if < 4.5 hours after onset and haemorrhage ruled out - alteplase (plasminogen activator), aspirin 300mg (PPI) for 2 weeks then lifelong clopidogrel
Can also do mechanical thrombectomy alongside thrombolysis (very limited resource), 6 hour window for identified proximal anterior circulation (up to 24h if good perfusion scan - limited infarct core), longer for basilar, risk of reperfusion injury
Carotid artery endarterectomy if in carotid territory and not severely disabled, > 70% stenosis
Long term: clopidogrel (not tolerated aspirin + dipyridamole), aspirin + clopidogrel in high risk, atorvastatin, lifestyle advice, hypertension ((TCA) thiazide, long acting CCB, ACE / ARB)
How are haemorrhagic strokes managed
Haemorrhagic: frequent GCS monitoring, any anticoagulants should be reversed (vitamin K + beriplex (W), andexanet alfa (DOAC), protamine (LMWH)), control hypertension, manual decompression + diuretic for raised ICP, surgery - clipping, endovascular coiling
What are the causes of TIA
Small vessel occlusion, atherothromboembolism from carotid is the chief cause
Also hyperviscosity: polycythaemia, sickle cell, myeloma
Hypoperfusion: cardiac dysrhythmia, postural hypotension, decreased flow through atheromatous arteries
Describe the presentation of TIAs
Sudden loss of function, symptoms usually < 60 mins but can be up to 24h
Much more focal than strokes, 90% anterior / carotid, one or few: numb contralateral leg, hemiparesis, hemi sensory disturbance, dysphagia, amaurosis fugax (transient loss of vision in one eye)
How is TIA diagnosed
Often solely on history
Carotid artery doppler ultrasound (stenosis/ atheroma), MRI (diffusion weighted + blood sensitive), echocardiogram, ECG
CT only indicated if still ongoing pathology or other disease suspected
Rule out: FBC (polycythaemia), ESR (vasculitis), glucose, cholesterol
How is TIA managed
TIA: Aspirin 300mg (with PPI) immediately, carotid doppler, reviewed within 24h, if imaging required - MRI
If bleeding disorder, immediate CT scan to exclude intracranial haemorrhage, no aspirin if on medication already
Long term: clopidogrel (not tolerated aspirin + dipyridamole), aspirin + clopidogrel in high risk, atorvastatin, lifestyle advice, hypertension (thiazide, long acting CCB, ACE / ARB)
Describe Cushing’s triad
Cushing’s triad are the classical signs of raised intracranial pressure; widening pulse pressure (increase in systolic to combat pressure), bradycardia + slow deep breathing due to brainstem compression (Cheyne-Stokes respiration)
What is the pathogenesis and presentation of subarchnoid haemorrhages
Subarachnoid: rupture of saccular ‘berry’ aneurysms, i.e. rupture of junctions in circle of willis. 10% arteriovenous malformations. Tissue ischaemia, raised ICP
Berry: associated with polycystic kidney disease, hypertension, ehlers-danlos, coarctation of A
SA: sudden onset worst ever / thunderclap headache, vomiting, collapse, seizures, coma
What is the pathogenesis and presentation of subdural haemorrhages
Subdural: acute = high impact injury; chronic = small brain, rupture of bridging veins, vulnerable to deceleration injuries also dural metastases, haematoma forms and stops bleeding, weeks later starts to autolyse and grow in size, ICP rises leading to herniation. (Trauma may not be obvious as weeks before and can be very minor)
Patients on anticoagulants have ~10x risk of SD and worse outcomes
SD: fluctuating levels of consciousness, sleepiness, headache, personality change
What is the pathogenesis and presentation of extradural haemorrhages
ED: most commonly due to traumatic head injury (fracture of pterion causing laceration of middle meningeal), blood accumulates rapidly over minutes or hours
Pterion (temple): parietal, temporal, sphenoid, frontal
ED: head injury, brief loss of consciousness, lucid interval between injury and loss of consciousness. Severe headache, N+V, confusion, seizures, drowsy
How are intracranial haemorrhages investigated
SA: CT within 6h - blood in basal cisterns (star shaped); LP (CT more than 6h and inconclusive or after 12h) - xanthochromia (bilirubin from broken down RBCs); confirmed, CT angiography to find cause and anatomy
Other: clotting profile for coagulopathy, troponin I often raised, ECG (looks like STEMI)
SD: CT - crescentic and can cross suture lines; acute = hyperdense, chronic = hypodense; may be midline shift or effacement of sulci. Consider MRI / X ray is CT inconclusive
ED: CT - biconvex (lentiform) hyperdense, limited by suture lines
How are intracranial haemorrhages managed
Refer all SAH to neurosurgeon immediately. ABCDE + sedate, maintain perfusion - IV fluids, BP below 160, nimodipine. Endovascular coiling (promotes thrombosis and ablation of aneurysm) - first line if angiography shows aneurysm, clipping, also intracranial stents and balloon remodelling
Nimodipine prevents vasospasm and increases blood flow downstream
SD: ABCs, stabilise + reduce ICP, irrigation / evacuation via burr hole / craniotomy (small can be left)
Management of raised ICP: head of bed 30d, analgesics + sedation + paralytics, hyperventilation to reduce pCO2, mannitol
ED like SD, ABCDE, stabilise + reduce ICP, craniotomy / burr hole + clot evacuation, ligation of bleeding vessel
Describe the presentations of different epileptic seizures
Last 30-120s, ictal and post ictal symptoms, typical phenomena (tongue biting, deja vu), may occur from sleep
Grand mal (generalised tonic-clonic): loss of consciousness, tonic phase (rigid and stiff), clonic phase (bilateral muscle jerking), eyes open, bite tongue, followed by confusion / coma
Complex partial: loss of awareness, symptoms depending on area affected: temporal (most common) - aura, sensory hallucinations, fear, automatisms; frontal - motor features (posturing, peddling), Jacksonian march (moves down homunculus), post ictal paralysis of involved; parietal - sensory and tingling; occipital - visual phenomena
⅔ of partial seizures will spread to a generalised
Simple partial: awareness is unimpaired with focal motor / sensory / autonomic, no postictal
Absent: just stops and stares, does not realise
Myoclonic: sudden isolated jerk of one limb / face / trunk
Tonic: sudden increased tone, stiffening without jerking
How is epilepsy managed
Men:
Generalised / myoclonic / tonic / atonic: sodium valproate
Focal: lamotrigine or levetiracetam (carbamazepine SL)
Absence: ethosuximide (sodium valproate SL) (carbamazepine contraindicated)
Women:
Generalised / focal: lamotrigine or levetiracetam (carbamazepine SL)
Tonic / atonic: lamotrigine
Myoclonic: levetiracetam
Absence: ethosuximide (lamotrigine or levetiracetam SL) (carbamazepine contraindicated)
Prolonged seizure (> 3min) or repeated - buccal midazolam FL community / IV lorazepam FL hospital (rectal diazepam) *2, not responding - IV phenytoin
Describe the pathogenesis of Parkinson’s
Mitochondrial dysfunction + oxidative stress, progressive degeneration of dopaminergic neurons in the substantia nigra, striatum receives less dopamine
Lewy-bodies (clumps of protein) become gradually widespread
1% purely genetic, combination of genetic susceptibility and environment (toxin exposure)
Describe the presentation of Parkinson’s
Classic triad: bradykinesia (slow, struggle with fine movements, gait), tremor at rest, rigidity
Up to 7 years before motor: anosmia (smell), depression / anxiety, aches, REM sleep disorders, urinary urgency, hypotension, constipation
Onset is asymmetrical (that side will stay worse), gradual onset, first is usually impaired dexterity / foot drop
How is parkinson’s investigated and managed
Clinical by neurologist (history and examination), confirm with response to levodopa
Parkinson’s is urgent referral
MRI initially normal (may show atrophy later), exclude tumours, hydrocephalus
Compensate for dopamine: levodopa (L-dopa) and co-careldopa - decarboxylase inhibitor (prevents peripheral conversion of L-dopa to dopamine)
Also dopamine agonists (bromocriptine, ropinirole - disinhibition), MAO-B inhibitors (selegiline, rasagiline) not very powerful but help in some
Symptomatic: occupational, aids, SSRIs for depression, constipation etc
Describe the parkinson’s plus conditions
Suspect in poor response to levodopa
Multiple system atrophy: parkinsonism, cerebellar signs (ataxia, dysarthria, nystagmus), autonomic disturbance (erectile dysfunction, postural hypotension, atonic bladder)
MSA-P = predominant parkinsonian symptoms, MSA-C predominant cerebellar
Progressive supranuclear palsy: early onset parkinsonism (bradykinesia), cognitive + frontal lobe impairment, postural instability + falls (stiff, broad based gait), impairment of vertical gaze, speech and swallowing difficulties
Corticobasal degeneration: asymmetric parkinsonism, cortical signs (apraxia, alien limb phenomenon, cortical sensory loss), cognitive (progressive dementia + language)
Also lewy body dementia, frontotemporal dementia
