Neurology Flashcards
Patterns of Motor Loss Cortical Lesions (3)
Unexpected pattern of weakness of all movements of a hand or foot
Normal/reduced tone
Increased reflexes more proximally in the arm or leg will suggest an UMN rather than LMN
Patterns of Motor Loss
Internal Capsule and Corticospinal Tract Lesions (3)
Cause contralateral hemiparesis
If occurs with epilepsy, reduced cognition or hoonymour hemianopia then lesion is in cerebral hemisphere
A cranial nerve palsy (III-XII) contralateral to a hemiplegia implicates the brainstem on the side of the cranial nerve palsy
Patterns of Motor Loss Cor lesions (2)
Paraparesis (both legs) or quadriparesis/tetraplegia (all limbs)
Find lesion by finding a motor and reflex level- power is unaffected above the lesion, with LMN signs at the level of the lesion and UMN signs below the lesion
Patterns of Motor Loss Peipheral neuropathies (4)
Most cause distal weakness eg. foot drop
In Guillain-Barre weakness if often proximal due to root involvement
Involvement of a single nerve (mononeuropathy) occurs with trauma or entrapment eg. carpal tunnel
Involvement of several nerves (mononeuritis multiplex) eg. DM/vasculitis
Patterns of Sensory Loss
Tracts (2)
Pain and temp. travel along small fibres in peripheral nerves and the spinothalamic (anterolateral) tracts in the cord and brainstem
Joint-position and vibration sense travel in large fibres in peripheral nerves and the large dorsal columns of the cord
Patterns of Sensory Loss
Distal Sensory Loss (3)
Suggests a neuropathy
May involve all sensory modalities or be selective, depending on size of involved fibre
Individual nerve lesions are identified by their anatomical territories, which are usually more sharply defined than dermatomes (root lesions)
Patterns of Sensory Loss Sensory level (2)
Hallmark of a cord lesion- ie. decreased sensation below lesion, normal sensation above
Hemicord lesions cause a Brown-Sequard picture with dorsal column loss on the side of the lesion and contralateral spinothalamic loss
Patterns of Sensory Loss
Dissociated sensory loss (3)
Occur in cervical cord lesions- loss of fine touch and proprioception without loss of pain and temp.
Lateral brainstem lesions show both dissociated and crossed sensory loss with pain and temp. loss on the side of the face ipsilateral to the lesion, and contralateral arm and leg sensory loss
Lesions above th ebrainstem give a contralateral pattern of generalised sensory loss
Patterns of Sensory Loss
Dissociated sensory loss (3)
Occur in cervical cord lesions- loss of fine touch and proprioception without loss of pain and temp.
Lateral brainstem lesions show both dissociated and crossed sensory loss with pain and temp. loss on the side of the face ipsilateral to the lesion, and contralateral arm and leg sensory loss
Lesions above the brainstem give a contralateral pattern of generalised sensory loss
Patterns of Sensory Loss Cortical lesions (1)
Sensory loss is confined to more subtle and discriminative sensory functions
Cerebral Artery Occlusion Carotid artery (2)
At worst, internal carotid artery occlusion causes total fatal infarction of the anterior 2/3rd of its hemisphere and basal ganglia
More often, the picture is like middle cerebral artery occlusion
Cerebral Artery Occlusion
Anterior cerebral artery (4)
Supplies the frontal and medial part of cerebrum
Occlusion may cause a weak, numb contralateral leg +/- similar (usually milder) arm symptoms
Face is spared
Bilateral infarction can cause akinetic mutism from damage to the cingulate gyri (also a rare cause of paraplegia)
Cerebral Artery Occlusion
Middle cerebral artery (2)
Supplies lateral part of each hemisphere
Occlusion may cause contralateral hemiparesis, hemisensory loss (especially face and arm), contralateral homonymous hemianopia due to involvement of optic radiation, cognitive change including dysphasia with dominant hemisphere lesions + visuospatial disturbance with non-dominant lesions
Cerebral Artery Occlusion
Posterior cerebral artery (2)
Supplies the occipital lobe
Occlusion gives contralateral homonymous hemianopia
Cerebral Artery Occlusion Vertebrobasilar Circulation (4)
Supplies the cerebellum, brainstem + occipital lobes
Occlusion causes signs relating to any or all 3: hemianopia, cortical blindness, diplopia, vertigo, nystagmus, ataxia, dysarthria, dysphasia, hemi/quadri-plegia, unilateral or bilateral sensory symptoms, coma
Infarctions of the brainstem can cause vertigo, vomiting, dysphagia, nystagmus
Locked in syndrome is due to pontine artery occlusion (can’t move but aware)
Causes of Acute Single Episodes of Headache
9
Meningitis (fever, photophobia, stiff neck, purpuric rash, coma)
Encephalitis (fever, odd behaviour, fits, reduced consciousness)
Subarachnoid haemorrhage (sudden onset)
Head injury (usually lasts 2 weeks but rule out subdural/extradural)
Venous sinus thrombosis (subacute/sudden, papilloedema)
Sinusitis (dull, constant ache over sinuses with tenderness, worse on bending)
Tropical illness (malaria)
Low pressure headache (CSF leak)
Acute glaucoma (elderly, constant ache around eye, reduced vision, cloudy cornea)
Causes of Acute Single Episodes of Headache
9
Meningitis (fever, photophobia, stiff neck, purpuric rash, coma)
Encephalitis (fever, odd behaviour, fits, reduced consciousness)
Subarachnoid haemorrhage (sudden onset)
Head injury (usually lasts 2 weeks but rule out subdural/extradural)
Venous sinus thrombosis (subacute/sudden, papilloedema)
Sinusitis (dull, constant ache over sinuses with tenderness, worse on bending)
Tropical illness (malaria)
Low pressure headache (CSF leak)
Acute glaucoma (elderly, constant ache around eye, reduced vision, cloudy cornea)
Migraine
Symptoms (6)
Visual or other aura lasting 15-30 mins followed by unilateral, throbbing headache Nausea Vomiting Photophobia Phonophoia Allodynia- all stimuli produce pain
Migraine
Associations (2)
Obesity
Patent foramen ovale
Migraine
Stages (4)
Prodrome: precedes headache by hours/days, yawning, cravings, mood/sleep change
Aura: precedes headache by mins
Headache
Postdrome: fatigue, cognitive changes, muscle pain
Migraine
Triggers (9)
Chocolate Hangovers Orgasms Cheese Oral contraceptives Lie-ins Alcohol Tumult Exercise
Migraine Differential diagnosis (4)
Cluster headache
Tension headache
Intracranial pathology
Sinusitis/otitis media
Migraine Acute therapy (5)
Restrict to 2 days a week
Aspirin 900mg
Ibuprofen 400-600mg
Triptans: sumatriptan 1st choice (contraindicated if IHD, uncontrolled high BP; side effect arrhythmias)
Add antiemetic if vomiting: metoclopramide
Migraine Preventative therapy (6)
Consider if migraine is disabling and reduced quality of life or prolonged severe attacks
Propranolol 1st
Topiramate (side effect reduced memory) 2nd
Amitriptyline/other TCA
Candesartan
Others: sodium valproate (not for young women), pizotifen
Cluster Headache
Symptoms of attack (6)
Rapid onset of excrutiating pain
Around on eye, may become watery and bloodshot
Strictly unilateral (almost always affects same side)
Lasts 15-60 min
Occurs once/twice daily
Often nocturnal
Cluster Headache
Symptoms of bout (2)
Clusters last 4-12 weeks
Followed by pain free periods of months or even 1-2 years
Cluster Headache
Treatment of acute attack (3)
100% O2
Sumatriptan SC
Zolmitriptan nasal spray
Cluster Headache Preventative treatment (4)
Suboccipital steroid injections
Verapamil
Lithium
Melatonin
Trigeminal Neuralgia
Symptoms (4)
Intense, stabbing pai
Lasts seconds
In trigeminal nerve distribution unilaterally (typically maxillary/mandibular)
Face screws up with pain
Trigeminal Neuralgia
Triggers (4)
Washing affected area
Shaving
Eating
Talking
Trigeminal Neuralgia Secondary causes (4)
Compression of trigeminal nerve root by aneurysmal intracranial vessels or a tumour
Chronic meningeal inflammation
MS
Skull base malformation
Trigeminal Neuralgia
Investigations (1)
MRI to exclude secondary causes (approx. 14%)
Trigeminal Neuralgia
Treatment (5)
Carbamazepine Lamotrigine Phenytoin Gabapentin Surgery if drugs fail
Giant Cell Arteritis
Aetiology (3)
Elderly
Takayasu’s if <55
Polymyalgia rheumatica
Giant Cell Arteritis
Symptoms (5)
Headache Temporal artery and scalp tenderness Jaw claudication Sudden blindness, typically in on eye Extracranial symptoms: dyspnoea, moring stiffness, unequal/weak pulses
Giant Cell Arteritis
Investigations (6)
ESR ++ CRP ++ Platelets + Alk Phos + Hb - Temporal artery biopsy
Giant Cell Arteritis
Treatment (2)
Prednisolone
Typically a 2 year course then complete remission
Tension Headache
Signs + Symptoms (3)
Bilateral
Non-pulsatile headache
+/- scalp tenderness
Tension Headache
Treatment (2)
Massage
Antidepressants
Raised Intracranial Pressure
Aetiology (7)
Head trauma Infections Tumours Stroke Epilepsy/seizures Hydrocephalus Meningitis
Raised Intracranial Pressure
Signs + Symptoms (6)
Headache worse on waking, lying, bending forward or coughing Vomiting Papilloedema Seizures False localising signs Odd behaviour
Raised Intracranial Pressure
Investigations (2)
Imaging to exclude a space-occupying lesion
LP contraindicated until after imaging (measure pressure )
Raised Intracranial Pressure
Treatment (4)
Head elevation to facilitate venous return
Reduce pressure by draining fluid through a shunt
Mannitol or hypertonic saline (remove fluid from body)
Sedation as anxiety raises BP which raises ICP
Medication Overuse Headache
Aetiology (3)
Mixed analgesics (paracetamol + codeine/opiates)
Ergotamine
Triptans
Medication Overuse Headache
Treatment (3)
Withdraw the analgesia- aspirin or naproxen may help rebound headache
Preventive may help once off other drugs (eg. tricyclics, valproate, gabapentin)
Limit use of over the counter analgesia (no more than 6 days/month)
Medication Overuse Headache
Treatment (3)
Withdraw the analgesia- aspirin or naproxen may help rebound headache
Preventive may help once off other drugs (eg. tricyclics, valproate, gabapentin)
Limit use of over the counter analgesia (no more than 6 days/month)
Vasovagal Syncope
Aetiology (1)
Due to reflex bradycardia +/- peripheral vasodilatation provoked by emotion, pain, fear or standing too long
Vasovagal Syncope
Signs + Symptoms (8)
Onset over seconds Often preceded by nausea, pallor, sweating and closing in of visual fields (pre-syncope) It cannot occur if lying down Unconscious approx. 2 mins Brief clonic jerking of the limbs may occur (due to cerebral hypoperfusion leading to reflex anoxic convulsion) Urinary incontinence rare No tongue biting Recovery rapid
Carotid Sinus Syncope Carotid sinus (3)
A collection of baroreceptors
Dilated area at the base of the internal carotid artery just superior to the bifurcation
Baroreceptors sense pressure changes by responding to change in the tension of the arterial wall
Carotid Sinus Syncope
Definition (1)
Hypersensitive baroreceptors cause excessive reflex bradycardia +/- vasodilatation on minimal stimulation eg. head turning, shaving
Epilepsy Seizure elements (3)
Prodrome lasting hours/days may rarely precede the seizure
Aura is part of seizure of which the patient is aware, may be strange feeling in the gut, sense of deja vu or smells/flashing lights (implying a focal seizure, often from the temporal lobe)
Epilepsy Seizure Classification (5)
Partial (focal) seizures: features referable to a part of one hemisphere, often structural disease
Primary generalised seizures: simultaneous onset of electrical discharge throughout cortex with no localising features referable to only one hemisphere, absence seizures, tonic-clonic seizures, myoclonic seizures
Absence seizures: brief (<10s) pauses, presents in childhood eg. suddenly stops talking mid-sentence then carries on where left off
Tonic-clonic: loss of consciousness, stiff limbs (tonic), then jerk (clonic), post-ictal drowsy
Myoclonic: sudden jerk of limb/face/trunk, may be thrown suddenly to the ground
Epilepsy
Aetiology (5)
2/3 idiopathic (often familial)
Structural: cortical scarring (eg. head injuries), developmental, space occupying lesion, stroke
Non-epileptic: trauma, stroke, haemorrhage, increased ICP, alcohol, drugs (cocaine), infection (meningitis)
Metabolic disturbance: hypoxia, high/low Na, low Ca, high/low glucose
Trigges: alcohol, stress, fevers, flickering lights
Epilepsy
Investigations (4)
EEG
MRI (structural lesions)
Drug levels
Bloods: Na, Ca, glucose
Epilepsy
Treatment of generalised tonic-clonic seizures (2)
1st sodium valproate/lamotrigine
2nd carbamazepine/topiramate
Epilepsy
Treatment of absence seizures (3)
Sodium valproate
Lamotrigine
Ethosuximide
Epilepsy
Treatment of myoclonic seizures (2)
1st sodium valproate/lamotrigine
Must avoid carbamazepine, which may worsen seizures
Epilepsy
Treatment of focal seizures (2)
1st carbamazepine
2nd sodium valproate/lamotrigine/topirimate
Epilepsy
Side effects of treatments (3)
Carbamazepine: blurred vision, impaired balance, drowsiness
Lamotrigine: maculopapular rash, Stevens-Johnson syndrome or TEN, blurred vision, photosensitivity
Sodium valproate: teratogenic, nausea v common, pancreatitis, weight gain
Acoustic Neuroma
Definition (1)
Schwannoma arising from the vestibular nerve
Acoustic Neuroma
Signs + Symptoms (3)
Often presents with unilateral hearing loss, vertigo occurs later
With progression- ipsilateral Vth, VIth, IXth and Xth nerves may be affected and ipsilateral cerebellar signs
Signs of increased ICP occur late and suggest large tumour
Gait Disorders
Spastic (1)
Stiff, circumduction of legs +/- scuffing of the toes of the shoes
Gait Disorders
Extrapyramidal (4)
Flexed posture, shuffling feet, slow to start, postural instability, apraxic
‘Gluing to the floor’ on attempting walk
Wide-based unsteady gait with a tendency to fall
Causes: normal pressure hydrocephalus, multi-infarct states
Gait Disorders
Ataxic (4)
Wide-based
Falls
Cannot walk heel-to-toe
Causes: cerebellar lesions (eg. MS, posterior fossa tumours, alcohol), proprioceptive sensory loss (eg. reduced B12)
Gait Disorders
Myopathic (2)
Waddle (hip girdle weakness)
Can’t climb steps or stand from sitting
Gait Disorders
Psychogenic (2)
Often a bizarre gait not conforming to any pattern of organic gait disturbance
Suspect if profound gait disturbance but without any signs on couch examination
Dyskinesia
Definition (2)
Abnormal involuntary movements
Impaired planning, control and execution of movement
Dyskinesia
Tremor (4)
Rest tremor: abolished on voluntary movement, caused by Parkinsonism
Intention tremor: irregular, large-amplitude, worse at end of purposeful acts eg. finger pointing, caused by cerebellar damage (eg. MS, stroke)
Postural tremor: absent at rest, present on maintained posture (arms outstretched) and may persist (but isn’t worse) on movement, caused by benign essential tremor (autosomal dominant), hyperthryoidism, anxiety
Re-emergent tremor: postural tremor developing after delay of approx 10 seconds (eg. Parkinson’s)
Dyskinesia
Chorea (2)
Non-rhythmic, jerky, purposeless movements flitting from one place to another, eg. facial grimacing, raising shoulders, flexing/extending fingers
Causes: Huntington’s disease
Dyskinesia
Hemiballismus (2)
Large amplitude, flinging hemichorea (affects proximal muscles) contralateral to a vascular lesion of the subthalamic nucleus (often elderly diabetics)
Recovers spontaneously over months
Dyskinesia
Athetosis (3)
Slow, confluent, purposeless movements (especially digits, hand, face, tongue)
Hard to distinguish from chorea
Causes: cerebral palsy
Dyskinesia
Tics (3)
Brief, repeated, stereotyped movements which patients may suppress for a while
Common in children and usually resolve
Common in Tourette’s (motor and vocal)
Dyskinesia
Myoclonus (2)
Sudden involuntary focal/general jerks arising from cord, brainstem or cerebral cortex
Seen in metabolic problems (low Na, high CO2) neurodegenerative disease and myoclonic epilepsies (infantile spasms)
Dyskinesia Tardive Syndromes (4)
Tardive means 'delayed onset' Common after chronic exposure to dopamine antagonists (eg. antiemetics, antipsychotics) Tardive dyskinesia (movements) Tardive dystonia (muscle spasms, twisting/turning character)
Dystonia
Definition (1)
Prolonged muscle contractions causing abnormal posture or repetitive movements
Dystonia
Idiopathic generalised dystonia (2)
Onset in childhood
Often starts with dystonia in one leg, spreading to that side of the body
Dystonia Focal dystonias (3)
Confined to one part of the body eg. writer’s cramp
Rarely generalise
Worsened by stress
Dystonia Acute dystonia (3)
May occur on starting neuroleptics and some antiemetics
May mistake for tetanus or meningitis
Rapidly disappear after a dose of anticholinergic
Stroke
Definition (1)
Rapidly developing clinical signs of focal (or global) disturbance of cerebral function, with symptoms lasting >24 hours
Stroke
Pathophysiology (2)
Ischaemic 85%
Haemorrhagic 15% (70% primary intracerebral haemorrhage, 30% secondary haemorrhage eg. SAH)
Stroke
Causes (5)
Small vessel occlusion
Cardiac emboli: AF, MI
Atherothromboembolism eg. from carotids
CNS bleeds: high BP, trauma, aneurysm rupture, anticoagulation, thrombolysis
Carotid dissection (spontaneous or from neck trauma)
Stroke
Blood supply to the brain (2)
Carotid system supplies most of the hemispheres and cortical deep white matter
Vertebro-basilar system supplies the brainstem, cerebellum and occipital lobes
Stroke
Non-modifiable risk factors (4)
Previous stroke
Age
Male
Family history
Stroke
Modifiable risk factors (8)
High BP (exacerbates atheroma and increases involvement of smaller distal arteries) Smoking Diabetes The pill Sedentary lifestyle Lipids Heavy drinking AF
Stroke
Total anterior circulation syndrome (TACS) (5)
Complete hemiparesis/numbness Loss of vision on one side (hemianopia) Loss of awareness on one side (inattention)- non dominant Main artery to one hemisphere Dysphasia on its own
Stroke
Partial anterior circulation syndrome (PACS) (4)
Branch of main artery
2 of the 3 TACS criteria
Or one higher cortical deficit: inattention or dysphasia
Or monoparesis
Stroke Lacunar syndrome (LACS) (5)
Small perforating artery (basal ganglia, internal capsule, thalamus, pons)
Weakness/numbness of: face + arm + leg OR face + arm OR arm + leg
May have dysarthria
Ataxic hemiparesis
No affect on higher function (no dysphasia, inattention or hemianopia)
Stroke
Posterior circulation syndrome (POCS)
Any posterior artery Loss of balance/coordination Vertigo Double vision Dysarthria Visual loss (hemianopia)
Stroke
Outcomes at 12 months (4)
TACS: 60% mortality at 1 year, 6% recurrence rate at 1 year
PACS: 16% mortality at 1 year, 17% recurrence rate at 1 year (common early)
LACS: 11% mortality at 1 year, 9% recurrence rate at 1 year
POCS: 19% mortality at 1 year, 20% recurrence rate at 1 year
Stroke Differential diagnoses (6)
Seizures Syncope Sugar (hypo or hyper) Sepsis (+ previous stroke) Severe migraine Space occupying lesions
Stroke
Investigations (8)
CT head: haemorrhagic- hyperdense lesion, ischaemic- normal/parenchymal darkness, loss of grey-white matter difference, hyperattenuation of artery (clot inside) FBC: exclude anaemia + thrombocytopenia U+E + creatinine: exclude electrolyte disturbance Glucose: exclude hypo/hyper Troponin: exclude MI Clotting screen ECG: exclude MI + AF Carotid doppler ultrasound
Stroke
Treatment of ischaemic stroke (4)
Thrombolysis (eg. tissue plasminogen activator- alteplase) if within 4.5 hours
Anti-platelet: aspirin
Secondary prevention: statin, anticoagulation if in AF (warfarin/DOAC), antiplatelet (clopidogrel)
Carotid endarterectomy
Stroke
Contraindications to thrombolysis (8)
Previous inrtacranial haemorrhage Seizure at stroke onset Intracranial neoplasm Lumbar puncture within 7 days Pregnancy Active bleeding Oesophageal varices Require CT 24 hours after to assess for haemorrhage
Stroke
Treatment of haemorrhagic stroke (3)
Rapid BP control if within 6h and systolic 150-220, aiming 130-140 within 1h
Neurosurgical opinion
Stop anticoagulants and antiplatelets
Stroke
Locating the infarct (4)
Ant. cerebral artery: supplies frontal + medial cerebrum, causes contralateral motor/sensory loss in legs > arms with face sparing
Middle cerebral artery: supplies lateral hemisphere, causes motor/sensory loss in face + arms > legs, contralateral homonymous hemianopia due to optic radiation involvement and cortical changes (dysphasia if dominant hemisphere; hemisensory neglect/apraxia if non-dominant)
Posterior cerebral artery: supplies occipital lobe causing contralateral homonymous hemianopia with macular sparing
Vertebrobasilar circulation: supplies brainstem, cerebellum + occipital lobe, causes hemianopia/cortical blindness, CN lesions, quadriplegia + sensory symptoms
Transient Ischaemic Attack
Definition (3)
Sudden onset of focal CNS phenomena due to temporary occlusion of part of the cerebral circulation
Usually embolic
Symptoms <24 h
Transient Ischaemic Attack
Aetiology (2)
Atherosclerotic thromboembolism (usually from carotids)
Cardioembolism (post mI, AF, valve disease)
Hyperviscosity (polycythaemia, sickle cell disease, myeloma)
Transient Ischaemic Attack
Signs + symptoms (3)
Mimic stroke in same arterial territory Global events (eg. syncope, dizziness) not typical Emboli may pass to the retinal artery, causing amaurosis fugax (one eye's vision is progressively lost)
Transient Ischaemic Attack Differential diagnoses (4)
Hypoglycaemia
Migraine aura (symptoms spread over seconds, often visual)
Focal epilepsy (symptoms spread over seconds, often twitching/jerking)
Retinal bleeds
Transient Ischaemic Attack
Investigations (6)
Bloods: FBC, U&E, ESR, glucose, lipids, clotting CXR ECG: exclude MI/AF Echo: valvular disease Carotid doppler CT/MRI
Transient Ischaemic Attack
Treatment (4)
Immediate anti-platelet: aspirin or clopidogrel
Carotid endarterectomy: if >70% stenosis
Anticoagulation eg. warfarin: if cardiac emboli eg. AF
Control cardiovascular risk factors: antihypertensives, statin, diabetic control, stop smoking
Subarachnoid Haemorrhage
Aetiology (3)
Berry aneurysm rupture (80%): usually at junction of posterior communicating artery with the internal carotid artery or anterior communicating artery with anterior cerebral artery or MCA bifurcation, berry aneurysms are associated with polycystic kidneys, coarctation, Ehlers-Danlos
Arterio-venous malformation
No cause is found in <15%
Subarachnoid Haemorrhage Risk factors (5)
Smoking Alcohol misuse Hypertension Bleeding disorders Post-menopausal
Subarachnoid Haemorrhage
Signs + symptoms (8)
Sudden (thunderclap) occipital headache Vomiting Collapse Seizures Coma Neck stiffness Terson's syndrome: retinal,macular and vitreous bleeds Kernig's sign: severe stiffness of hamstrings causes inability to straighten leg when hip flexed to 90 degrees
Subarachnoid Haemorrhage Differential diagnoses (4)
Meningitis
Migraine
Intracerebral bleeds
Cortical vein thrombosis
Subarachnoid Haemorrhage
Investigations (6)
CT: detects 90% in first 48h LP: if CT -ve and no contraindications 12h after headache onset, CSF is bloody early then becomes xanthochromic (yellow) due to breakdown of haemoglobin to bilirubin FBC: leucocytosis Clotting: raised prolonged INR and PT U&E: hyponatraemia Troponin: elevated
Subarachnoid Haemorrhage
Treatment (4)
Immediate neurosurgery referral
Maintain cerebral perfusion by keeping well hydrated and aim SBP >160 (only treat BP if very severe)
Nimodipine: reduces vasospasm
Endovascular coiling > surgical clipping
Subarachnoid Haemorrhage
Complications (4)
Rebleeding commonest cause of death, usually in first few days
Cerebral ischaemia due to vasospasm and causes permanent CNS defect
Hydrocephalus due to blockage of arachnoid granulations
Hyponatraemia is common but shouldn’t be managed with fluid restriction
Intracranial Venous Thrombosis
Dural venous sinus thrombosis (3)
Most commonly sagittal/transverse sinus thrombosis
Symptoms come on gradually over days/weeks
Thrombosis within a dural venous sinus may extend into the cortical veins and cause infarction within a venous territory
Intracranial Venous Thrombosis
Cortical vein thrombosis (5)
Often causes venous infarcts
Stroke-like focal symptoms that develop over days
May have an associated thunderclap headache
Seizures are common and focal
Usually occurs with sinus thromboses
Intracranial Venous Thrombosis
Aetiology (4)
Common: pregnancy, OCP, head injury, dehydration, recent LP
Systemic: hyperthyroidism, heart failure, SLE, nephrosis, ketoacidosis
Infections: meningitis, TB, cerebral abscess, septicaemia
Drugs: androgens, antifibrinolytics, infliximab
Intracranial Venous Thrombosis
Signs + symptoms (4)
Sagittal sinus: headache, vomiting, seizures, reduced vision, papilloedema
Transverse sinus: headache +/- mastoid pain, seizures, papilloedema, focal CNS signs
Sigmoid sinus: cerebellar signs, lower cranial nerve palsies
Cavernous sinus: often due to spread from facial pustules/folliculitis, headache, oedematous eyelids, fever
Intracranial Venous Thrombosis Differential diagnoses (3)
Subarachnoid haemorrhage
Meningitis
Encephalitis
Intracranial Venous Thrombosis
Investigations (3)
Must rule out SAH and meningitis
CT/MRI venography: absence of sinus
Lumbar puncture: raised opening pressure indicates venous thrombosis if there is a persistent headache and SAH is excluded
Intracranial Venous Thrombosis
Treatment (2)
LMWH then warfarin once INR 2-3
Fibrinolytics eg. streptokinase
Subdural Haemorrhage
Aetiology (3)
Trauma (can be delayed)
Intracranial hypotension
Dural metastases
Subdural Haemorrhage
Pathology (3)
Bleeding from bridging veins between cortex and venous sinuses (vulnerable to deceleration injury)
Blood accumulates between arachnoid and dura matter
Gradually increases ICP shifting midline sutures away from side of clot
Subdural Haemorrhage Risk factors (3)
Elderly (cerebral atrophy makes bridging veins vulnerable)
Falls (epilepsy, alcohol)
Anticoagulation
Subdural Haemorrhage
Signs + symptoms (7)
Fluctuating level of consciousness Headache Personality change Unsteadiness Increased ICP Seizures Localising neurological symptoms (eg. unequal pupils, hemiparesis) occur late after injury
Subdural Haemorrhage
Investigations (1)
CT shows crescent cell shaped haematoma over 1 hemisphere +/- midline shift
Subdural Haemorrhage Differential diagnoses (3)
Stroke
Dementia
CNS masses (eg. tumours, abscess)
Subdural Haemorrhage
Treatment (2)
Irrigation and evacuation with Burr-hole craniostomy 1st line
Craniotomy 2nd line if clot has organised
Extradural Haemorrhage
Aetiology (1)
Fractured temporal or parietal bone causing laceration of middle meningeal artery and vein, typically after trauma to a temple (blood accumulates between bone and dura)
Extradural Haemorrhage
Signs + symptoms (3)
Lucid interval: head injury with no loss of consciousness, may last a few hours –> days
Subsequent features: reduced GCS (from rising ICP), severe headache, vomiting, confusion, fits +/- hemiparesis with brisk reflexes and upgoing plantars
Bleeding continues: dilation of ipsilateral pupil, GCS decreases more, bilateral limb weakness
Extradural Haemorrhage
Investigations (2)
CT: biconvex/lens shaped haematoma
Skull X-ray may show fracture lines across course of middle meningeal vessels
Extradural Haemorrhage
Treatment (1)
Craniotomy with clot evacuation +/- bleeding vessel ligation
Delirium
Epidemiology (3)
20-30% hospital inpatients
50% post-op
85% of patients in last weeks of life
Delirium
Aetiology (10)
Systemic infection: pneumonia, UTI
Intracranial infection: encephalitis, meningitis
Drugs: opiates, anti-convulsants, sedatives, levodopa
Withdrawal: alcohol, drugs
Metabolic: uraemia, high/low Na, high/low glucose
Hypoxia: resp/cardiac failure
Vascular: stroke, MI
Increased ICP: head injury, SOL
Epilepsy: post-ictal state
Nutritional: thiamine/B12 deficiency
Delirium
Symptoms (8)
Impaired attention Anterograde memory impairment Disorientation in time, place or person Fluctuating levels of arousal Disordered sleep/wake cycle Disorganised thinking (rambling/incoherent) Perceptual distortions eg. illusions, hallucinations Mood changes
Delirium
Signs (7)
Acute onset and fluctuant Disturbed consciousness Change in cognition Delusions Emotional disturbance Sleep/wake cycle disturbance Psychomotor function disturbance
Delirium
Investigations (3)
4AT (>4 = possible delirium/cognitive impairment, 1-3 = possible cognitive impairment, 0 = both unlikely)
FBC, U&E, LFT, glucose
Septic screen: urine dipstick, CXR, blood cultures
Delirium
Treatment (2)
Exclude and treat possible triggers (sepsis, blood glucose, medications, retention/constipation)
Drug management not usually necessary but if disruptive may need haloperidol for sedation
Dementia
Aetiology (5)
Alzheimer's disease (50%) Vascular dementia (25%) Lewy body dementia (15-25%) Fronto-temporal dementia Others: alcohol and drug abuse, repeated head trauma, Whipple's disease, Huntington's
Dementia Reversible causes (7)
Hypothyroidism B12/folate deficiency Syphilis Subdural haemorrhage Parkinsons HIV Normal pressure hydrocephalus
Dementia
Investigations (4)
MMSE/MOCA
Bloods: FBC, ESR, U&E, Ca, LFT, TSH, B12, folate
CT/MRI: vascular damage, haemorrhage, structural pathology
Functional imaging: FDG, PET, SPECT
Dementia Diagnostic criteria (3)
Present for >6 months Functional decline in ADLs Memory impairment +1 of: -dysphagia (expressive/receptive) -dyspraxia (motor skills) -dysgnosia (difficulty recognising objects) -dysexecutive functioning
Alzheimer’s Disease
Aetiology (2)
Accumulation of B-amyloid peptide results in neuronal damage, tangles, increased amyloid plaques + loss of acetylcholine
Usually temporal lobes affected first
Alzheimer's Disease Risk factors (7)
1st degree relative affected Down's syndrome Vascular risk factors: high BP, AF, diabetes Smoking Alcohol Reduced physical and cognitive activity Depression and loneliness
Alzheimer’s Disease
Signs + symptoms (7)
Enduring, progressive and global cognitive impairment (unlike other dementias which may affect certain domains but not others)
Reduced visuospatial skill (get lost)
Reduced memory
Reduced verbal abilities
Reduced executive functioning
Anosognosia (lack of insight into the problems caused by the disease)
Later on: irritability, mood disturbance, behavioural change (eg. disinhibition), psychosis
Alzheimer’s Disease
Treatment (2)
Acetylcholinesterase inhibitors eg. donepezil, galantamine, rivastigimine- SE: D+V, cramps, incontinence, dizziness, insomnia
Antiglutamatergic: memantine (NMDA antagonist) for late stage disease- SE: hallucinations, confusion, hypersexuality
Vascular Dementia
Aetiology (1)
Cumulative effects of many small strokes
Vascular Dementia Risk factors (5)
Diabetes Previous strokes Hypertension Peripheral vascular disease Ischaemic heart disease
Vascular Dementia
Signs + symptoms (2)
Stepwise deterioration
Often predominant executive dysfunction and gait abnormalities
Lewy Body Dementia
Signs + symptoms (7)
Fluctuating cognitive impairment Detailed visual hallucinations Parkinsonism later Amnesia not prominent REM sleep disorder Falls + syncope Frontal-executive and visuospatial defects
Fronto-Temporal Dementia
Signs + symptoms (5)
Younger onset
Behavioural disorder (personality change)
Early preservation of episodic memory and spatial orientation
Disinhibition
Speech disorder
Parkinson’s Disease
Aetiology of Parkinsonism (2)
Idiopathic (Parkinson’s Disease)
Drugs (neuroleptics, prochloperazine)
Parkinson’s Disease
Pathology (3)
Mitochondrial DNA dysfunction causes degeneration of dopaminergic neurones in substantia nigra
Reduced input to striatum
Reduced dopamine levels
Parkinson’s Disease
Signs + symptoms (7)
Tremor: worse at rest, pill-rolling of thumb over fingers
Rigidity: with tremor gives cogwheel rigidity
Bradykinesia: slow initiation of movement and slow repetitive actions
Postural instability
REM sleep disorders
Reduced sense of smell
Poor executive functioning
Parkinson’s Disease
Treatment (6)
Levodopa + co-beneldopa (dopa-decarboxylase inhibitor), but efficacy reduces over time
Dopamine agonists eg. ropinirole can delay starting levodopa
Anticholinergics can help tremor but cause confusion in the elderly
MAO-B inhibitors eg. selegiline, as alternative to dopamine agonists
COMT inhibitors
Deep brain stimulation
Multiple Sclerosis
Aetiology (5)
Discrete plaques of demyelination at multiple CNS sites due to T-cell mediated immune response
Demyelination heals poorly, causing relapsing and remitting symptoms
Prolonged demyelination causes axonal loss and clinically progressive symptoms
Lack of sunlight and vit D exposure
Genetic
Multiple Sclerosis
Presenting signs + symptoms (5)
Usually monosymptomatic Unilateral optic neuritis (pain on eye movement and rapid reduction in central vision) Limb paraesthesia Brainstem/cerebellar: ataxia, diplopia May worsen with heat and exercise
Multiple Sclerosis
Progresssive signs + ymptoms (9)
Sensory: pins + needles, reduced vibration sense
Motor: spastic weakness, myelitis
GU: erectile dysfunction, retention, incontinence
GI: swallowing disorder, constipation
Eyes: diplopia, hemianopia, pupillary defect
Cerebellum: trunk/limb ataxia, intention tremor, falls
Cognitive/visuospatial decline: amnesia, mood disturbed
Transverse myelitis: loss of motor, sensory, autonomic reflex and sphincter function below level of lesion
L’hermitte’s sign: neck flexion causes electric shock in trunk and limbs
Multiple Sclerosis
Poor prognostic signs (4)
Older male
Motor signs at onset
Many relapses early on
Many MRI lesions and axonal loss
Multiple Sclerosis
Investigations (4)
McDonald criteria
MRI
CSF: oligoclonal bands of IgG on electrophoresis that are not present in serum suggests CNS inflammation
Bloods: FBC, TFT, B12, U&E to exclude other causes
Multiple Sclerosis Differential diagnoses (5)
SLE HIV Tumour Stroke Vasculitis
Multiple Sclerosis
treatment of acute relapses (2)
Steroids: IV methylprednisolone (don’t use more than 2x/year)
Plasma exchange if severe
Multiple Sclerosis Ongoing treatment (3)
Interferons (IFN-1B + IFN-1a): reduce relapses by 30% in active relapsing remitting disease and reduce lesion accumulation
Monoclonal antibodies: eg. alemtuzumab, natalizumab for relapsing remitting
Azathioprine for relapsing remitting
Multiple Sclerosis
Palliation (3)
Spasticity: baclofen, diazepam
Tremor: botulinum injection
Urgency/frequency: self catheterisation
Space Occupying Lesions
Primary brain tumours (7)
Astrocytoma: low grade tumour of CNS supporting cells, low grade diffuse tumours tend to occur in young people
Glioblastoma multiforme: high grade tumour of CNS supporting cells, may arise from pre-existing astrocytoma, v. aggressive, most common adult brain tumour
Oligodendroglioma: arise rom myelin sheath
Ependymoma: ventricular tumour in children
Medulloblastoma: neuroectoderm tumour that tends to occur in children in the brainstem
Primary CNS lymphoma: usually diffuse large B cell
Meningioma non-invasive but locally advanced, arise from arachnoid cells
Space Occupying Lesions
Secondary brain tumours (3)
Lung
Breast
Melanoma
Space Occupying Lesions
Signs + symptoms (4)
Increased ICP: headache worse on waking, lying down, bending forward or with coughing, vomiting, papilloedema
Seizures
Evolving focal neurology: VIth nerve palsy commonest due to long intracranial course
Subtle personality change
Space Occupying Lesions
Investigations (3)
CT
MRI good for posterior fossa masses
Consider biopsy
Space Occupying Lesions
Treatment (3) Prognosis (1)
Treatment:
- Benign: surgical excision unless inaccessible
- Malignant: surgical excision and adjuvant radiotherapy
- Lone chemo-radiotherapy if inoperable
Prognosis:
- <50% 5 year survival
Space Occupying Lesions
Localising the lesion (5)
Temporal lobe: dysphasia, contralateral homonymous hemianopia, amnesia
Frontal lobe: hemiparesis, personality change, Broca’s dysphasia
Parietal lobe: hemisensory loss, dysphasia
Occipital lobe: contralateral visual field defects
Cerebellar: DANISH- Dysdiadokinesis (inability to perform rapidly alternating movements), Ataxia, Nystagmus, Intention tremor, Slurred speech, Hypotonia
Bell’s Palsy
Definition (1)
Idiopathic facial nerve palsy
Bell’s Palsy
Other causes of VIIth nerve palsy (7)
Ramsay Hunt syndrome Lyme disease Meningitis Stroke Tumour MS Guillain-Barre
Bell’s Palsy
Signs + symptoms (8)
Abrupt onset Complete unilateral facial weakness Ipsilateral numbness/pain around ear Reduced taste Drooling Food trapped between gum and cheek Speech difficulties Ask to wrinkle forehead and close eyes forcefully (under bilateral cortical control so spared in uMN lesion)
Bell’s Palsy
Investigations (2)
Blood: ESR, glucose, increased Borrelia antibodies in Lyme disease (indistinguishable from Bell’s clinically), increased VZV antibodies in Ramsay Hunt
MRI: space occupying lesion, stroke, MS
Bell’s Palsy
Treatment (3)
Prednisolone within 72h of onset
May need plastic surgery if eye closure remains a problem and to straighten drooping face
Botulinum toxin can augment facial symmetry
Mononeuropathies Definition (2)
Lesions of individual peripheral/cranial nerves, usually caused by trauma or entrapment (eg. tumour), except for carpal tunnel syndrome
Mononeuritis multiplex is when 2+ nerves are affected, causes tend to be systemic eg. AIDS, RA, diabetes
Mononeuropathies Median nerve (5)
C6-T1
Nerve of precision grip
LOAF: 2 Lumbricals, Opponens pollicis, Abductor pollicis brevis, Flexor pollicis brevis
Trauma (lacerations) or carpal tunnel
Weakness of abductor pollicis brevis and sensory loss over radial 3.5 fingers and palm
Mononeuropathies Ulnar nerve (3)
C7-T1
Vulnerable to elbow trauma
Wasting/weakness of medial wrist flexors, interossei and medial two lumbricals (claw hand), hypothenar wasting
Mononeuropathies Radial nerve (5)
C5-T1
Nerve that opens the fist
Damaged by compression against the humerus
Wrist and finger drop
Muscles: BEST- Brachioradialis, extensors, Supinator, Triceps
Mononeuropathies Phrenic nerve (3)
C3-5 (C3, 4, 4 keeps the diaphragm alive)
Consider phrenic nerve palsy if orthopnoea with raised hemidiaphragm on CXR
Causes: lung cancer, myeloma, thymoma, thoracic surgery, MS, HIV
Mononeuropathies Sciatic nerve (3)
L4-S3
Damaged by pelvic tumours/fractures to pelvis/femur
Lesions affect hamstrings and all muscles below the knee (foot drop), with loss of sensation below the knee
Mononeuropathies
Common peroneal nerve (5)
L4-S1 Originates from sciatic nerve just above knee, often damaged as it winds round the fibular head Foot drop Weak ankle dorsiflexion/eversion Sensory loss over dorsum of foot
Mononeuropathies Tibial nerve (4)
L4-S3
Originates from sciatic nerve just above knee
Lesions lead to inability to stand on tiptoe (plantar flexion), invert foot, flex toes
Sensory loss over the sole
Polyneuropathies
Definition (1)
Disorders of peripheral/cranial nerves, distribution is symmetrical and widespread, often with distal weakness and sensory loss (‘glove and stocking’)
Polyneuropathies
Aetiology (5)
Metabolic: diabetes and renal failure (mostly sensory)
Vasculitides: RA, Wegener’s
Inflammatory: Guillain-Bare syndrome (mostly motor)
Infections: leprosy (mostly sensory), HIV, syphilis
Alcohol
Polyneuropathies
Signs + symptoms of sensory neuropathy (5)
Numbness
Pins and needles/burning
Affects extremities 1st (glove and stocking distribution)
Difficulty handling small objects like buttons
Trauma/joint deformity
Polyneuropathies
Signs + symptoms of motor neuropathy (5)
Often progressive Weak/clumsy hands Difficulty walking (falls, stumbling) Difficulty breathing LMN lesion signs
Polyneuropathies
Signs + symptoms of cranial neuropathy (2)
Swallowing/speaking difficulties
Diplopia
Polyneuropathies
Signs + symptoms of autonomic neuropathy (5)
Sympathetic and parasympathetic neuropathies may be isolated or part of generalised sensorimotor peripheral neuropathy Postural hypotension Erectile dysfunction Reduced sweating Constipation and urinary retention
Guillain-Barre Syndrome
Pathology (4)
Acute inflammatory demyelinating polyneuropathy
Triggered by Campylobacter jejuni, CMV, HIV, EBV
Trigger causes antibodies which attack nerves but very often no cause is found
May advance quickly and cause paralysis, unlike other neuropathies, proximal muscles are more affected (trunk, respiratory, cranial nerves)
Guillain-Barre Syndrome
Signs + symptoms (4)
A few weeks after infection a symmetrical ascending muscle weakness starts (progression over days-weeks)
Pain common
Autonomic dysfunction: sweating, tachycardia, BP changes, arrhythmias
Areflexia
Guillain-Barre Syndrome
Investigations (2)
Nerve conduction studies: slow conduction
CSF: high protein, normal WCC
Guillain-Barre Syndrome
Treatment (3)
Ventilate with respiratory involvement
IV immunoglobulin
Plasma exchange
Guillain-Barre Syndrome
Prognosis (3)
85% make complete or near complete recovery
10% unable to walk 1 year
Mortality 10%
Motor Neuron Disease
Definition (2)
Cluster of major degenerative diseases characterised by selective loss of neurons in motor cortex, cranial nerve nuclei and anterior horn cells
Upper and lower motor neurons are affected but there is no sensory loss/sphincter disturbance
Motor Neuron Disease
Classification (4)
ALS: loss of motor neurons in motor cortex and the anterior horn of the cord, so weakness and UMN signs + LMN signs
Progressive bulbar palsy: only affects cranial nerves IX-XII (LMN lesion of tongue and muscles of talking/swallowing, can also be caused by Guillain-Barre, myasthenia
Corticobulbar palsy: UMN lesion of muscles of swallowing/talking, due to bilateral lesions (increased jaw jerk, slow speech, also see in MS/stroke)
Progressive muscular atrophy: anterior horn lesion only, thus no UMN signs
Motor Neuron Disease
Signs + symptoms (7)
Stumbling spastic gait Foot drop Proximal myopathy Weak grip Shoulder abduction UMN signs LMN signs
Motor Neuron Disease
Treatment (3)
Antiglutamatergic drugs may prolong life
Treat symptoms such as drooling, dysphagia, spasticity, joint pain
Non-invasive ventilation
Duchenne Muscular Dystrophy
Pathology (1)
X-linked recessive mutation in dystrophin gene results in near-total loss of dystrophin (muscles get replaced by fibroadipose tissue)
Duchenne Muscular Dystrophy
Signs + symptoms (4)
Boys aged 1-6
Waddling, clumsy gait
Gower’s manoeuvre: on standing, he uses his hands to climb up his legs
Wheelchairs required by 9-12
Duchenne Muscular Dystrophy
Investigations (2)
CK increases (measure in all boys not walking by 1.5 years) Muscle biopsy (abnormal fibres surrounded by fat and fibrous tissue)
Duchenne Muscular Dystrophy
Prognosis (3)
Prednisolone slows decline in muscle strength and function in short term
Mechanical ventilation improves longevity
Median age at death 31 years
Myasthenia Gravis
Pathology (3)
Autoimmune disease mediated by antibodies to acetylcholine receptors (AChR)
Interfering with the neuromuscular transmission via depletion of working post-synaptic receptor sites
Both B+T cells implicated
Myasthenia Gravis
Signs + symptoms (5)
Increasing muscular fatigue Muscle groups affected in order: extraocular --> bulbar (swallowing, chewing) --> face --> neck etc. Ptosis Diplopia On counting to 50 the voice fades
Myasthenia Gravis
Associations (2)
If under 50 commoner in women and associated with other autoimmune diseases and thymic hyperplasia
If over 50 commoner in men and associated with thymic atrophy/tumour
Myasthenia Gravis
Investigations (3)
Anti-AChR antibodies
Neurophysiology
CT thymus
Myasthenia Gravis
Treatment (3)
Symptom control: anticholinesterase
Immunosuppression: treat relapses with prednisolone (may combine with azathioprine/methotrexate)
Thymectomy
Spinal Cord Injury
Aetiology (5)
Most due to trauma, especially RTAs Falls in elderly population Tumours Prolapsed discs Inflammatory disease
Spinal Cord Injury
Assessment (8)
ATLS principles
Log-roll technique for movement
C-spine immobilisation
Prevent and treat hypotension (due to neurogenic shock)
Restore intravascular volume (don’t overload)
Monitor and treat symptomatic bradycardia
Monitor and regulate temp.
Perform serial neurological examinations
Spinal Cord Injury
Root lesion tests (10)
C5: shoulder abduction C6: elbow flexion C7: elbow extension C8: finger flexion (grip) T1: finger abduction L2: hip flexion L3: knee extension L4: ankle dorsiflexion L5: great toe extension S1: ankle plantarflexion
Spinal Cord Injury
Consequences (5)
Injury to cervical spine causes tetraplegia but injury above level of phrenic nerve (C3-5) results in paralysis of diaphragm
Thoracic spine: paraplegia
Lumbar spine: cauda equina
Respiratory insufficiency: from neurological dysfunction and associated trauma
Hypotension below lesion (sympathetic interruption and resultant neurogenic shock- low BP + HR)
Spinal Cord Injury
Treatment (5)
Early transfer to spinal injuries unit Steroids Early surgical decompression and stabilisation Traction for cervical injuries Anticoagulation: v high risk of VTE
Brown-Sequard Syndrome
Definition (1)
Hemisection (lesion in one half) of spinal cord
Brown-Sequard Syndrome
Aetiology (1)
Penetrating injuries
Brown-Sequard Syndrome
Signs + symptoms (4)
Ipsilateral UMN weakness below lesion (severed corticospinal tract causing spastic paraparesis, brisk reflexes, extensor plantars)
Ipsilateral paralysis
Ipsilateral loss of proprioception and vibration (1 dorsal column severed)
Contralateral loss of pain and temp. (severed spinothalamic tract which is crossed over)
Spinal Shock
Definition (1)
Transient physiological loss of function, often due to haemorrhage
Spinal Shock
Signs + symptoms (5)
Anaesthesia
Flaccid paralysis below the level
Urinary retention
Over time flexion at hip and knee may be induced by stimuli (cold) and reflexes return
Overall, temporary loss of sensory and motor function tends to recover
Spinal Cord Compression
Aetiology (5)
Bone displacement Disc prolapse Local tumour (secondary malignancy- breast, lung, prostate) Abscess Haematoma
Spinal Cord Compression
Signs + symptoms (6)
Spinal/root pain
Leg weakness
LMN signs at level of lesion
UMN signs and sensory changes below lesion (spastic weakness, brisk reflexes, upgoing plantars, loss of coordination, joint position sense and vibration sense)
Joint position and vibration affected on same side
Pain and temp affected on other side
Spinal Cord Compression Differential diagnoses (5)
Transverse myelitis MS Trauma Guillain-Barre Cord vasculitis (eg. syphilis)
Spinal Cord Compression
Investigations (4)
MRI
Biopsy/surgical exploration may be needed to identify nature of mass
Bloods: FBC, ESR, syphilis serology, U&E, LFT, PSA
CXR: primary lung malignancy or secondaries
Spinal Cord Compression
Treatment (2)
If malignancy: IV dexamethasone while considering chemo/radio +/- decompressive laminectomy
If epidural abscess: surgical decompression and antibiotics
