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Phase 2a > Neurology > Flashcards

Neurology Flashcards

1
Q

What are the two nervous systems? How many cranial and spinal nerves are there? What are collections of cell bodies called in the different nervous systems?

A
  • CNS = brain and spinal cord. Collections of cell bodies are called nuclei (singular = nucleus)
  • PNS) = outside the CNS. Collections of cell bodies are called ganglia (singular = ganglion)
  • 12 pairs of cranial nerves: connect brain / brainstem and the head and neck
  • 31 pairs of spinal nerves: connect spinal cord and the periphery (muscles, skin, organs etc.)
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2
Q

What does the autonomic nervous system control? Which nervous system does it belong to? What are its two divisions?

A
  • Control viscera; smooth muscle, glands, heart
  • Beyond conscious control
  • Parts in the CNS, parts in the PNS
  • Sympathetic and parasympathetic divisions
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3
Q

What can we find on the lateral surface of the brain?

A
  • Cerebral hemispheres
  • Important regions of cerebral cortex
  • Brainstem
  • Cerebellum
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4
Q

What can we find on the medial surface of the brain?

A
  • Cerebral hemispheres and cerebral cortex
  • Diencephalon (thalamus and hypothalamus)
  • Brainstem
  • Cerebellum
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5
Q

What can we find in the deep brain?

A
  • Internal capsule
  • Diencephalon (thalamus and hypothalamus)
  • Basal ganglia:
  • Caudate
  • Putamen
  • Globus pallidus
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6
Q

Where does the spinal cord start and end? What are the pairs of spinal nerves?

A
  • Starts just below the medulla. Ends at L1-2
  • 31 pairs of spinal nerves (8 cervical, 12 thoracic, 5 lumbar, 5 sacral and 1 coccygeal (Come Through Little Saint)
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7
Q

What is a dermatome? What is a myotome?

A
  • Dermatome = area of skin supplied by a single spinal nerve
  • Myotome = muscles supplied by a single spinal nerve
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8
Q

What is the difference between an ascending and descending tract?

A
  • Ascending tracts bring sensory info. from periphery to CNS
  • Descending tracts carry motor info. from CNS to periphery
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9
Q

What are the key ascending tracts?

A
  • Dorsal columnar medial lemniscus
  • Spinothalamic tract
  • Spinocerebellar tract
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10
Q

What sensations does the dorsal column medial lemniscus carry? Where are the synapses? Where are the decussations?

A
  • Carry proprioception, vibration + discriminative touch
  • Fasciculus cuneatus = LATERAL + carries info from UPPER BODY to cuneat tubercle in medulla
  • Fasciculus gracilis = MEDIAL + carries info from LOWER BODY to gracile tubercle in medulla
  • Ascends to medulla + then DECUSSATES and SYNAPSES to become medial lemniscus + then ascends to thalamus + SYNAPSES to primary somatosensory cortex
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11
Q

What sensations does the spinothalamic tract carry? Where does it synapse?

A
  • LATERAL: pain + temperature
  • MEDIAL: crude touch
  • Ascend on same side for 2-3 vertebra. SYNAPSE and DECUSSATE
  • Up to medulla
  • SYNAPSE
  • Up to primary somatosensory cortex
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12
Q

What sensations does the spinocerebellar tract carry? What are the two tracts?

A
  • Carries unconscious proprioception
  • Ventral (anterior) spinocerebellar
  • Dorsal (posterior) spinocerebellar
  • Enter dorsal grey horn, SYNAPSE at nucleus dorsal is (C8-L3)
  • Majority of fibres decussate to form ventral spinocerebellar tract (dorsal fibres remain ipsilateral)
  • Ascend through medulla to cerebellar cortex
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13
Q

What are the three types of descending tracts?

A
  • Corticospinal
  • Corticobulbar
  • Vestibulospinal, Reticulospinal, Tectospinal, Rubrospinal
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14
Q

What does the corticospinal tract do? Where does it decussate?

A
  • Transmits control of voluntary muscles (motor)
  • Provides axial and limb motor function via upper motor neurons and lower motor neurons
  • Primary motor cortex –> internal capsule –> medullary pyramids
  • 90% decussate here (lateral)
  • 10% decussate at white commissures (anterior), i.e. stay ipsilateral
  • SYNAPSE with LMN, out of spinal cord via anterior horn
  • Terminate at neuromuscular junction within motor units
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15
Q

What does the corticobulbar tract provide? What is its path?

A
  • Voluntary movement of face and neck
  • Motor and premotor cortex –> internal capsule –> brainstem
  • SYNAPSE with cranial nerve nuclei (lower motor neurone)
  • To face and neck muscles
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16
Q

What does the extrapyramidal tract provide?

A
  • Vestibulospinal: muscle tone and posture
  • Reticulospinal: spinal reflexes
  • Tectospinal: head turning to view stimuli
  • Rubrospinal: assists motor functions
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17
Q

What are the twelve cranial nerves?

A

On Occasion Our Trusty Truck Acts Funny Very Good Vehicle Any How

  • 1: Olfactory
  • 2: Optic
  • 3: Oculomotor
  • 4: Trochlear
  • 5: Trigeminal
  • 6: Abducens
  • 7: Facial
  • 8: Vestibulocochlear
  • 9: Glossopharyngeal
  • 10: Vagus
  • 11: Accessory
  • 12: Hypoglossal
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18
Q

What are the sensory and motor functions of the cranial nerves?

A

(Remember: Some Say Money Matters But My Brother Says Big Brains Matter More)

  • 1: Olfactory = sensory
  • 2: Optic = sensory
  • 3: Occulomotor = motor
  • 4: Trochlear = motor
  • 5: Trigeminal = both
  • 6: Abducens = motor
  • 7: Facial = both
  • 8: Vestibulocochlear = sensory
  • 9: Glossopharyngeal = both
  • 10: Vagus = both
  • 11: Accessory = motor
  • 12: Hypoglossal = motor
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19
Q

Where do the twelve cranial nerves emerge from?

A
  • First two (olfactory + optic) emerge from cerebrum
  • Remaining ten emerge from the brainstem (CN IX, X, XI and XII emerge from the medulla oblangata)
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20
Q

What are the four autonomic (parasympathetic) cranial nerves?

A
  • 10, 9, 7 and 3 (remember 1973)
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21
Q

What are the functions of the twelve cranial nerves?

A
  • Olfactory (1) = smell (sensory)
  • Optic (2) = vision (sensory)
  • Occulomotor (3) = eye movements, sympathetic = pupil dilation, parasympathetic = pupil constriction, accommodation (motor)
  • Trochlear (4) = SO4 LR6, all other muscles are innervated by CN 3
  • Trigeminal (5) = sensory = anterior 2/3 tongue, face, motor = jaw movement, three branches (ophthalmic, maxillary, and mandibular) (motor)
  • Abducens (6) = lateral rectus (motor)
  • Facial (7) = motor = facial expressions, lacrimal/salivary/sublingual, sensory = taste bud anterior 2/3 tongue (both)
  • Vestibulocochlear (8) = hearing and balance (sensory)
  • Glossopharyngeal and Vagus (9 and 10) = motor = swallowing and gag reflex, sensory = posterior 1/3 of tongue, secretion of parotid gland (both)
  • Accessory (11) = sternocleidomastoid and trapezius (motor)
  • Hypoglossal (12) = tongue movement (motor)
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22
Q

What are the meninges?

A
  • PAD OUT:
  • Dura – outermost, tough, fibrous
  • Arachnoid – soft, thin, loose
  • Pia – innermost, adhered to the surface of the brain
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23
Q

What are the two layers of the dura mater? What happens in some places?

A
  • Periosteal – outer layer, adhered to skull
  • Meningeal – inner layer
  • In places the layers diverge to form dural venous sinuses
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24
Q

What does the pia mater contribute to? Can it be seen?

A
  • Pia mater contributes to the blood brain barrier
  • Thin layer - cannot be seen with the naked eye
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25
Q

What are the spaces in between the meninges called?

A
  • Skull and outer dura = narrow extradural space (in some regions)
  • Inner dura and arachnoid = narrow subdural space
  • Arachnoid and pia = subarachnoid space - continuous with ventricular system
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26
Q

What can we find in each of the spaces between the meninges?

A
  • Extradural space – meningeal vessels
  • Subdural space – bridging veins
  • Subarachnoid space – Circle of Willis and branches
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27
Q

What is the blood supply to the lateral surface of the brain? How about the medial region?

A
  • Lateral surface: most from the middle cerebral artery
  • Medial surface: mostly from the anterior cerebral artery
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28
Q

Where is the lower limb represented? How about the upper limb and face?

A
  • Lower limb - represented on the medial surface of the cerebral hemisphere = territory of the anterior cerebral artery
  • Upper limb and face represented on the lateral surface = middle cerebral artery territory
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29
Q

What are the different types of cerebrovascular events? Which ones are classified as ischaemic events and which are classified as haemorrhagic events? Which are classified as a stroke and which are not classified as stroke?

A
  • Ischaemic events:
  • Transient Ischaemic Attack (TIA) (not a stroke)
  • Cerebral Infarction (ischaemic stroke) (stroke)
  • Haemorrhagic events:
  • Intracerebral haemorrhage (stroke)
  • Subarachnoid haemorrhage (stroke)
  • Subdural haemorrhage (not a stroke)
  • Extradural haemorrhage (not a stroke)
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30
Q

What is a transient ischaemic attack (TIA)? What is it caused by? When are symptoms maximal? What is its classical time period? Without intervention, how many TIA sufferers will have a stroke within one week?

A
  • A sudden onset, brief episode of neurological deficit caused by temporary, focal cerebral ISCHAEMIA (lack of O2 + nutrients to the brain)
  • Symptoms are maximal at ONSET (usually last 5-15 minutes)
  • Usually last <24 HOURS
  • Without intervention, 1/12 will have a stroke WITHIN A WEEK
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31
Q

What is the epidemiology of a TIA?

A
  • 15% of FIRST STROKES are PRECEDED by a TIA
  • Can also foreshadow an MI
  • More common in MALES and BLACK PEOPLE - predisposition to hypertension & atherosclerosis
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32
Q

What are the risk factors for a TIA?

A
  • AGE
  • HYPERTENSION
  • SMOKING
  • DIABETES
  • Hyperlipidaemia
  • Heart disease - ATRIAL FIBRILLATION
  • Combined oral CONTRACEPTIVE PILL
  • Peripheral arterial disease, clotting disorder, vasculitis
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33
Q

What is the aetiology of a TIA?

A
  • ATHEROTHROMBOEMBOLISM = from carotid artery - main cause - listen for a CAROTID BRUIT
  • CARDIOEMBOLISM: in ATRIAL FIBRILLATION, after an MI, valve disease/prosthetic valve
  • Hyperviscosity
  • Hypoperfusion
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34
Q

What are the main differential diagnoses for a TIA?

A
  • Hypoglycemia
  • Migraine aura
  • Focal epilepsy
  • Vasculitis
  • Syncope, e.g. due to an arrhythmia
  • Retinal bleed
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35
Q

What is the clinical presentation of a TIA?

A
  • Carotid artery (90%):
  • AMAUROSIS FUGAX - caused by temporary occlusion of retinal artery. Unilateral sudden vision loss. Transient – only lasts minutes. “Like a curtain descending”
  • Aphasia
  • Hemiparesis
  • Hemisensory loss
  • Hemianopic vision loss
  • Vertebrobasilar artery (10%):
  • Diplopia, vertigo, vomiting
  • Choking and dysarthia
  • Ataxia
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36
Q

In what cases can we say that it is not a TIA?

A
  • NOT a TIA if these occur on their own:
  • Syncope
  • Dizziness
  • Temporary loss of consciousness
  • Temporary memory loss
  • Gradual onset – suggests demyelination, tumour, migraine
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37
Q

What score is used to calculate the risk of stroke after a TIA? What does it stand for?

A

ABCD2:

  • Age (>60 years)
  • Blood pressure (>140/90)
  • Clinical features (e.g., unilateral weakness)
  • Duration of TIA
  • Diabetes mellitus
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38
Q

What are the investigations for TIA?

A
  • Clinical diagnosis based off SYMPTOMS DESCRIPTION
  • BLOOD TESTS: glucose, FBC (looking for polycythemia), ESR (raised in vasculitis), U&Es, cholesterol, INR (if on Warfarin)
  • FIRST LINE = BRAIN IMAGING - diffusion weighted MRI or CT
  • SECOND LINE = CAROTID imaging - DOPPLER ULTRASOUND. MR/CT angiography if stenosis is found
  • ECG
  • Echocardiogram
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39
Q

Describe the management for TIA.

A
  • Immediate management: ASPIRIN 300mg. Refer to specialist – to be seen WITHIN 24h of symptom onset
  • Control CV risk factors: BP control, smoking cessation, statin, e.g. simvastatin, no driving for 1 month
  • Antiplatelet therapy: standard treatment is ASPIRIN 75mg daily (with modified-release Dipyridamole) OR Clopidogrel daily
  • Anticoagulation (e.g. Warfarin) for patients with Atrial Fibrillation
  • Carotid Endarterectomy: if >70% carotid stenosis, reduces stroke/TIA risk by 75%
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40
Q

What is stroke? What is it caused by?

A
  • RAPID ONSET NEUROLOGICAL DEFICIT lasting for OVER 24 HOURS
  • POOR BLOOD FLOW to the brain causes CELL DEATH
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41
Q

What is the epidemiology of stroke?

A
  • 3rd MOST COMMON cause of death worldwide - death rate of 20-25%
  • In the UK, someone has a stroke every 3.5 minutes
  • 1 in 4 people who suffer a stroke die WITHIN 1 year
  • 1 in 2 stroke survivors have PERMANENT DISABILITY
  • Most common in OLDER PEOPLE - rare aged <40
  • Slightly more common in MALES
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42
Q

What are the two types of stroke? How do we determine which type is present?

A
  • ISCHAEMIC (85%) - blood clot in blood vessel to brain
  • HAEMORRHAGIC (15%) - bleed in small blood vessel in/around brain
  • An URGENT CT/MRI is needed to determine which type is present - treating the wrong type would be devastating
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43
Q

What is the public health campaign for stroke recognition?

A

F.A.S.T:

  • Face - has it fallen on one side?
  • Arms - can they raise them?
  • Speech - is it slurred?
  • Time - if you notice any of these, do not hesitate to call 999
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44
Q

What is a cerebral infarction (ischaemic stroke)?

A
  • Blood vessel to/in brain OCCLUDED by a CLOT
  • Ischaemia & INFARCTION follow:
  • Infarcted area DIES, resulting in FOCAL neurological SYMPTOMS
  • Infarcted area is surrounded by a swollen area (OEDEMA) which can REGAIN FUNCTION with neurological recovery
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45
Q

What are the risk factors for ischaemic stroke?

A
  • AGE, MALE, HYPERTENSION, SMOKING, DIABETES, recent/past TIA
  • Hyperlipidaemia
  • Heart disease - IHD, AF, valve disease
  • Combined oral CONTRACEPTIVE pill
  • Black, Asian, peripheral vascular disease, clotting disorder, vasculitis, alcohol, infective endocarditis, carotid bruit
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46
Q

What is the aetiology of ischaemic stroke?

A
  • Small vessel occlusion by THROMBUS
  • ATHEROTHROMBOEMBOLISM, e.g. from carotid artery
  • CARDIOEMBOLISM - AF, post-MI, valve disease, infective endocarditis
  • Hyperviscosity
  • Hypoperfusion
  • Vasculitis
  • Fat emboli from a long bone fracture
  • Venous sinus thrombosis
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47
Q

What is the clinical presentation of a cerebral infarct (ischaemic stroke)?

A

Depends on site (ACA, MCA, PCA etc.):

  • ACA: CONTRALATERAL WEAKNESS AND SENSORY LOSS OF THE LOWER LIMB, incontinence, drowsiness
  • MCA: CONTRALATERAL MOTOR WEAKNESS AND SENSORY LOSS, APHASIA/DYSPHAGIA (due to Wernicke’s and Broca’s area being affected), FACIAL DROOP
  • PCA: HOMONYMOUS HEMIANOPIA, visuo-spatial deficit
  • Vertebrobasilar artery: coordination and balance
  • Lateral medullary syndrome: ipsilateral HORNER’S syndrome = reduced sweating, facial numbness, dysarthria, limb ataxia, dysphagia
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48
Q

What is the clinical presentation of brainstem infarcts (ischaemic stroke)?

A
  • Varies depending on the site:
  • QUADRIPLEGIA
  • LOCKED-IN SYNDROME
  • Facial numbness & paralysis
  • Gaze & vision disturbances
  • Dysarthria & speech impairment
  • Vertigo, nausea, vomiting
  • Cerebellar signs
  • Palatal paralysis & diminished gag reflex
  • Altered consciousness
  • Coma
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49
Q

What is a lacunar infarct (ischaemic stroke)? Where do they come from? Where can they happen?

A
  • Small infarcts from occlusion of a single small perforating artery supplying a subcortical area
  • Can happen in:

– Internal capsule

– Basal ganglia

– Thalamus

– Pons

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50
Q

What is the clinical presentation of a lacunar infart (ischaemic stroke)?

A
  • Depends on the area affected. One of:
  • Sensory loss
  • Weakness (unilateral)
  • Ataxic hemiparesis
  • Dysarthria - motor speech problems
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51
Q

What are the investigations for ischaemic stroke?

A
  • NON-CONTRAST CT HEAD SCAN ASAP: DISTINGUISHES ISCHAEMIC from HAEMORRHAGIC. Shows site of infarct. Identifies conditions mimicking a stroke
  • Diffusion-weighted MRI scan: more sensitive. CT might be negative in first few hours after infarct. Indicated if diagnosis is uncertain
  • BLOOD TESTS: glucose (to rule out hypoglycaemia), FBC (looking for polycythemia), ESR (raised in vasculitis), U&Es, cholesterol, INR (if on Warfarin)
  • ECG: AF, MI
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52
Q

Describe the management for ischaemic stroke.

A
  • Immediate management: haemorrhagic stroke must be EXCLUDED. Immediate loading dose: ASPIRIN 300MG
  • Antiplatelet therapy: aspirin 300mg daily for 2 weeks, then Clopidogrel daily long term
  • Anticoagulation (e.g., Warfarin) for patients with Atrial Fibrillation
  • THROMBOLYSIS: must happen WITHIN 4.5 HOURS of symptoms onset (the window in which the benefits outweigh the risks). IV ALTEPLASE (loads of CONTRAINDICATIONS as it can cause massive bleeds)
  • MECHANICAL THROMBOECTOMY: endovascular removal of thrombus - only suitable for some patients and not others
  • Admit to an acute stroke unit
  • Swallowing & feeding support
  • Eventual rehabilitation
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53
Q

What is the clinical scoring tool for stroke in an emergency room?

A

ROSIER

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54
Q

What is an intracerebral haemorrhage (haemorrhagic stroke)? What is it due to? What percentage of strokes does an intracerebral haemorrhage make up and what is its mortality?

A
  • SUDDEN BLEEDING into brain tissue
  • Due to RUPTURE of a BLOOD VESSEL WITHIN the BRAIN
  • Like an ischaemic stroke, this leads to INFARCTION, due to O2 DEPRIVATION
  • Pooling blood INCREASES intracranial pressure (ICP)
  • ~10% of strokes, higher mortality: up to 50%
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55
Q

What are the major risk factors for intracerebral haemorrhage?

A
  • HYPERTENSION
  • ANTICOAGULATION drugs
  • Just been given THROMBOLYSIS
  • Age
  • Alcohol
  • Smoking
  • Diabetes
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56
Q

What is the aetiology of intracerebral haemorrhage?

A
  • HYPERTENSION: can lead to stiff & brittle vessels = prone to rupture and microaneurysms
  • SECONDARY to ISCHAEMIC stroke: bleeding after reperfusion
  • Head trauma
  • Arteriovenous malformations
  • Vasculitis
  • Vascular tumours
  • Brain tumours
  • Cerebral amyloid angiopathy
  • Carotid artery dissection
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57
Q

When we have a bleed in the brain, the intercranial pressure is raised. Explain what can happen.

A
  • Puts pressure on skull, brain & blood vessels - healthy tissue can die
  • CSF outflow obstruction = hydrocephalus
  • Midline shift = displacement of brain tissue across the centre line of the brain
  • Tentorial herniation = movement of brain tissue from one intercranial compartment to another
  • Coning = compression of brainstem = stop breathing because respiratory centre is there = death
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58
Q

What is the clinical presentation of intracerebral haemorrhage?

A
  • Similar to an ischaemic stroke
  • Pointers to haemorrhage (these are unreliable, as CT scan is needed for differentiation):
  • Sudden loss of consciousness
  • Severe headache
  • Meningism
  • Coma
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59
Q

What are the investigations for intracerebral haemorrhage?

A
  • Same as ischaemic stroke
  • Brain imaging (CT/MRI) is essential
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60
Q

Describe the management of intracerebral haemorrhage.

A
  • Stop anticoagulants immediately: effects reversed with clotting factor replacement, decision to restart after 1-2 weeks on a case by case basis
  • Control of BP - IV drugs
  • Reducing ICP: mechanical ventilation, IV Mannitol to reduce ICP
  • Referred for neurosurgical evaluation if:
  • Hydrocephalus
  • Coma
  • Brainstem compression
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61
Q

What is a subarachnoid haemorrhage? What percentage of strokes are made up by subarachnoid haemorrhages?

A
  • Spontaneous BLEEDING into SUBARACHNOID SPACE (space between arachnoid mater and pia mater)
  • Can be CATASTROPHIC
  • About 5% of strokes
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62
Q

What is contained with the subarachnoid space?

A

Circle of Willis

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63
Q

What is the epidemiology of subarachnoid haemorrhage?

A
  • Typical AGE 35-65
  • Make up 5% of strokes
  • ~50% of people DIE STRAIGHT AWAY or soon after
  • 10-20% more DIE from REBLEEDING within weeks
  • HALF the survivors are left with SIGNIFICANT DISABILITY
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64
Q

What are the risk factors for subarachnoid haemorrhage?

A
  • HYPERTENSION
  • KNOWN ANEURYSM
  • PREVIOUS ANEURYSMAL SAH
  • Smoking
  • Alcohol
  • Family history
  • Bleeding disorders
  • Associated with BERRY ANEURYSMS (things that cause Berry aneurysms = PKD, coarctation of aorta, Ehlers-Danlos syndrome + Marfan syndrome
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65
Q

What is the aetiology of subarachnoid haemorrhages?

A
  • Traumatic injury
  • Aneurysmal RUPTURE - BERRY ANEURYSMS. 70-80% of cases, at common points around Circle of Willis (junction of anterior communicating artery with anterior cerebral artery (40%) and bifurcation of the middle cerebral artery (34%))
  • ARTERIOVENOUS MALFORMATIONS = abnormal tangle of blood vessels connecting arteries and veins, 15% of SAH cases
  • Idiopathic = 15-20% of cases
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66
Q

What is the pathophysiology of subarachnoid haemorrhage, i.e. its complications?

A
  • Tissue ISCHAEMIA: less blood can reach tissue due to bleeding loss, so less O2 & nutrients reach tissue, causing cell death
  • Raised ICP: fast flowing arterial blood pumped into cranial space
  • SPACE-OCCUPYING LESION = puts pressure on brain
  • Blood IRRITATES MENINGES: these inflame – meningism symptoms, can obstruct CSF outflow – hydrocephalus
  • VASOSPASM - bleeding irritates other vessels, e.g. arteries so they constrict = ischaemic injury
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67
Q

What are the symptoms of subarachnoid haemorrhage?

A
  • SUDDEN ONSET EXCRUCIATING HEADACHE: “THUNDERCLAP”, “WORST EVER headache of life”, typically OCCIPITAL. Can get a sentinel headache before main rupture, sign of a ‘warning leak’ - in ~6%
  • NAUSEA
  • VOMITING
  • COLLAPSE
  • LOSS of/DEPRESSED CONSCIOUSNESS
  • Seizures
  • Vision changes
  • Coma
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68
Q

What are the signs of subarachnoid haemorrhage?

A
  • Signs of meningeal irritation:
  • NECK STIFFNESS
  • KERNIG’S SIGN (knee and hip flexed to 90 degrees + extension of knee is painful or limited in extension)
  • BRUDZINSKI’S SIGN (passive flexion of neck causes hip and knee flexion)
  • Retinal, subhyaloid & vitreous bleeds = worse prognosis, with/without also papilloedema
  • Focal neurological signs, e.g. 3rd nerve palsy
  • Increased BP
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69
Q

What are the main differential diagnoses for subarachnoid haemorrhage?

A
  • Headache:
  • MIGRAINE
  • Cluster headache
  • MENINGITIS
  • Intracerebral haemorrhage
  • Cortical vein thrombosis
  • Carotid/vertebral artery dissection
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70
Q

What are the investigations for subarachnoid haemorrhage? What will they show?

A
  • Brain CT = ASAP!. Detects >95% of SAH in first 24 hours. Subarachnoid and/or intraventricular blood. “STAR” shaped sign
  • LUMBAR PUNCTURE but only if normal ICP to prevent coning. Perform if -ve CT but strong suspicion of SAH remains. PERFORMED AFTER 12 HOURS as we are looking for XANTHACROMIA = confirms SAH, CSF is yellowish - filled with breakdown products of RBCs, e.g. bilirubin
  • MRI/CT angiography = to establish source of bleeding, e.g. aneurysm, in all patients fit for surgery
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71
Q

Describe the management for a subarachnoid haemorrhage.

A
  • Once SAH is proven, IMMEDIATELY REFER TO NEUROSURGEON
  • NIMODIPINE for 3 weeks - Ca2+ antagonist, reduces vasospasm so reduces cerebral ischaemia
  • Surgery:
  • ENDOVASCULAR COILING (preferred) OR surgical clipping if angiography has shown an aneurysm
  • IV fluids - maintain cerebral perfusion
  • Ventricular drainage for hydrocephalus
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72
Q

What is a subdural haematoma? What are these due to? What is the usual cause of a subdural haematoma? How long is the latent interval?

A
  • BLEEDING into SUBDURAL SPACE (space between dura mater & arachnoid mater)
  • Due to rupture of a BRIDGING VEIN - run from cortex to venous sinuses, vulnerable to deceleration injury
  • Usually due to HEAD TRAUMA - other causes include dural metastases
  • Massive LATENT INTERVAL - WEEKS TO MONTHS
  • Very treatable
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73
Q

What is the epidemiology/risk factors for a subdural haematoma?

A
  • BABIES - traumatic injury, e.g. “shaking baby syndrome”
  • BRAIN ATROPHY - veins are more susceptible to rupture, e.g. DEMENTIA, ELDERLY, ALCOHOLICS. These people are also more ACCIDENT-PRONE and at risk of FALLS, along with epileptics
  • People on ANTICOAGULANTS
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74
Q

What is the pathophysiology of subdural haematoma?

A
  • Bleeding from bridging veins into subdural space
  • Forms a haemotoma (SOLID SWELLING of CLOTTED blood)
  • Then BLEEDING STOPS
  • WEEKS/MONTHS LATER, haematoma starts to AUTOLYSE. This creates a MASSIVE INCREASE in ONCOTIC AND OSMOTIC PRESSURE. Water sucked in, haematoma ENLARGES
  • GRADUAL RISE in ICP over weeks
  • MIDLINE STRUCTURES SHIFTED AWAY from side of clot - TENTORIAL HERNIATION, CONING
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75
Q

What are the symptoms of subdural haematoma?

A
  • FLUCTUATING level of CONSCIOUSNESS
  • DROWSINESS
  • HEADACHE
  • CONFUSION - may fluctuate
  • Insidious physical & intellectual slowing
  • Personality change
  • Unsteadiness
  • They can often not remember the traumatic injury as it was long ago!
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76
Q

What are the signs of subdural haematoma?

A
  • RAISED ICP
  • Seizures
  • Localising neurological signs:
  • Unequal pupils
  • Hemiparesis
  • Occur late (often >1 month after injury)
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77
Q

What are the investigations for subdural haematoma? What will these show?

A
  • NON-CONTRAST HEAD CT SCAN:
  • Shows haematoma - crescent-shaped - BANANA
  • Shows MIDLINE SHIFT
  • MRI scan
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78
Q

Describe the management of a subdural haematoma.

A
  • SURGERY:
  • 1st line = BURR-HOLE washout
  • 2nd line = craniotomy
  • IV MANNITOL to reduce ICP
  • Reverse clotting abnormalities
  • Address cause of trauma, e.g. falls, trauma
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79
Q

What is an extradural haematoma? What are these usually a result of? How long is the interval?

A
  • BLEEDING into EXTRADURAL SPACE (space between dura mater & skull bone)
  • Usually after TRAUMA to TEMPLE:
  • FRACTURE to TEMPORAL/parietal BONE
  • RUPTURE of MIDDLE MENINGEAL ARTERY
  • Can also be due to tear to dural venous sinus
  • LUCID INTERVAL – can be HOURS. Initial drowsiness/unconsciousness, then recovery, then rapid deterioration later on
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80
Q

What is the epidemiology and risk factors for extradural haematoma?

A
  • Mostly in YOUNG PEOPLE, but rare in small children due to plasticity of skull
  • Rare in >60s as the dura mater is more tightly adherent to skull
  • More common in MALES
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81
Q

What is the pathophysiology of extradural haematoma after the lucid interval?

A
  • After lucid interval:
  • Rapid rise in ICP
  • Pressure on brain
  • Midline shift
  • Tentorial herniation
  • Coning
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82
Q

What is the initial clinical presentation of extradural haematoma?

A
  • Initial head trauma: injury to temple/pterion, short episode of drowsiness or unconsciousness
  • Lucid interval: hours to days, period of recovery
  • Then sudden, rapid deterioration follows…
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83
Q

What is the clinical presentation of an extradural haematoma after the lucid interval?

A
  • RAPIDLY DECLINING GCS (consciousness level)
  • Increasingly severe HEADACHE
  • VOMITING
  • SEIZURES
  • Hemiparesis
  • UMN signs
  • Ipsilateral pupil dilation
  • Bilateral limb weakness
  • COMA
  • Deep and irregular breathing due to coning (brainstem compression)
  • Late signs include:
  • Bradycardia
  • Raised BP
  • Death from respiratory arrest
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84
Q

What are the investigations for extradural haematoma? What will these show?

A
  • CT scan: shows haematoma, LEMON-SHAPED LESION, doesn’t cross suture lines. Unilateral, shows midline shift
  • Skull X-ray: fracture lines might be seen in temporal or parietal bone
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85
Q

Describe the management for an extradural haematoma. What should we not give?

A
  • Stabilise patient
  • URGENT SURGERY: clot evacuation, ligation of bleeding vessel
  • IV MANNITOL to reduce ICP
  • Airway care: intubation, ventilation
  • DO NOT GIVE ASPIRIN!!
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86
Q

What are the different types of headache?

A
  • Migraine
  • Cluster headache
  • Tension headache
  • Secondary headache, e.g. drug-induced
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87
Q

What is a migraine? What is it the most common cause of? Who is it more common in? What percentage of migraine patients have an onset before 40? What are the risk factors?

A
  • Migraine: RECURRENT throbbing headache often preceded by an AURA + ASSOCIATED WITH NAUSEA, VOMITING and VISUAL CHANGES
  • Most common causes of EPIDSODIC HEADACHE i.e. recurrent
  • More common in FEMALES (roughly 3x) + 90% have onset before 40yrs
  • Risk factors: genetics > FHx, female, age (majority of first migraines are in adolescence)
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88
Q

What may migraines stem from?

A

There is some evidence suggesting that migraines are due to irritation of the trigeminal nuclei within the brainstem due to changes in arterial blood flow; this is why the pattern pictured above is seen (same as trigeminal neuralgia)

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89
Q

What is the aetiology of migraines?

A
  • There are no know definite causes, however a number of triggers are known
  • Mnemonic – CHOCOLATE:
  • Chocolate
  • Hangovers
  • Orgasms
  • Cheese
  • Oral contraceptives
  • Lie-ins
  • Alcohol
  • Tumult i.e. loud noises
  • Exercise
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90
Q

What do the terms prodrome and aura mean?

A
  • PRODROME = yawning, cravings, mood/sleep changes
  • AURA = PRECEDES ATTACK AND CAN BE A VARIETY OF SYMPTOMS:
  • Visual disturbance, e.g. lines, dots, zig-zags
  • Somatosensory, e.g. paraesthesia, pins & needles
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91
Q

What is the clinical presentation of a migraine?

A
  • Migraines are classified as WITH OR WITHOUT AURA, but to be classified as a migraine a set of general features must also be met:
  • AT LEAST 2 OF:
  • Unilateral pain (usually 4-72hrs)
  • Throbbing-type pain of a moderate>severe intensity
  • Motion sensitivity

PLUS, AT LEAST ONE OF:

  • Nausea/vomiting
  • Photophobia/phonophobia
  • THERE MUST ALSO BE A NORMAL EXAMINATION AND NO ATTRIBUTABLE CAUSE
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92
Q

What are the investigations for migraine?

A
  • Usually, diagnosis is made clinically with few/no investigations required; however, in certain cases other causes for headaches must be rules out:
  • Lab tests, e.g. CRP, ESR
  • CT/MRI if RED FLAGS i.e. indications:
  • Worst/severe headache i.e. Thunderclap
  • Change in pattern of migraine
  • Abnormal neurological exam
  • Onset >50yrs
  • Epilepsy
  • Posteriorly located headache
  • Lumbar puncture indications
  • Thunderclap headache
  • Severe, rapid onset headache/progressive headache/unresponsive headache
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93
Q

Describe the treatment of migraine. What should we never give?

A
  • TRIPTANS, e.g SUMATRIPTAN (first line and most important for exams). C/I in IHD, uncontrolled HTN. S/Es = arrhythmias, angina > MI. Work on 5-HT receptor
  • NSAIDS, e.g. naproxen
  • Anti-emetics, e.g. prochlorperazine
  • AVOID OPIOIDS AND ERGOTAMINE no matter how bad the pain is
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94
Q

On which receptor do triptans work?

A

5-HT receptor

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95
Q

Describe the prevention of migraine.

A
  • Required if >2 attacks per month OR require acute meds >2x per week
  • BETA BLOCKERS, e.g. propanolol - but contra-indicated in asthmatics etc.
  • TCAs, e.g. amitryptyline
  • Anti-convulsant, e.g. Topiramate
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96
Q

What is a cluster headache? What are they considered? Describe its epidemiology.

A
  • EPISODIC HEADACHES lasting from 7 days up to 1 year (although usually 2-3wks) with PAIN-FREE PERIODS in between that last ~4wks
  • Considered the MOST DISABLING OF PRIMARY HEADACHES
  • Much rarer than migraines, and MORE COMMON IN MALES (~4x)
  • Typically affects adults with onset usually 20-40yrs
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97
Q

What are the risk factors for cluster headaches?

A
  • SMOKER
  • ALCOHOL
  • Male
  • Genetics - autosomal dominant gene has a link
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98
Q

What is the clinical presentation of cluster headache?

A
  • RAPID ONSET OF EXCRUCIATING PAIN, CLASSICALLY AROUND THE EYE, however other common areas are the temples or forehead
  • Pain is strictly UNILATERAL and LOCALISED TO ONE AREA. It rises to a CRESCENDO over a few minutes and last for 15-160 minutes, once or twice a day usually around the same time of day
  • IPSILATERAL AUTONOMIC FEATURES:
  • WATERY + BLOODSHOT EYE
  • MIOSIS (PUPILLARY CONSTRICTION) +/- PTOSIS (SEEN IN 20%)
  • Facial flushing
  • Rhinorrhoea (blocked nose)
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99
Q

Describe the management of cluster headaches.

A
  • Acute attacks:
  • Analgesics are unhelpful
  • 15L 100% O2 FOR 15 MINS VIA A NON-REBREATHER MASK (first line for acute)
  • TRIPTANS, e.g. SUMATRIPTAN
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100
Q

Describe the prevention for cluster headaches.

A
  • VERAPAMIL (CCB) = 1st line prophylaxis
  • Prednisolone
  • REDUCE ALCOHOL CONSUMPTION AND STOP SMOKING
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101
Q

How common is a tension headache? Is it episodic or chronic? What are the causes?

A
  • MOST COMMON CHRONIC DAILY + RECURRENT HEADACHE
  • Can be EPISODIC <15 DAYS/month or CHRONIC > 15 DAYS/month (for at least 3 months)
  • There is no known organic cause, however a number of triggers exist
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102
Q

What are the triggers for tension headache?

A

Triggers:

  • Stress
  • Sleep deprivation
  • Bad posture
  • Hunger
  • Eyestrain
  • Anxiety
  • Noise
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103
Q

What is the clinical presentation of tension headache?

A
  • Usually at least one of the following:
  • BILATERAL
  • PRESSING/TIGHT + NON-PULSATILE (LIKE AN ELASTIC BAND). Mild/moderate intensity
  • +/- scalp tenderness
  • NO AURA, vomiting or sensitivity to head movement
  • CAN BE SOME ‘PRESSURE’ BEHIND EYES, but pain isn’t localised to be around the eye
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104
Q

Describe the management of tension headache. Which type of medication should we avoid?

A
  • Avoidance of triggers & stress relief
  • Symptomatic relief:
  • Aspirin
  • Paracetamol
  • Ibuprofen
  • AVOID OPIOIDS
  • LIMIT ANALGESICS TO NO MORE THAN 6 DAYS PER MONTH TO REDUCE THE RISK OF MEDICATION-OVERUSE
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105
Q

Primary headaches (migraine, cluster, and tension) are without causes but have triggers. Secondary headaches have causes. Give examples of secondary headaches.

A
  • Giant cell/temporal arteritis (most important = vascular disease affecting the temporal artery. One-sided pain in the temple, scalp tenderness when you touch it. Important to rule out in people >55. Important as can cause BLINDNESS if left untreated)
  • Sentinel headache
  • Thunderclap headache
  • Headache of a morning
  • Trauma
  • Medication overuse
  • Trigeminal neuralgia
  • Systemic infection
  • Meningitis/encephalitis
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106
Q

What is the definition of epilepsy?

A

Epilepsy - the recurrent tendency to spontaneous, intermittent, abnormal electrical activity in part of the brain, manifesting in seizures

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107
Q

What is the criteria for the diagnosis of epilepsy?

A

Criteria, one of:

  • AT LEAST 2 UNPROVOKED SEIZURES OCCURING MORE THAN 24 HOURS APART
  • One unprovoked seizure and a probability of future seizures (considered >60% risk in 10yrs)
  • Diagnosis of an epileptic syndrome
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108
Q

When is the onset of epilepsy most common?

A

Can occur at any age, but onset is most common in the extremes of life, e.g. <20 years and >60 years

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109
Q

What is the aetiology of epilepsy?

A
  • 2/3RDS IDIOPATHIC, often familial
  • Cortical scarring, e.g. trauma, cerebrovascular disease, infection
  • Tumours/space-occupying lesions
  • Strokes
  • Alzheimer’s
  • Alcohol withdrawal (delirium tremens)
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110
Q

What are the risk factors for epilepsy?

A
  • FHx
  • Premature babies, especially if they are small for their gestational age
  • Abnormal cerebral blood vessels
  • Drugs, e.g. cocaine
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111
Q

What are the 3 different components of a seizure? What is post-ictal Todd’s palsy? What do we got following a temporal lobe seizure?

A
  • PRODROME = precedes the seizures, usually by hours/days. Weird feeling, e.g. mood/behaviour changes
  • AURA = just before a seizure. Part of the seizure where the patient is aware & often precedes other manifestations, e.g. strange feelings in gut, déjà vu, strange smells, flashing lights. Often implies a PARTIAL SEIZURE
  • POST-ICTAL = the period after a seizures. HEADACHE, CONFUSION, MYALGIA, SORE TONGUE (OFTEN BITTEN). Temporary weakness after focal seizure in motor cortex = POST-ICTAL TODD’S PALSY (this will go away after a few hours). DYSPHASIA following TEMPORAL LOBE seizure
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112
Q

What are the different types of seizure in epilepsy?

A
  • Primary generalized (40%):
  • Simultaneous electrical discharge throughout the whole cortex, with no features that suggest localisation to only one hemisphere/lobe
  • Bilateral and symmetrical motor manifestations
  • ALWAYS ASSOCIATED WITH LOSS OF CONSCIOUSNESS & LACK OF AWARENESS (patient will wake up and be told they’ve had a seziure)
  • Partial (focal) (60%):
  • Focal onset with features that can be referrable to a single lobe, e.g. temporal lobe
  • Often seen with underlying structural disease i.e. there is an underlying cause
  • Electrical discharge is limited to one lobe, in one hemisphere
  • These may later PROGRESS to become GENERALIZED SEIZURES (secondary)
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113
Q

What are the different types of primary generalized seizures?

A
  • TONIC seizure = high tone (hence the name) = RIGID, STIFF LIMBS. Will fall to floor if standing due to stiff limbs
  • CLONIC seizure = RHYTHMIC MUSCLE JERKING (i.e. clonus, the UMN sign)
  • TONIC-CLONIC SEIZURE (“Grand Mal”) = combination of tonic & clonic seizures. STEREOTYPICAL ‘SHAKING’ SEIZURES due to the mix of on/off rigidity and muscle jerking
  • MYOCLONIC seizure = isolated jerking of a limb/face/trunk. “DISOBEDIENT LIMB” or “thrown to the floor”
  • ATONIC seizure = LOSS OF MUSCLE TONE = FLOPPY
  • ABSENCE seizure (“Petit Mal”) = common in CHILDHOOD but usually goes by adulthood, however there is an INCREASED RISK OF DEVELOPING GENERALIZED TONIC-CLONIC SEIZURES AS AN ADULT. Will go PALE and ”STARE BLANKLY” for a few seconds. Often suddenly stop talking mid-sentence & do not realise they have had an attack
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114
Q

What are the different types of partial (focal) seizures?

A
  • SIMPLE PARTIAL SEIZURE = NO EFFECT on CONSCIOUSNESS OR MEMORY. Awareness unimpaired but will have focal motor, sensory, autonomic or psychic symptoms depending on the affected lobe. NO POST-ICTAL SYMPTOMS
  • COMPLEX PARTIAL SEIZURE = memory/awareness is affected before, during or immediately after the seizure. Most commonly arises from the TEMPORAL LOBE > affects speech, memory & emotion. Post-ictal confusion is COMMON if temporal lobe, whereas RECOVERY is often swift if the FRONTAL LOBE is affected
  • PARTIAL SEIZURE WITH SECONDARY GENERALISATION. 2/3 patients with partial seizures will develop generalized seizures, usually generalized tonic-clonic. These start focally & spread widely throughout the cortex
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115
Q

What are the characteristics of seizures if they affect the:

a) temporal lobe
b) frontal lobe
c) parietal lobe
d) occipital lobe

A

a) Temporal lobe i.e. memory, understanding speech, emotion:
- AURA (80%): deja-vu, auditory hallucinations, funny smells, fear
- Anxiety, out-of-body experiences
- AUTOMATISMS (set of brief unconscious behaviours), e.g. lip smacking
b) Frontal lobe i.e. motor, thought processing:
- Motor features, e.g. posturing, peddling movements of leg
- JACKSONIAN MARCH - seizures march up/down the motor homunculus
- POST-ICTAL TODD’S PALSY - starts distally in a limb & works its way upwards to the face
c) Parietal lobe i.e. sensation:
- Sensory disturbances, e.g. TINGLING/NUMBNESS
d) Occipital lobe i.e. vision:
- VISUAL PHENOMENA, e.g. spots, lines, flashes

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116
Q

What is the difference between a non-epileptic seziure and an epileptic seizure?

A
  • Non-epileptic seizures are entirely situational, e.g. metabolic disturbances (low Na+, hypoxia). Can be related to syncope (afterwards)
  • Non-epileptic seizures are typically longer with closed eyes & mouth
  • Non-epileptic do not occur during sleep and do not involve incontinence or tongue-biting
  • There are pre-ictal anxiety symptoms in non-epileptic, e.g. they know they are about to happen
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117
Q

What are the epilepsy-sensitive signs that differentiate it from syncope?

A
  • Epilepsy-sensitive signs:
  • Tongue-biting
  • Head turning
  • Muscle pain
  • LOC
  • Cyanosis
  • Post-ictal symptoms
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118
Q

What are the investigations for epilepsy?

A
  • DIAGNOSIS IS MADE CLINICALLY, but there are a number of tests to help:
  • ELECTROENCEPHALOGRAM (EEG) = not diagnostic, but may help determine the TYPE of epileptic syndrome
  • MRI/ CT head = used to rule out other potential causes, e.g. space-occupying lesions
  • Bloods = FBC, Ca2+, electrolytes, U&Es, LFTs, blood glucose. To rule out other potential causes, e.g. metabolic disturbances
  • Genetic testing = if suspected genetic cause, e.g. juvenile myoclonic epilepsy
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119
Q

Describe the management for epilepsy.

A
  • Usually only started after the second epileptic episode, and the drug of choice varies dependent on the type of epileptic syndrome and the individual (esp. age, gender)
  • You basically give SODIUM VALPROATE unless:
  • Female of childbearing potential, then LAMOTRIGINE for all generalized except:
  • Myoclonic = LEVETIRACETAM/TOPIRAMATE
  • Absence = ETHOSUXIMIDE
  • Partial (focal) seizure = Lamotrigine
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120
Q

What is the general rule for giving sodium valproate?

A

Male = SODIUM VALPROATE

Female = LAMOTRIGINE (as most will of childbearing potential)

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121
Q

Why is sodium valproate contraindicated in females of child bearing potential?

A

IT IS HIGHLY TERATOGENIC!

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122
Q

What is status epilepticus? What is its management?

A

Continuous seizure lasting over 5 minutes or repeated seizures with no recovery of consciousness in-between

  • Management:
  • BENZODIAZEPINES (1st line) - IV LORAZEPAM
  • If ineffective within 10 mins, 2nd line = PHENYTOIN, sodium valproate, levetiracetam, phenobarbital
  • If no response within 30 mins from onset - induction of GA with Propofol
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123
Q

What are the primary brain tumours? How common are they compared to secondary brain tumours?

A
  • Gliomas (tumours of the glial cells, listed from most to least malignant):
  • Astrocytoma (GLIOBLASTOMA MULTIFORME is the most common)
  • Oligodendroglioma
  • Ependymoma
  • Others:
  • Meningioma (tumour of the meninges)
  • Schwannoma
  • Craniopharyngiomas
  • Much less common than secondary brain tumours
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124
Q

What are the origins of the secondary brain tumours? How common are they?

A
  • Most common origins:
  • Non-small cell lung cancer = most common
  • Small cell lung cancer
  • Breast
  • Melanoma
  • Renal cell carcinoma
  • GI
  • MUCH MORE COMMON than primary brain tumours
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125
Q

What is the clinical presentation of brain tumours?

A
  • Often brain tumours do not have any symptoms, particularly when they are small
  • As they develop they present with FOCAL NEUROLOGICAL SYMPTOMS depending on the location of the lesion, e.g. classic example: patient has an unusual change in personality and behaviour = tumour in the frontal lobe
  • Also present with signs and symptoms of RAISED INTERCRANIAL PRESSURE - key finding is PAPILLOEDEMA on FUNDOSCOPY
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126
Q

What is Wernicke’s encephalopathy? What is its clinical presentation?

A
  • Depletion of THIAMINE (VITAMIN B1)
  • Classic triad:
  • CONFUSION
  • Ataxia
  • Ophthalmoplegia
  • Sign:
  • ASTERIXIS (‘liver flap’) = general sign of a metabolic encephalopathy
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127
Q

In which individuals does Wernicke’s encephalopathy tend to occur in?

A

Occurs in patients with poor nutritional absorption, intake, or loss:

  • CHRONIC ALCOHOLISM
  • Severe starvation
  • Prolonged vomiting
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128
Q

What are the investigations for Wernicke’s encephalopathy?

A
  • Diagnosis is clinical
  • Low blood thiamine
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129
Q

Describe the treatment for Wernicke’s encephalopathy.

A
  • PABRINEX (IV B vitamins including thiamine)
  • DO NOT give glucose before thiamine
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130
Q

If Wernicke’s encephalopathy is not managed appropriately, what can happen?

A
  • If not managed appropriately:
  • Fatal in 20%
  • Can progress to KORSAKOFF’S SYNDROME
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131
Q

What is Korsakoff’s syndrome? What are its symptoms?

A
  • Irreversible, long-term brain damage (due to B1 deficiency)
  • Symptoms:
  • Decreased ability to acquire new memories
  • Retrograde amnesia
  • Confabulation (invented memories)
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132
Q

What is dementia? What are the different types?

A
  • Dementia is a term used to describe a group of symptoms such as poor memory and difficulty learning new information, which can make it really hard to function independently
  • Different types:
  • Alzheimer’s disease
  • Frontotemporal dementia (Pick’s)
  • Vascular dementia
  • Dementia with Lewy bodies
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133
Q

What is Alzheimer’s disease? What is its epidemiology?

A
  • Alzheimer’s disease is a chronic neurodegenerative disease with an insidious onset and progressive but slow decline
  • Most common form of dementia
  • Mainly affects those over 65
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134
Q

What are the risk factors for Alzheimer’s disease?

A
  • Increased age
  • Family history
  • Down’s syndrome (Trisomy-21)
  • Apolipoprotein E-e4 (ApoEe4) allele homozygosity (ApoE normally breaks down beta amyloid, e4 alleles encode less effective ApoE)
  • Reduced cognitive activity
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135
Q

What is the pathophysiology of Alzheimer’s disease?

A
  • Extracellular deposition of BETA-AMYLOID PLAQUES: signalling obstruction -> deposits around vessels -> increased haemorrhage risk -> initiates inflammatory response
  • In AD, Tau proteins become hyperphosphorylated -> aggregate, stop supporting microtubules -> form NEUROFIBRILLARY TANGLES -> obstruct neuronal signalling -> neuron apoptosis
  • Damaged synapses
  • Atrophy
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136
Q

What are the signs and symptoms of Alzheimer’s disease?

A
  • Memory - episodic and semantic
  • Language - difficulty understanding or finding words
  • Attention and concentration issues
  • Psychiatric changes, e.g. withdrawal, delusions
  • Disorientation, e.g. time and surroundings
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137
Q

What are the investigations for Alzheimer’s disease?

A
  • MMSE
  • Bloods - TFTs, B12 (check for other causes)
  • CT/MRI scan - exclude other dementia causes. AD will show cortical (especially hippocampus) atrophy, gyri narrowing, sulci widening and ventricle enlargement
  • Memory clinic assessment
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138
Q

Describe the management for Alzheimer’s disease.

A
  • No cure
  • Supportive therapy, e.g. carers, changes to the home, help with daily activities
  • Medication to manage symptoms: acetylcholinesterase (AChE) inhibitors, e.g. rivastigmine, galantamine, memantine
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139
Q

What is frontotemporal dementia? What type of dementia is it? What is its epidemiology?

A
  • Frontotemporal dementia (Pick’s) = atrophy of the frontal and temporal lobes. It is a progressive dementia
  • 5% of dementias
  • More common in those under 65 - average onset is between 45-65 years
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140
Q

What is the pathophysiology of frontotemporal dementia?

A
  • Loss of neurons, but no plaque formation
  • Pick bodies
  • Tau +ve or TDP-43 +ve inclusions
141
Q

What are the signs and symptoms of frontotemporal dementia?

A
  • Onset tends to be insidious and progressive. Present with 3 main symptoms:
  • Behavioural issues, e.g. loss of inhibition/empathy, compulsive behaviours, difficulty planning
  • Progressive aphasia, e.g. slow, difficult speech, grammatical errors
  • Semantic dementia, e.g. loss of vocabulary, problems understanding
142
Q

What are the investigations for frontotemporal dementia?

A
  • Bloods - B12, TFTs, U&Es (?other causes)
  • MRI/CT - frontal/temporal atrophy
  • FBC and LFTs for suspected encephalopathy
  • MMSE
143
Q

Describe the management for frontotemporal dementia.

A
  • No cure
  • Supportive therapy, e.g. carers, help setting up a stable routine, home changes for motor difficulties, speech and language therapy
  • SSRIs - help with behaviour symptoms
  • Levodopa/carbidopa if Parkinson’s symptoms present
  • Stopping exacerbating drugs
144
Q

What is vascular dementia? What is it the result of? What is its epidemiology? What are its risk factors? What is its pathophysiology based on? By how much does a single stroke raise the risk of having vascular dementia?

A
  • Vascular dementia is a chronic progressive disease of the brain bringing about cognitive impairment. The executive functions of the brain such as planning are more prominently affected than memory. It is the result of multiple, small infarcts
  • Second most common dementia globally - 17% of dementia in the UK
  • Risk factors: smoking, history of TIAs, AF, hypertension, DMT1, hyperlipidaemia, obesity, coronary heart disease
  • Detailed pathophysiology is based on the location and size of the original infarct, and number and location of consequent infarcts
  • A single stroke doubles the risk of developing vascular dementia
145
Q

What is a feature of vascular dementia that it is characterised by?

A

Characterised by STEPWISE PROGRESSION - periods of stable symptoms, followed by a sudden increase in severity

146
Q

What is the clinical presentation of vascular dementia? What would we expect to see if the infarct was subcortical?

A
  • Presentation varies massively but can include:
  • Visual disturbances
  • UMN signs (e.g. muscle weakness, overactive reflexes, clonus)
  • Attention deficit
  • Depression
  • Incontinence
  • Emotional disturbances
  • If infarct was subcortical, then expect to see dysarthria and parkinsonisms
147
Q

What are the investigations for vascular dementia?

A
  • Full history important - previous stroke/TIA?
  • Cognitive impairment screen - orientation, attention, language function, visuospatial functions, motor control
  • Medication review - ?other cause
  • MRI - looking for previous infarcts
148
Q

Describe the management for vascular dementia. What is the prognosis of vascular dementia?

A
  • Supportive therapy, e.g. carers, home changes, routine help, cognitive simulation programmes
  • SSRIs or anti-psychotics to control symptoms, e.g. lorazepam
  • Prognosis is 3-5 years from diagnosis
149
Q

What is dementia with Lewy bodies characterised by? Is it on a spectrum?

A
  • Characterised by eosinophilic intracytoplasmic neuronal inclusion bodies (Lewy bodies) in the brainstem and neocortex. Also see substantia nigra depigmentation and amyloid deposits
  • Lewy body disease includes three overlapping disorders, so this dementia is on a spectrum - DLB is when the dementia is the presenting issue, Parkinson’s dementia is when Parkinson’s is the presenting issue
150
Q

What are the signs and symptoms of dementia with Lewy bodies?

A
  • Dementia is often presented initially: memory loss, spatial awareness difficulties, loss of cognitive function
  • Parkinsonisms, e.g. tremor, rigidity, change in gait
  • Visual hallucinations
  • Sleep disorders, restless leg syndrome
151
Q

What are the investigations for dementia with Lewy bodies?

A
  • International criteria used:
  • Presence of dementia with 2 of: fluctuating attention and concentration, recurrent well-formed visual hallucinations, spontaneous Parkinsonism
  • If there is only 1 of the 3 core features, diagnosis can also be made with a SPECT or PET scan showing low dopamine transporter uptake in basal ganglia
  • MMSE or 6-item cognitive impairment test (6-CIT)
  • Bloods - B12, TFTs, U&E, MRI (?other cause)
  • MSU to check for urine infection
152
Q

Describe the management for dementia with Lewy bodies. What should be be avoided and why?

A
  • Refer to a specialist
  • Supportive therapy - cognitive stimulation, exercise programmes, at-home care
  • Cholinesterase inhibitors, e.g. rivastigmine suggested to treat cognitive decline
  • Avoid use of neuroleptic drugs, e.g. haloperidol, as they can produce severe sensitivity reactions
153
Q

What is Parkinson’s disease? Which area of the brain is affected the most? What is its epidemiology?

A
  • Parkinson’s disease is a condition where there is a progressive REDUCTION of DOPAMINE in the BASAL GANGLIA of the brain, leading to disorders of movement
  • Ventral tier of the zona compacta in the substantia nigra is affected the most
  • Second most common neurodegenerative disorder (after Alzheimer’s). Typically develops between 55-65 years of age
154
Q

What is the aetiology of Parkinson’s disease? What are its risk factors?

A
  • Usually idiopathic
  • Drug-induced Parkinsonism is caused by dopamine antagonists, e.g. clozepine
  • Can also be caused by encephalitis or exposure to certain toxins, e.g. manganese dust
  • Risk factors: age, male sex, pesticide exposure
155
Q

What is the clinical presentation of Parkinson’s disease?

A
  • The symptoms are characteristically asymmetrical, with one side affected more than the other. There is a classic triad of features in Parkinson’s disease:
  • RESTING TREMOR
  • RIGIDITY (COG-WHEEL WALK)
  • BRADYKINESIA
  • Other clinical signs include: impaired dexterity, fixed facial expressions, foot drag
  • Common associated symptoms: dementia, depression, urinary frequency, constipation, sleep disturbances
156
Q

What are the investigations for Parkinson’s disease? What is used to confirm the diagnosis of Parkinson’s?

A
  • Almost entirely clinical diagnosis. 3 step diagnosis:
    1) Diagnosis of Parkinsonian syndrome: bradykinesia (required) plus one of rigidity, resting tremor, or postural instability
    2) Exclusion criteria (none to be met): history of stroke, repeated head injury, neuroleptic treatment, unilateral features after 3 years, cerebellar signs, Babinski’s sign, early severe dementia, negative response to large L-dopa dose
    3) Supportive criteria (3 or more required): unilateral onset, rest tremor present, progressive, excellent response to L-dopa (70-100%), visual hallucinations
  • DaT SCAN IS USED TO CONFIRM THE DIAGNOSIS OF PARKINSON’S DISEASE
157
Q

Describe the management of Parkinson’s disease. What can happen after years of taking L-dopa?

A

Young onset + biologically fit:

  1. Dopamine agonist: ropinirole
  2. MOA-B inhibitor: rasagiline
  3. L-DOPA: co-careldopa = most effective for symptomatic management. Offered in early disease as well tolerated. Wear-off phenomenon can happen after years of taking levodopa - where dose is no longer effective. Can be combated by taking a COMT inhibitor alongside

Biologically frail and comorbidities:

  1. L-DOPA
  2. MOA-B inhibitor
158
Q

What is Huntington’s disease? What is the mean age of onset? What is its pathophysiology?

A
  • Huntington’s disease is an autosomal dominant genetic condition that causes a progressive deterioration in the nervous system. It causes the LOSS of main inhibitory neurotransmitter GABA
  • Mean age of onset is 30-50 years
  • It is a ‘TRINUCLEOTIDE REPEAT’ disorder that affects CAG gene on the Huntington gene, on chromosome 4
159
Q

As Huntington’s disease is a result of trinucleotide repeats, what does that mean it displays?

A
  • ANTICIPATION. This is where successive generations have more repeats in the gene, resulting in:
  • Earlier age of onset
  • Increased severity of disease
160
Q

What is the clinical presentation of Huntington’s disease?

A
  • Main sign is hyperkinesia
  • Characterised by: CHOREA, DYSTONIA, and INCOORDINATION
  • EYE MOVEMENT PROBLEMS
  • Psychiatric issues
  • Depression
  • Cognitive impairment, behavioural difficulties
  • Irritability, agitation, anxiety
161
Q

What are the investigations for Huntington’s disease?

A
  • Diagnosis is made in a specialist genetic centre using a genetic test (CAG repeat testing) for the faulty gene. It involves pre-test and post-test counselling regarding the implications of the results
  • MRI/CT - loss of striatal volume
162
Q

Describe the management for Huntington’s disease. What is its prognosis and leading causes of death?

A
  • No treatment options for slowing or stopping the progression of the disease
  • Benzodiazepines/valproic acid - chorea
  • SSRIs if depression present
  • Haloperidol for psychosis
  • Prognosis is poor. Most common death is from respiratory illness, e.g. pneumonia. Suicide is the 2nd most common cause
163
Q

What is the key differential diagnosis for Huntington’s disease?

A

SYDENHAM’S CHOREA (rheumatic fever)

164
Q

What is spinal cord compression? What is its aetiology?

A
  • Spinal cord compression (SCC) results from processes that compress or displace arterial, venous, and cerebrospinal fluid spaces, as well as the cord itself
  • Causes: trauma, tumours, central disc protrusion, prolapsed disc (L4-5 and L5-S1 most common), epidural haematoma, infection, cervical spondylitic myelopathy. Tumours: most common spinal metastases are breast, prostate and lung cancer
165
Q

What is the clinical presentation of spinal cord compression?

A
  • Red flag signs:
  • Loss of bladder or bowel function
  • UMN signs in the lower limbs (e.g. clonus, hyperreflexia)
  • LMN signs in the upper limbs (e.g. atrophy)
  • Symptoms depend on the injury type and site. Can include paraplegia, pain, paraesthesia, changes to tendon reflexes etc.
166
Q

What are the investigations for spinal cord compression?

A
  • X-ray whole spine
  • MRI if indicated, e.g. cancer
  • Renal function
  • Haemoglobin - monitor blood loss
167
Q

Describe the treatment for spinal cord compression.

A
  • Acute spinal cord compression is a neurosurgical emergency
  • Dexamethasone until treatment plan confirmed
  • Catheterisation
  • Analgesia
  • Surgical decompression if indicated
  • Chemotherapy if indicated
168
Q

What is Brown-Sequard syndrome? What are most cases caused by? Which vertebral region is most commonly affected?

A
  • Hemisection of the spinal cord (damage limited to one half -> paralysis on side of lesion (ipsilateral hemiplegia), loss of sensation on the opposite side (contralateral pain and temperature sensation deficits) - this is due to the crossing of fibres in the spinothalamic tract)
  • Most commonly caused by penetrating trauma
  • Most cases seen in the cervical region
169
Q

What is the clinical presentation of Brown-Sequard syndrome?

A
  • Ipsilateral hemiparesis
  • Contralateral loss of pain and temperature below the lesion
170
Q

What are the investigations for Brown-Sequard syndrome?

A
  • Plain radiographs for penetrating or blunt trauma
  • MRI to determine extent of injury
  • Neurological examination to establish level of injury
171
Q

Describe the treatment for Brown-Sequard syndrome.

A
  • No specific treatment:
  • Spine immobilisation
  • Steroids to decrease swelling
  • Physical therapy
  • Occupational therapy
  • Surgery if indicated
172
Q

What is cauda equina syndrome? What is the cauda equina? What is its aetiology?

A
  • Cauda equina syndrome is a rare and severe type of spinal stenosis where all of the nerves in the lower back suddenly become severely compressed
  • The cauda equina is formed by the nerve roots caudal to spinal cord termination
  • Causes: herniation of lumbar at L4/5 or L5/S1 level, tumours, trauma, infection, late-stage ankylosing spondylitis, postoperative haematoma, sarcoidosis
173
Q

How quick is the onset on symptoms for Cauda equina syndrome? What is the clinical presentation of Cauda equina syndrome?

A
  • Sudden onset - hours
  • SADDLE PARASTHESIA = loss of sensation in the perineum - around the genitals and anus (red flag)
  • BLADDER/BOWEL DYSFUNCTION, i.e. loss of sensation, urinary incontinence
  • BILATERAL SCIATICA
  • Sexual dysfunction (red flag)
  • Motor problems
  • Lower back pain (if severe, red flag)
  • Bilateral LMN weakness, absent ankle reflex
174
Q

What are the investigations for cauda equina syndrome?

A
  • Medical emergency - immediate referral
  • Rectal exam - loss of anal tone/sensation
  • MRI spine (most important)
175
Q

Describe the treatment for cauda equina syndrome.

A
  • CAUDA EQUINA SYNDROME IS A NEUROSURGICAL EMERGENCY:
  • LUMBAR DECOMPRESSION SURGERY
  • Immobilise spine
  • Anti-inflammatory agents
  • Antibiotics if infection present
  • Chemotherapy if indicated
176
Q

What is sciatica?

A

Sciatica refers to the symptoms associated with irritation of the SCIATIC NERVE

177
Q

Describe the anatomy of the sciatic nerve. What does it divide into? What does it supply?

A

The spinal nerves L4 – S3 come together to form the SCIATIC NERVE. It exits the posterior part of the pelvis through the GREATER SCIATIC FORAMEN, in the buttock area on either side. It travels down the back of the leg. At the knee, it divides into the TIBIAL NERVE and the COMMON PERONEAL NERVE

The sciatic nerve supplies SENSATION to the lateral lower leg and the foot. It supplies MOTOR function to the posterior thigh, lower leg and foot

178
Q

What are the main causes of sciatica? What is a red flag for cauda equina syndrome?

A
  • The main causes of sciatica are lumbosacral nerve root compression by:
  • HERNIATED DISC
  • SPONDYLOLISTHESIS (anterior displacement of a vertebra out of line with the one below)
  • SPINAL STENOSIS
  • BILATERAL SCIATICA is a RED FLAG for CAUDA EQUINA syndome
179
Q

What is the clinical presentation of sciatica?

A
  • UNILATERAL PAIN from the buttock radiating down the back of the thigh to below the knee or feet - might be described as an “electric” or “shooting” pain
  • PARASTHESIA
  • NUMBNESS
  • MOTOR WEAKNESS
  • REFLEXES may be affected depending on the affected nerve root
180
Q

What are the investigations for sciatica?

A
  • X-ray, MRI - confirms disc herniation, stenosis, tumours as its aetiology
  • SCIATIC STRETCH TEST can be used to help diagnose sciatica. The patient lies on their back with their leg straight. The examiner lifts one leg from the ankle with the knee extended until the limit of hip flexion is reached (usually around 80-90 degrees). Then the examiner dorsiflexes the patient’s ankle. Sciatica-type pain in the buttock/posterior thigh indicates sciatic nerve root irritation. Symptoms improve with flexing the knee
181
Q

Describe the treatment for sciatica.

A
  • Initial management = self-management, education, reassurance, analgesia
  • NICE guidelines state NOT to use medications such as gabapentin, pregabalin, diazepam or oral corticosteroids for sciatica. They suggest considering a NEUROPATHIC MEDICATION if symptoms are persisting or worsening at follow up: AMITRIPTYLINE or DULOXETINE
  • Chronic sciatica management options: epidural CORTICOSTEROID injections, local anaesthetic injections, radiofrequency denervation, spinal decompression
182
Q

What is a nerve lesion? What does it result in? What are the three categories of peripheral nerve injuries?

A
  • Damage to a nerve through compression, trauma, infection etc.
  • Results in the interruption of axonal continuity
  • 3 categories of peripheral nerve injuries: stretch related, lacerations, and compressions
183
Q

What is the clinical presentation of a nerve lesion?

A
  • Depends on the nerve affected

Can include: numbness, tingling, muscle weakness, dropping objects, sharp pains, buzzing sensations in limbs

184
Q

How do we grade nerve lesions?

A
  • Grades of nerve injury (Seddon 1942):
  • Neuropraxia (conduction block)
  • Axonotmesis (axons divided)
  • Neurotmesis (nerves divided)
185
Q

What are the investigations for nerve lesions?

A
  • Neurological examination
  • MRI
  • Again, depends on the nerve affected
186
Q

Describe the treatment for nerve lesions.

A
  • Splints/braces
  • Physical therapy
  • Exercise
  • Analgesia
  • Surgery in some severe cases
187
Q

What is carpal tunnel syndrome? What is the function of the affected nerve? What is its epidemiology? What is its aetiology? What are the risk factors?

A
  • Compression of the median nerve in the carpal tunnel
  • There are 8 carpal bones in the wrist and a ligament that lies across the front of the wrist - between the ligament and the carpal bones is the carpal tunnel
  • Median nerve gives feeling to thumb, index finger, middle finger, and half of the ring finger
  • More common in late 50s and late 70s, and pregnant women
  • IDIOPATHIC. There are a number of key risk factors: ACROMEGALY, HYPOTHYROIDISM, diabetes, rheumatoid arthritis, repetitive strain, obesity, perimenopause
188
Q

What is the clinical presentation of carpal tunnel syndrome? When are the symptoms typically worse?

A
  • SENSORY symptoms of the thumb, index finger and middle finger, and the lateral half of the ring finger: NUMBNESS, parasthesia, burning sensation, pain
  • Symptoms can come and go but are typically WORSE at NIGHT
189
Q

What are the investigations for carpal tunnel syndrome?

A
  • Clinical diagnosis
  • NERVE CONDUCTION STUDIES (first-line)
  • USS or MRI if other damage suspected
  • PHALEN’S test (fully flexing the wrist) and TINNEL’S TEST (tapping the wrist at the location of the median nerve passing through the carpal tunnel)
190
Q

Describe the management for carpal tunnel syndrome.

A
  • 1 in 4 cases will be self-limiting (usually 1 year). Pregnancy cases will resolve postpartum
  • Rest the wrist, and try to avoid gripping/squeezing actions
  • Splint (1st line) - common for night wear only
  • Steroid injections
  • Surgery in severe cases to decompress the carpal tunnel
191
Q

What is foot drop? Which nerve is affected? What is it caused by?

A
  • Difficulty in lifting the front part of the foot, resulting in dragging of the toes. Can be permanent or temporary
  • Caused by damage to the COMMON PERONEAL NERVE (also called common fibular nerve)
  • Causes include: injury, lower back damage, tumour, hip replacement, cauda equina syndrome, and multiple sclerosis
192
Q

What is the clinical presentation of foot drop?

A
  • Unilateral symptoms:
  • Complaint of one foot dragging across the floor when walking
  • Tripping
  • Numbness in the same side
  • Weakness in the same side
193
Q

What are the investigations for foot drop?

A
  • Foot drop itself can be a clinical diagnosis
  • Need to find the underlying cause:
  • X-ray, USS, CT, MRI
  • Nerve conduction study
194
Q

Describe the treatment for foot drop.

A
  • Brace or splint
  • Physiotherapy
  • Specialised shoes - prevent foot drop when walking
  • Nerve stimulation
  • Surgery if indicated
195
Q

What is Charcot-Marie-Tooth disease? What is its mode of inheritance?

A
  • Heterogeneous group of inherited peripheral neuropathies. It affects the PERIPHERAL MOTOR and SENSORY nerves and causes dysfunction in the MYELIN or the AXONS
  • Most common inherited neuromuscular disorder. Autosomal dominant inheritance (can be recessive but rare)
  • No predilection for race or sex
  • Disease course is extremely varied
196
Q

What are the four types of Charcot-Marie-Tooth disease?

A
  • 4 major categories: CMT1, CMT2, CMT3, CMTX:
  • CMT1 - production of abnormal, unstable myelin
  • CMT2 - primarily an axonal disorder
  • CMT3 - characterised by marked segmental demyelination
  • CMTX - demyelinating neuropathy
197
Q

What is the clinical presentation of the different types of Charcot-Marie-Tooth syndrome?

A
  • Onset is insidious and slowly progressive
  • CMT1: onset by 10 years old. Muscle weakness starting in feet and working up (INVERTED CHAMPAGNE BOTTLE LEGS), sensory loss in the same pattern as weakness, foot drop and spinal deformities can be seen
  • CMT2: onset between 10-20 years old (can be later). Weakness and wasting pattern same as CMT1
  • CMT3: infantile onset, usually by 2 years old. Hypertonia or floppy baby syndrome
  • CMTX: more severe in males. Similar presentation as CMT1
198
Q

What are the investigations for Charcot-Marie-Tooth disease?

A
  • Bloods - FBC, TFTs, LFTs, B12, folate
  • CSF examination
  • MRI brain and spinal cord
  • Genetic studies
  • Nerve conduction studies
  • Nerve biopsy if genetic studies inconclusive
199
Q

Describe the management for Charcot-Marie-Tooth syndrome. Which type of drug should we avoid?

A
  • No cure or effective treatment
  • MDT care
  • Supportive therapy and rehabilitation
  • Surgical correction of spinal deformity
  • Analgesia
  • Avoid neurotoxic drugs, e.g. vincristine, as this can exacerbate the condition
200
Q

What is muscular dystrophy? What are the two important types to know about?

A
  • Muscular dystrophy is an umbrella term for genetic conditions that cause gradual wasting and weakening of the muscles
  • Duchenne muscular dystrophy
  • Becker muscular dystrophy
201
Q

What is Duchenne muscular dystrophy? What is its mode of inheritance? What is its pathophysiology? What is its prognosis?

A
  • Inherited disorder characterised by progressive muscle wasting and weakness
  • X-linked recessive condition - male
  • Results in damage to the DYSTROPHIN gene, so no dystrophin is produced. Function = strengthen muscle fibres and protect from injury
  • Prognosis - wheelchair by 12, death by 30
202
Q

What is the clinical presentation of Duchenne muscular dystrophy?

A
  • Present in early childhood, before 3
  • Progressive proximal muscular dystrophy with characteristic pseudohypertrophy of the calves
  • Major milestones delayed
  • Inability to run, hop or jump
  • Recurrent falls
  • Speech delay
  • Fatigue - really common
203
Q

What are the investigations for Duchenne muscular dystrophy?

A
  • Initial investigation - serum creatinine kinase = very high
  • Genetic analysis
  • Muscle biopsy with assay for dystrophin protein
  • Muscle strength test
  • Gait assessment
204
Q

What are the complications of Duchenne muscular dystrophy? What is the most common cause of death in Duchenne muscular dystrophy?

A
  • Joint contractures
  • Cardiomyopathies and heart failure
  • Gastric dilation
  • Learning difficulties
  • Constipation, osteoporosis, hypertension
  • Respiratory failure - most common cause of death
205
Q

Describe the management for Duchenne muscular dystrophy.

A
  • MDT care. Specialist referral
  • CORTICOSTEROIDS - 1st line
  • Immunisations - influenza and pneumococcal
  • Physiotherapy
  • Vitamin D and bisphosphonates for bone health
  • Mobility help - wheelchair once cannot walk
  • Nutritional care
  • End-of-life directive and palliative set-up
206
Q

What is Beckers muscular dystrophy? When do symptoms start to appear? What is its management?

A
  • Beckers muscular dystrophy is very similar to Duchennes, however the DYSTROPHIN gene is LESS SEVERELY AFFECTED and maintains some of its function. The clinical course is less predictable than Duchennes
  • Symptoms only start to appear around 8-12 years. Some patient require wheelchairs in their late 20s or 30s. Others able to walk with assistance into later adulthood
  • Management is similar to Duchennes
207
Q

What is Lambert-Eaton syndrome? What is it caused by? Who does it typically occur in? What is its presentation very similar to?

A
  • Disorder of neuromuscular transmission caused by impaired presynaptic release of acetylcholine. Rare disorder
  • Caused by an autoimmune attack on P/Q subtype of VOLTAGE-GATED CALCIUM CHANNELS (VGCCs). These VGCSs are responsible for assisting the release of acetylcholine into the synapse of the neuromuscular junction
  • Typically occurs in patients with SMALL-CELL LUNG CANCER
  • Presentation can be very similar to MYASTHENIA GRAVIS - be aware of this
208
Q

What is the clinical presentation of Lambert-Eaton syndrome?

A
  • Insidious onset:
  • PROXIMAL MUSCLE WEAKNESS
  • DYSPHAGIA
  • EYELID PTOSIS (drooping)
  • DIPLOPIA
  • Depressed tendon reflexes
  • Gait changes
  • Dry mouth
  • Impotence in male patients
209
Q

What are the investigations for Lambert-Eaton syndrome?

A
  • Nerve conduction studies
  • Nerve stimulation using 50Hz
  • Serum test for VCGC antibodies
  • Detection of ACh receptor antibodies indicate Myasthenia gravis
  • MRI for malignancy. This should be done after 2 years if patient did not present with SCLC
210
Q

Describe the treatment for Lambert-Eaton syndrome.

A
  • Initial treatments aimed at any cancers present
  • AMIFAMPRIDINE - improves muscle strength
  • Acetylcholinesterase inhibitors
  • Immunosuppression in severe cases, e.g. prednisolone
  • Plasmapheresis
  • Surgical intervention possible
211
Q

What is myasthenia gravis? What is its epidemiology? What is myasthenia gravis associated with?

A
  • Myasthenia gravis is an autoimmune condition that causes muscle weakness that gets progressively worse with activity and improves with rest
  • Affects men and women of different ages - typical patients are either a woman under the age of 40 or a man over the age of 60
  • There is a strong link between THYOMA (tumours of the thymus gland) and myasthenia gravis
212
Q

What is the pathophysiology of myasthenia gravis?

A
  • Caused by the binding of autoantibodies (85% - ACETYLCHOLINE RECEPTOR ANTIBODIES, 15% = MuSK and LRP4 antibodies) to POSTSYNAPTIC neuromuscular junction receptors - most commonly on the acetylcholine receptor
  • These antibodies also activate the COMPLEMENT system within the neuromuscular junction, leading to damage to cells at the postsynaptic membrane. This further worsens the symptoms
213
Q

What is the clinical presentation of myasthenia gravis?

A
  • Muscle weakness that is worse on exertion and gets better with rest
  • Almost all patients will have ocular manifestations at some point in the disease (DIPLOPIA, PTOSIS)
  • Weakness is more marked in proximal muscles. Weakness might be seen in: small muscle of the hands, deltoid and triceps muscles, bulbar muscles, muscles involved in chewing
  • No muscle wasting, sensation is unimpaired
  • Seizures can occur
214
Q

What are the investigations for myasthenia gravis?

A
  • Diagnosis is mostly clinical
  • POSITIVE TENSILON/EDROPHONIUM TEST - muscles get stronger after being injected with Tensilon
  • Detection of ACh receptor antibodies (85%), MuSK (10%), LRP4 (5%)
  • Pulmonary function tests
  • TFTs
  • Crushed ice test - ice is applied to ptosis for 3 minutes, if it improves it is likely myasthenia gravis
215
Q

Describe the treatment for myasthenia gravis.

A
  • REVERSE ACETYLCHOLINESTERASE INHIBITORS - PYRIDOSTIGMINE = increases the amount of acetylcholine in the neuromuscular junction and improve symptoms
  • IMMUNOSUPPRESSION (e.g. prednisolone or azathioprine) suppresses the production of antibodies
  • THYMECTOMY can improve symptoms even in patients without a thymoma
  • Monoclonal antibodies, e.g. rituximab
216
Q

Name three drugs that can exacerbate myasthenia gravis.

A
  • Ciprofloxacin
  • Azithromycin
  • Propranolol
217
Q

What is amaurosis fugax? What are its five types of causes?

A
  • The painless, temporary loss of vision in one or both eyes
  • 5 causes: embolic, haemodynamic, ocular, neurological, and idiopathic
218
Q

What are the

a) haemodynamic and embolic
b) ocular
c) neurological causes of amaurosis fugax?

A

a) Embolic and haemodynamic causes can include: cardiac emboli, giant cell arteritis, SLE, thrombocytosis, malignancy hypotension
b) Ocular causes can include: keratitis, closed-angle glaucoma, myopia, intraocular haemorrhage
c) Neurological causes can include: optic neuritis, multiple sclerosis, migraine

219
Q

What is the most common cause of amaurosis fugax? Describe this.

A
  • Most common cause is ATHEROSCLEROTIC EMBOLI
  • This results in the narrowing (stenosis) or occlusion of the INTERNAL CAROTID ARTERY or the CENTRAL RETINAL ARTERY, leading to hypoperfusion (i.e., low blood supply) of the retina
220
Q

What is the clinical presentation of amaurosis fugax? How long can it last?

A
  • Described as ‘black curtain coming down vertically into the field of vision’
  • Vision loss, blurring, fogging, dimming
  • Can last seconds to hours (depends on cause)
221
Q

What are the investigations for amaurosis fugax?

A
  • Clinical diagnosis due to transient nature. Full history
  • Ophthalmic exam - look for signs of ocular ischaemia
  • ESR level
  • CT head if indicated
  • More concerned with cause of episode
222
Q

Describe the treatment for amaurosis fugax. What can happen if it is left untreated?

A
  • Treat the underlying cause, e.g. anticoagulants
  • If left untreated, it can lead to a stroke
223
Q

What is peripheral neuropathy? What is the most common cause? What are the causes of axonal and segmental degeneration?

A
  • Damage to one or more peripheral nerves. Results in transmission blockages between the PNS and CNS. Can be acute or chronic
  • Diabetes is the most common cause of peripheral neuropathy. Can also be caused by dietary deficiencies, medicines, alcohol excess, CKD, injury, infection, connective tissue disorders, inflammatory conditions, or some hereditary diseases
  • Axonal degeneration results from DM, B12 deficiency, lead poisoning, paraneoplastic syndrome
  • Segmental demyelination results from GBS, CMT
224
Q

What are the sensory and motor signs and symptoms of peripheral neuropathy?

A
  • Sensory:
  • Loss of touch, proprioception, temperature/pain sensation, paraesthesia
  • Numbness, tingling, burning/shooting pains
  • +ve Romberg test (patient cannot stand with feet together and eyes closed) - sensory ataxia
  • Motor:
  • Distal weakness - tripping, difficulty opening jars
  • Proximal weakness - difficulty climbing stairs
  • Muscle wasting
  • Fasciculations
  • Absent tendon reflexes
225
Q

What are the investigations for peripheral neuropathy?

A
  • Full history - past medical history, drug history, family history etc.
  • Bloods - glucose, B12, LFTs, TFTs, FBC, U&Es, ESR, immunoglobulins (?cause)
  • NERVE CONDUCTION STUDIES useful for classification
  • Electromyography
  • Nerve biopsy
226
Q

Describe the treatment for peripheral neuropathy.

A
  • TREAT THE UNDERLYING CAUSE
  • Pregabalin or gabapentin for pain
  • Supportive therapy, e.g. walking aids
227
Q

What is depression? What is major depressive disorder? What are the risk factors? What is the clinical presentation? What are the investigations? Describe the treatment.

A
  • Depression can describe both a mood and an illness. Major depressive disorder is a clinical syndrome involving mood, neurovegetative functions, cognition, and behaviour - it is characterised by at least 5 symptoms
  • Risk factors: prior depression, family history of depression, recent bereavement, stress, or medical illness, postnatal, dementia, corticosteroids
  • Clinical presentation: depressed mood, anhedonia, weight change, libido changes, sleep disturbance
  • Investigations: clinical diagnosis, metabolic panel, FBC, thyroid function tests
  • Treatment: moderate = antidepressant, e.g. citalopram, psychotherapy
228
Q

What is Herpes Zoster (shingles)? Is it more or less contagious than the primary infection? What are the risks?

A
  • Painful rash caused by REACTIVATION of a nerve infection caused by the varicella-zoster virus. First presents as chickenpox in childhood, remains dormant in the dorsal root ganglia, and travels through peripheral sensory nerves to the skin
  • Less contagious than primary infection
  • Risks include: immunocompromised, HIV, malignancy
229
Q

What is the clinical presentation of Herpes Zoster virus?

A
  • Red, painful rash - dermatomal distribution. Most commonly cervical, trigeminal, thoracic and lumbar dermatomes
  • Fluid-filled blisters
  • Stabbing or burning pain
  • Fever, headache, fatigue
  • Itching
230
Q

What are the investigations for Herpes Zoster?

A
  • Often a CLINICAL DIAGNOSIS
  • PCR test
  • CSF analysis
  • Bloods and cultures
231
Q

Describe the treatment for Herpes Zoster.

A
  • ORAL ANTIVIRAL THERAPY (1st line): acyclovir, valacyclovir, famciclovir
  • Immunocompromised patients should be treated with IV acyclovir
  • Analgesia
  • Antipyretics
232
Q

What is encephalitis? What are the causes? What is the most common cause? In which individuals are infections most severe?

A
  • Inflammation of the brain parenchyma due to a viral infection (most commonly)
  • Can be caused by other conditions: TB, Lyme disease, toxoplasmosis, ticks
  • HSV-1 is the most common cause, others: CMV, EBV
  • Infections are most severe in children and the elderly
233
Q

What is the clinical presentation of encephalitis? What happens if encephalitis is caught too late/not caught at all?

A
  • TRIAD of FEVER, HEADACHE, and ALTERED MENTAL STATUS
  • Many present with signs of meningitis (stiff neck, vomiting, headache)
  • Symptoms of raised ICP - vertigo, nausea, severe headache, photophobia
  • If not caught, or caught too late, patient’s can rapidly slip into coma
234
Q

What are the investigations for encephalitis?

A
  • Bloods - FBC, U&Es, LFTs, TFS, B12, lactate etc.
  • CSF - viral PCR to detect specific virus - lymphocytosis with normal CSF:plasma glucose ratio
  • CT/MRI - often bilateral but asymmetrical (MRI preferred)
  • Blood cultures/gram stain
235
Q

Describe the treatment for encephalitis.

A
  • Urgent hospital admission
  • IV ACICLOVIR STAT (1st line) as soon as encephalitis is suspected
  • Immediate antibiotics - IV Benzylpenicillin
  • Careful with fluids - cerebral oedema
  • ICU admission may be required with ventilation
  • Sedatives may be required
236
Q

What is Guillain-Barré syndrome? What is its aetiology? What is its epidemiology?

A
  • Guillain-Barré syndrome is an “ACUTE PARALYTIC POLYNEUROPATHY” that affects the peripheral nervous system. It results in demyelination and axonal degeneration. It causes acute, symmetrical, ascending weakness and can also cause sensory symptoms
  • It is usually triggered by an infection (particularly ~6 weeks post-GI infection) and is particularly associated with to campylobacter jejuni, cytomegalovirus and Epstein-Barr virus
  • Increased incidence in males. Peak ages are 15-35, and 50-75
237
Q

What is the pathophysiology of Guillain-Barré syndrome?

A
  • Guillain-Barré is thought to occur due to a process called MOLECULAR MIMICRY
  • The B cells of the immune system create ANTIBODIES against the antigens on the pathogen that causes the preceding infection. These antibodies also match proteins on the nerve cells. They may target proteins on the MYELIN SHEATH of the motor nerve cell or the nerve axon
238
Q

What is the clinical presentation of Guillain-Barré syndrome?

A
  • Characterised by weakness, paraesthesia, and hyporeflexia
  • Sudden onset - TOES TO NOSE WEAKNESS. SYMMETRICAL ASCENDING WEAKNESS
  • Absent reflexes (LMN sign)
  • Neuropathic pain - can develop in the legs, back pain is rare
  • Peripheral loss of sensation - sensory loss in the lower extremities
  • Involvement of autonomic nervous system: reduced sweating, reduced heat tolerance, paralytic ileus - intestinal obstruction w/o blockage, urinary hesitancy
239
Q

What are the investigations for Guillain-Barré syndrome?

A
  • Diagnosis is made CLINICALLY - BRIGHTON CRITERIA can be used
  • Other investigations:
  • Nerve conduction studies
  • Lumbar puncture. Raised protein >0.55g/L. Normal WCC at <5 WBC per mm^2. These results are called cyto-protein dissociation
  • Bloods - B12, FBC, U&Es, LFTs, TFTs etc.
  • Spirometry - to monitor respiratory function
  • ECG - identify any abnormalities & monitor
240
Q

Describe the treatment for Guillain-Barré syndrome. Which type of medication should we avoid? What is the prognosis?

A
  • IV IMMUNOGLOBULIN 0.44g/kg/day for 5 days (1st line)
  • Plasmapheresis (plasma exchange)
  • DVT prophylaxis - LMWH
  • AVOID CORTICOSTEROIDS - these can make the condition worse
  • Good prognosis - most fully recover (80%)
241
Q

What is chronic traumatic encephalopathy? What is it associated with?

A
  • Chronic traumatic encephalopathy is a progressive brain condition that’s thought to be caused by repeated blows to the head and repeated episodes of concussion
  • It is particularly associated with contact sports, such as boxing or American football
242
Q

What are the symptoms of chronic traumatic encephalopathy?

A
  • Similar to other types of degenerative brain disorders, particularly Alzheimer’s:
  • Short-term memory loss
  • Changes in mood
  • Increasing confusion and disorientation
  • Difficulty thinking
  • As it progresses: dysarthria, significant memory problems, parkinsonism
243
Q

What are the investigations for chronic traumatic encephalopathy?

A
  • There is currently no test to diagnose CTE. A diagnosis is based on a HISTORY of participating in contact sports, plus the symptoms and clinical features
  • MRI/CT scan - may not show anything
244
Q

Describe the management for chronic traumatic encephalopathy.

A

Similar to dementia - supportive treatment

245
Q

ILA 6 – Stroke

Margaret Mills is an 88-year-old who presents urgently to your GP Practice complaining of a sudden onset of loss of vision and weakness in her right arm, which lasted less than 10 minutes before completely resolving. This happened late last night but they were alone and because it resolved quickly, decided not to call 999. Margaret has a past medical history of hypertension and osteoarthritis.

On further questioning, she admits to occasional palpitations and shortness of breath. On examination heart rate is 100 beats per minute and is irregularly irregular; blood pressure is 157/87 mmHg.

  1. What cardiac rhythm is this likely to be?
  2. Explain in pathophysiological / coagulation terms how this caused their symptoms.
A
  1. Atrial fibrillation – see AF, think stroke
  2. Fibrillating atria will result in stasis and pooling of blood, particularly in the pockets of the auricular appendages. AF is irregularly irregular as electrical signals randomly make it across to the Bundle of His in the ventricles, and these contract at disorganised intervals.

The stasis of the atrial blood (as per Virchow’s triad) will contribute to the likelihood of clot formation in the heart, which if dislodged may be carried as an embolus through the heart and into the aorta. The path of least resistance tends to be straight into the carotid arteries, though there’s a slight increase in the risk of thromboembolisms going elsewhere in the body.

246
Q

The patient’s condition deteriorates and the nurse looking after them is concerned because the patient’s blood pressure is gradually increasing, the heart rate is slowing and their breathing is becoming erratic.

What pathophysiological process is occurring intra-cranially to cause these signs?

A

Cushing’s reflex.

Raised intracranial pressure:

Ischaemic/necrosing tissue creates an inflammatory response. This in turn perpetuates swelling and oedema, which in a large area of the brain is not very helpful and cerebral oedema will cause an increase in the intracranial pressure. If there’s a haemorrhagic stroke, a similar process occurs as frank blood coming in contact with cerebral neurons creates an inflammatory response, as well as bleeding simply taking up space in the brain and raising pressure.

When the pressure reaches a point where CSF, venous system, and then arteries have all become squashed, the cerebral perfusion pressure in the arteries is not high enough to properly perfuse the brain, and it starts to become more ischaemic. The arterial smooth muscle will increase the blood pressure by vasoconstricting to try to reperfuse the brain, but the baroreceptors in the aorta will get stressed out with the blood pressure increase, and result in a bradycardia to calm the BP down.

247
Q

What is multiple sclerosis? What is it characterised by? What is its epidemiology? What is the aetiology of multiple sclerosis?

A
  • Multiple sclerosis (MS) is a CHRONIC and PROGRESSIVE condition that involves DEMYELINATION of the MYELINATED neurones in the central nervous system. This is caused by an INFLAMMATORY process involving the activation of IMMUNE CELLS against the MYELIN
  • Characterised by repeated episodes of inflammation of the nervous tissue in the brain and spinal cord
  • Female to male ratio; 2:1, <50. Peak incidence is in young females
  • Causes not fully understood - genetic and environmental factors
248
Q

What is the pathophysiology of multiple sclerosis? What is the characteristic feature of multiple sclerosis?

A
  • Results in the loss of the myelin sheath in the CNS due to inflammation. This slows or blocks the transmission of signal to and from the brain
  • Oligodendrocytes affected (CNS), NOT Schwann cells
  • A characteristic feature of MS is that lesions vary in their location over time, meaning that different nerves are affected and symptoms change over time. The key expression to remember to describe the way MS lesions change location over time is that they are “DISSEMINATED IN TIME AND SPACE”
249
Q

What are the three main patterns of multiple sclerosis?

A

There are 3 main patterns of MS:

1) Relapsing-remitting MS: symptoms come and go, periods of good health followed by sudden symptoms, most common presentation
2) Secondary progressive MS: follows from relaxing-remitting, gradually worsening symptoms with fewer remissions, ~50% of those with relapsing-remitting MS develop this
3) Primary progressive MS: from the beginning of the disease, symptoms gradually develop and worsen over time, 10-15% of people at onset

250
Q

What are acute attacks of multiple sclerosis in early disease followed by? What happens as the disease progresses?

A

In early disease, RE-MYELINATION can occur and symptoms can resolve. In the later stages of the disease, re-myelination is incomplete and symptoms gradually become more permanent

251
Q

What are the symptoms of multiple sclerosis?

A
  • Symptoms - TEAM:
  • Tingling
  • Eye: OPTIC NEURITIS (loss of vision in one eye, most common presentation). Also double vision (due to lesions in the SIXTH CRANIAL NERVE - two key phrases = INTERNUCLEAR OPTHALMOPLEGIA + CONJUGATE LATERAL GAZE DISORDER)
  • Ataxia
  • Motor: paraparesis
252
Q

What are the signs of multiple sclerosis?

A
  • Usually UMN signs
  • Loss of COLOUR VISION
  • LHERMITTE SIGN - electric jolt felt down the spine when flexing neck
  • UHTHOFF PHENOMENON - symptoms worse with heat, e.g. hot bath/exercise
253
Q

What are the investigations for multiple sclerosis?

A
  • Symptoms must be disseminated in time (>1 month apart) and space (clinically or MRI)
  • Gold standard - MRI BRAIN AND SPINAL CORD = GD-enhancing lesions
  • Lumbar puncture
  • Often a clinical diagnosis: McDonald Criteria
  • Bloods - B12, FBC, U&Es, LFTs, TFTs, HIV serology, calcium, glucose (?other causes)
254
Q

Describe the management for multiple sclerosis.

A

MIMO:

  • Acute relapse - METHYLPREDNISOLONE (1st line)
  • Relapsing-remitting MS - immunomodulators, e.g, INTERFERON BETA 1A (1st line)
  • Secondary progressive - SIPONIMOD or METHYLPREDNISOLONE (1st line), CLADRIBINE (2nd line)
  • Primary progressive - OCRELIZUMAB (1st line)
255
Q

What is trigeminal neuralgia? What are the two types? What are the triggers?

A
  • Trigeminal neuralgia is sudden, severe facial pain. It’s often described as a sharp shooting pain or like having an electric shock in the jaw, teeth or gums
  • Two types:
  • Classic = caused by artery/vein compressing the trigeminal nerve (CN V)
  • Secondary = non-vascular lesion compressing the trigeminal nerve
  • Triggers: touching/moving tongue/lips/face, chewing, shaving, brushing teeth
256
Q

What is the clinical presentation of trigeminal neuralgia?

A
  • Pain paroxysms - last ONE-SEVERAL SECONDS, may REPEAT, usually UNILATERAL
  • Dull pain between paroxysms
  • Facial muscle spasms
257
Q

What are the investigations for trigeminal neuralgia?

A
  • MRI/CT head - may identify lesion/vascular compression
  • Clinical diagnosis
258
Q

What is the treatment for trigeminal neuralgia?

A
  • CARBAMAZEPINE (first line)
  • Surgery
259
Q

What is syncope?

A

Syncope is the term used to describe the event of temporarily LOSING CONSCIOUSNESS due to a disruption of blood flow to the brain, often leading to a fall. Syncopal episodes are also known as vasovagal episodes, or simply fainting

260
Q

What is the pathophysiology of syncope?

A

Syncope caused by a problem with the AUTONOMIC nervous system regulating blood flow to the brain

  • When the vagus nerve receives a strong stimulus, e.g change in temperature it can stimulate the parasympathetic nervous system. Parasympathetic activation counteracts the sympathetic nervous system, which keeps the smooth muscles in blood vessels CONSTRICTED
  • As the blood vessels delivering blood to the brain relax, the blood pressure in the cerebral circulation drops, leading to hypoperfusion of brain tissue. This causes the patient to lose consciousness and “faint”
261
Q

What is the clinical presentation of syncope? What is essential when gathering a history?

A
  • Patients often remember the event and can recall how they felt prior to fainting. This is called the PRODROME, and involves feeling: hot or clammy, sweaty, heavy, dizzy or lightheaded, vision going blurry or dark, headache
  • May be bit groggy but different to POST-ICTAL period after a seizure. May be INCONTINENCE with both seizures and syncopal episodes
  • A COLLATERAL history from someone that witnessed the event is essential. During a vasovagal episode they may describe the person: suddenly losing consciousness and falling to the ground, unconscious on the ground for a few seconds to a minute as blood returns to their brain, there may be some twitching, shaking or convulsion activity, which can be confused with a seizure
262
Q

What are the primary and secondary causes of syncope?

A
  • Primary syncope (simple fainting): dehydration, missed meals, extended standing in a warm environment, a vasovagal response to a stimuli, e.g. sudden surprise, pain or the sight of blood
  • Secondary causes: hypoglycaemia, anaemia, infection, anaphylaxis, arrhythmias, valvular heart disease, hypertrophic obstructive cardiomyopathy
263
Q

Compare syncope and seizure.

A
  • Syncope: prolonged upright position before the event, lightheaded before the event, sweating before the event, blurring or clouding of vision before the event, reduced tone during the episode, return of consciousness shortly after falling, no prolonged post-ictal period
  • Seizure: epilepsy aura (smells, tastes or deja vu) before the event, head turning or abnormal limb positions, tonic clonic activity, tongue biting, cyanosis, lasts more than 5 minutes, prolonged post-ictal period
264
Q

What are the key examinations for syncope?

A
  • Full history and examination. Are there any physical injuries as a result of the faint, for example a head injury? Is there a concurrent illness, for example an infection or gastroenteritis?
  • ECG, particularly assessing for arrhythmia and the QT interval for long QT syndrome
  • 24 hour ECG if paroxysmal arrhythmias are suspected
  • Echocardiogram if structural heart disease is suspected
  • Lying and standing blood pressure
  • Bloods
265
Q

What are the investigations for syncope?

A
  • ECG, particularly assessing for arrhythmia and the QT interval for long QT syndrome. 24 hour ECG if paroxysmal arrhythmias are suspected
  • Echocardiogram if structural heart disease is suspected
  • Bloods, including a full blood count (anaemia), electrolytes (arrhythmias and seizures) and blood glucose (diabetes)
266
Q

Describe the management for syncope.

A
  • SEIZURES or UNDERLYING PATHOLOGY need to be managed by an appropriate specialist
  • Once a simple vasovagal episode is diagnosed, reassurance and simple advice can be given to:
  • Avoid dehydration + missing meals
  • Avoid standing still for long periods
  • When experiencing prodromal symptoms such as sweating and dizziness, sit or lie down, have some water or something to eat and wait until feeling better
267
Q

What is meningitis? What are the different types? Which age are most at risk? What are the risk factors?

A
  • Inflammation of the meninges. Notifiable disease
  • Can be caused by a virus, bacteria or fungi
  • Bacterial meningitis is often more serious than viral. Viral is more common
  • Infants and teenagers are most at risk
  • Risk factors: immunosuppression, smoking, CSF shunts, DM, IVDU, adrenal insufficiency, malignancy, sickle cell disease, and crowding (university!)
268
Q

What are the most common causes of bacterial meningitis in children and adults? How about in neonates?

A
  • Neonates = GROUP B STREP.
  • Babies, young children and adults = STREPTOCOCCUS PNEUMONIAE
  • Teens and young adults = NEISSERIA MENINGITIDIS
269
Q

What are the most common causes of viral meningitis?

A
  • HERPES SIMPLEX VIRUS
  • ENTEROVIRUS
  • VARICELLA ZOSTER VIRUS
270
Q

What is the clinical presentation of meningitis?

A
  • Non-specific symptoms: fever, headache, vomiting, nausea, lethargy, irritability, muscle pain, chills, shivering, sore throat
  • Stiff neck
  • Photophobia
  • NON-BLANCHING RASH, i.e. do not disappear (meningococcal only - Neisseria meningitidis)
  • KERNIG’S SIGN (pain on passive knee extension)
  • BRUDZINSKI’S SIGN (patient lying flat, lift their head and flex their chin to their chest - this causes them to involuntarily flex their hips and knee)
  • Raised ICP - decreased GCS, seizure, focal deficits
  • Septic shock
271
Q

What are the investigations for menigitis?

A
  • If suspected do NOT delay treatment
  • LUMBAR PUNCTURE - CONTRAINDICATED with raised ICP, shock
  • Bloods - cultures, FBC, U&Es, glucose, lactate
  • ABG
272
Q

Describe the lumbar puncture results in bacterial, viral and fungal meningitis.

A
  • Bacterial: appearance = cloudy, opening pressure = elevated, WBC = high >1000-2000 (neutrophils), protein = high >200, glucose = low <40
  • Viral: appearance = clear, opening pressure = normal, WBC = low <300 (lymphocyte), protein = mildly raised or normal <200, glucose = normal
  • Fungal: appearance = normal, opening pressure = normal/elevated, WBC = <500, protein = high >200, glucose = normal/low
  • TIP: interpreting lumbar puncture results is a common exam question. It is easier to think about what will happen to the CSF with bacteria or viruses living in it rather than trying to rote learn the results. It makes sense that bacteria swimming in the CSF will release proteins and use up the glucose. Viruses don’t use glucose but may release a small amount of protein. The immune system releases neutrophils in response to bacteria and lymphocytes in response to viruses
273
Q

Describe the treatment for bacterial meningitis.

A
  • ABCDE + support
  • Empirical therapy = IV Benzylpenicillin
  • Assess GCS
  • FIRST LINE = CEFTRIAXONE/Cefotaxime. Add IV BENZYLPENICILLIN for RASH
  • CONTACTS = single dose of CIPROFLOXACIN
  • Penicillin allergy = CHLORAMPHENICOL
  • Immunocompromised (risk of listeria) = Amoxicillin / Ampicillin
274
Q

Describe the treatment for viral meningitis. Describe the prophylaxis for meningitis.

A
  • Viral meningitis = ACYCLOVIR
  • Prophylaxis = RIFAMPICIN and CIPROFLOXACIN
275
Q

What is motor neurone disease? What are the different motor neurone diseases? What is the epidemiology?

A
  • An umbrella term for a variety of neurodegenerative disorders selectively affecting motor neurons (mostly the anterior horn cells of the spinal cord and the motor cranial nuclei). Can affect upper or lower motor neurons. NO sensory problems as no effect on sensory neurones
  • Mostly sporadic. Few familial variants - SOD1 gene, C90RF72 gene. Men slightly more affected; 3:2
  • The majority of cases are AMYOTROPHIC LATERAL SCLEROSIS (ALS), however there are 3 other categories of MND (progressive muscular atrophy (PMA), primary lateral sclerosis (PLS), progressive bulbar palsy (PBP))
276
Q

What is the general clinical presentation for motor neurone disease?

A
  • Results in a mixed UMN and LMN presentation
  • LMN signs typically predominate, e.g. weakness, atrophy, muscle fasciculations
  • Onset in the limb is the typical presentation:
  • Look for wrist/foot drop
  • Change in appearance of hands - wasting
  • Gait disorders/tendencies to trip
  • Excessive fatigue
277
Q

What are the general investigations for motor neurone disease?

A
  • El Escorial Criteria:
    1) Presence of: LMN degeneration by clinical, electrophysiological, or neuropathological examination; UMN degeneration by clinical examination; progressive symptoms as determined by the history
    2) Absence of: electrophysiological and pathological evidence of other disease processes; neuroimaging evidence of disease processes
278
Q

What is the general management for motor neurone disease? What is its prognosis?

A
  • MDT Care
  • Supportive therapy
  • Regular physical and occupational therapy
  • Speech and language therapy
  • Diet and nutrition support
  • Non-invasive ventilation
  • RILUZOLE - neuroprotective glutamate-release inhibitor; life-prolonging treatment
  • End of life care and advance directives
  • Prognosis - average survival post-diagnosis is 2-4 years
279
Q

What is amyotrophic lateral sclerosis? Which genes is it associated with? What is its typical age of onset?

A
  • Progressive disease characterised by degeneration of the motor neurons with cortical, brainstem, and ventral cord locations
  • Most common form of MND ~50%
  • Some familial inheritance with the SOD1 and C90RF72 genes
  • Common ages of onset 40-50 (familial) and 58-63 (sporadic)
280
Q

What is the clinical presentation of amyotrophic lateral sclerosis? What indicates a worse prognosis?

A
  • Presents with signs of degeneration of upper and lower motor neurons (upper extremity weakness, stiffness, with poor-cordination and balance, unsteady gait). Asymmetric onset
  • Babinski sign +ve
  • Fasciculations of the tongue
  • Any corticobulbar signs indicate a worse prognosis:
  • Brisk jaw reflex
  • Dysarthria (difficulty speaking)
  • Dysphagia (difficulty swallowing)
  • Sialorrhoea (excess salivation)
281
Q

What are the investigations for amyotrophic lateral sclerosis?

A
  • Diagnosis via the El Escorial Criteria
  • There are no specific investigations for MND but tests include:
  • Nerve conduction studies
  • EMG
  • CT or MRI brain and spinal cord (?other cause)
  • Bloods - B12, folate, HIV serology, Lyme disease serology, creatinine kinase, serum protein electrophoresis (?other causes)
  • Muscle biopsy
282
Q

Describe the management for amyotrophic lateral sclerosis.

A
  • MDT Care
  • Supportive therapy, physical therapy
  • Diet and nutrition care
  • RILUZOLE - life prolonging medication
  • Quinine/baclofen - cramps
  • Hyoscine - sialorrhoea
  • PEG tube for nutrition
  • NIV - respiration help
283
Q

How common is progressive bulbar palsy? Where does it occur? What is its prognosis compared to ALS?

A
  • Around 2 in 10 people with MND have PBP
  • Bulbar = medulla oblongata (ORIGIN OF CRANIAL NERVES 9-12)
  • WORST PROGNOSIS
284
Q

What is the clinical presentation of progressive bulbar palsy?

A
  • UMN and LMN
  • First affected muscles are those used for talking, chewing, and swallowing
  • Present with palsy of the tongue, difficulty swallowing and palsy of facial muscles
285
Q

What are the investigations for progressive bulbar palsy?

A
  • Diagnosis via the El Escorial Criteria
  • There are no specific investigations for MND but tests include:
  • Nerve conduction studies
  • EMG
  • CT or MRI brain and spinal cord (?other cause)
  • Bloods - B12, folate, HIV serology, Lyme disease serology, creatinine kinase, serum protein electrophoresis (?other causes)
  • Muscle biopsy
286
Q

Describe the management for progressive bulbar palsy.

A
  • MDT Care
  • Supportive therapy, physical therapy
  • Diet and nutrition care
  • RILUZOLE - life prolonging medication
  • Quinine/baclofen - cramps
  • Hyoscine - sialorrhoea
  • PEG tube for nutrition
  • NIV - respiration help
287
Q

Compare ALS, PBP, PLS and PMA: affected neuron, clinical features, and genes affected.

A
  • ALS: UMN and LMN, progressive paralysis, eventual respiratory failure, SOD1, C90RF72, ALS2, SETX, VAPB, ANG
  • PBP: LMN in the brainstem, pharyngeal muscle weakness, progressive loss of speech, tongue atrophy, none
  • PLS: UMN of the arms, legs and face, movements become slower, pseudobulbar effect, UMN signs, none
  • PMA: progressive degeneration of only the LMNs, muscle wasting, clumsy hand movements, fasciculations, muscle cramps, LMN only, none
288
Q

What are the signs and symptoms for both progressive muscular atrophy and primary lateral sclerosis?

A
  • Progressive muscular atrophy: anterior horn cells affected, LMN ONLY; distal muscle affected first then proximal
  • Primary lateral sclerosis: rare, progressive tetraparesis (UMN ONLY)
289
Q

What happens if the cranial nerves are damaged (go through each one)?

A
  • Olfactory (I): may notice altered taste, rather than a loss of sense of smell. Disorders can manifest as anosmia, hyposmia, distortions (dysosmias), or spontaneous olfactory hallucinations (phantosmias)
  • Optic (II): typically produce monocular visual loss, which can be sudden or gradual, and may or may not be associated with pain
  • Occulomotor (III): controls most extra-ocular muscles. Present with paralysis of adduction, elevation, and depression, and when the pupil is involved a large unreactive pupil is noted. This presentation can suggest serious neurological disorders
  • Trochlear (IV): innervates the superior oblique muscle, which controls depression, intorsion, and adduction of the eye. It is the most common cause of vertical diplopia
  • Trigeminal (V): biggest cranial nerve (opthalmic (V1), maxillary (V2) and mandibular (V3)). Symptoms depend on the location and aetiology of the lesion and may include loss of sensation in the distribution of one or more trigeminal nerve branches, neuropathic pain, or weakness of the muscles of mastication
  • Abducens (VI): innervates the lateral rectus muscle and controls abduction. Patients typically present with horizontal double vision
  • Facial (VII): most common cranial nerve mononeuropathy. There are many aetiologies, and the most important initial step is to rule out central causes of facial weakness, including ischaemic stroke and pontine neoplasms. The most common cause of a peripheral facial palsy is BELL’S PALSY
  • Vestibulocochlear (VIII): symptoms of dysfunction include hearing loss, tinnitus, and vertigo
  • Glossopharyngeal (IX): isolated glossopharyngeal neuropathy is rare, as lesions often involve other cranial nerves in close proximity (VIII, X, XI, and XII). Additionally, isolated palsy of the glossopharyngeal nerve can often be asymptomatic, due to redundant innervation of target structures by other cranial nerves
  • Vagus (X): can result in hoarseness, dysphagia, and dyspnoea, as well as palatal droop and deviation of the uvula to the contralateral side
  • Accessory (XI): trapezius weakness results in a drooping shoulder at rest and mild scapular winging with attempted shoulder elevation and arm abduction >90°. When the patient shrugs his or her shoulders against resistance, unilateral weakness may be detected. SCM weakness results in difficulty when turning the head in the opposite direction to the injury. To test, the patient is asked to turn his or her head to the side against resistance
  • Hypoglossal (XII): unilateral or bilateral tongue weakness with deviation towards the affected side on tongue protrusion, tongue atrophy (with scalloping or accentuation of the midline groove), fasciculation of the tongue at rest, tongue flaccidity, or the inability to move the tongue rapidly from side to side or vertically
290
Q

What is Bell’s palsy? What are the risk factors?

A
  • Bell’s palsy is an acute, sudden-onset, unilateral facial palsy of probable viral aetiology
  • Risk factors: age, diabetes mellitus, pregnancy (third trimester)
291
Q

What are the symptoms of Bell’s palsy?

A
  • Can be remembered by BELLS Palsy:
  • Blink reflex abnormal
  • Ear sensitivity
  • Lacrimation - deficient or excess
  • Loss of taste
  • Sudden onset
  • Palsy (CN VII muscles)
292
Q

What are the function of UMNs and LMNs?

A
  • UMN: transmits information from brain to spinal cord or brainstem
  • LMN: transmit signals from spinal cord to skeletal muscle
293
Q

What are the causes of UMN lesions?

A
  • Damage to the brain: stroke, infection, tumour
  • Injury to the white matter of the spinal cord
294
Q

What are the causes of LMN lesions?

A
  • Injury to the axons leaving the spinal cord
  • Injury to the ventral grey matter of the spinal cord
295
Q

What is the clinical presentation of an UMN lesion?

A
  • HYPERTONIA (everything goes up)
  • Spasticity
  • Clonus (involuntary muscle contractions)
  • Overactive reflexes, tight muscles
  • Babinski sign –> dorsiflexed toe
296
Q

What is the clinical presentation of LMN lesions?

A
  • HYPOTONIA (everything goes down)
  • Muscle ATROPHY
  • Reduced reflexes
  • Fasciculations (muscle twitching)
297
Q

A 72 year old woman attends A&E after suffering a sudden severe headache and collapse at 4:00am. On examination she has nuchal rigidity and her BP is 173/118. Despite the most likely diagnosis, the CT scan shows no significant abnormalities.

You are the on-call F1 on the evening shift. The patient’s GCS is scoring 11. What investigation should you order?

a. Diffusion weighted MRI scan
b. Carotid doppler ultrasound
c. Lumbar puncture
d. Liver function tests (LFTs)
e. CT angiography

A

C. Lumbar puncture

298
Q

A 72 year old woman attends A&E after suffering a sudden severe headache and collapse at 4:00am. On examination she has nuchal rigidity and her BP is 173/118. Despite the most likely diagnosis, the CT scan shows no significant abnormalities.

The lumbar puncture is positive for xanthochromia, and a diagnosis of a subarachnoid haemorrhage is made. Which of these drugs should be used to reduce cerebral ischemia in someone who has suffered an SAH?

a. Olanzapine
b. Amlodipine
c. Terlipressin
d. Nimodipine
e. Verapamil

A

d. Nimodipine

299
Q

Why is an ECG an important investigation after a stroke?

A

To look for cardiac causes of thrombotic emboli

  • Atrial fibrillation
  • Myocardial infarction in the past

You may also want to do an echocardiogram to look for valvular disease, heart muscle abnormalities, mural thrombi and infective endocarditis

300
Q

Give three reasons why someone might not be given Alteplase after suffering a stroke?

A
  • The stroke has not yet been confirmed as ischaemic
  • The stroke has been confirmed as haemorrhagic
  • It has been more than 4.5 hours since the onset of their symptoms
  • They/their family decline thrombolytic therapy
  • Contraindications: recent surgery, recent trauma, previous CNS bleed, stroke is mild/non-disabling, AVM or aneurysm is present, severe liver disease, serious head injury or stroke in past 3 months, recent GI or GU haemorrhage, known clotting disorder, on anticoagulants, low platelet count

High BP

301
Q

A 28 year old man was playing baseball this morning when the side of his head was struck by the ball. After initially feeling drowsy, he told his teammates he felt ok. However, 20 minutes ago he suddenly vomited and then collapsed, and has been unconscious since. He is unresponsive when you assess him.

Which of these has most likely been ruptured?

a. Arteriovenous malformation
b. Middle meningeal artery
c. Berry aneurysm
d. Carotid artery
e. Bridging veins

A

b. Middle meningeal artery

302
Q

A 28 year old man was playing baseball this morning when the side of his head was struck by the ball. After initially feeling drowsy, he told his teammates he felt ok. However, 20 minutes ago he suddenly vomited and then collapsed, and has been unconscious since. He is unresponsive when you assess him.

Describe three essential steps in the management of this patient.

A
  • IV mannitol - to reduce ICP, if midline shift or hydrocephalus is seen on CT scan
  • Urgent neurosurgery - to remove the clot and ligate the bleeding vessel
  • Intubation & ventilation
303
Q

Which of these is not a typical symptom of an anterior circulation territory TIA?

a. Weakness in one arm for 10 minutes
b. Sudden one-sided visual loss for 10 minutes
c. Unilateral sensory loss for 10 minutes
d. Difficulty speaking for 10 minutes
e. Dizziness and loss of coordination for 10 minutes

A

e. Dizziness and loss of coordination for 10 minutes

304
Q
A
305
Q
A
306
Q

A 42 year-old gentleman presents to you in your GP practice complaining of a headache. He tells you it hurts quite a lot. When you ask him some more questions, you find out that the pain is localised around his left eye and these headaches have been occurring for the last 5 days. You examine his eye and note that it is very bloodshot and that the eye is constricted.

Which type of headache do you think he is most likely suffering from?

a) Tension headache
b) Migraine
c) Trigeminal Neuralgia
d) Increased ICP
e) Cluster headache

A

e) Cluster headache

307
Q

Which of these is NOT a known trigger for migraines?

a) Hangovers
b) Orgasms
c) Cheese
d) Lack of sleep
e) Chocolate

A

d) Lack of sleep

308
Q

Which of these is considered the first line management for a migraine?

a) Paracetamol
b) Co-Codamol
c) Sumatriptan
d) Ergotamine
e) Ibuprofen

A

c) Sumatripan

309
Q

Which of these is NOT a classic feature of cluster headaches?

a) Watery & bloodshot eye
b) Hyperhidrosis
c) Facial flushing
d) Rhinorrhoea
e) Miosis

A

b) Hyperhidrosis

310
Q

A 15 year old girl presents to you in A&E with her mum after having a “fit”. The mum shows you a video of her “fitting”. In the video, you see high legs for stiff and she falls to the floor. Her memory of the episode is completely missing and she was unconscious during the episode. According to her mum, this is the second such episode in about 3 months.

What is the girls most likely type of epilepsy?

a) Tonic seizure generalised seizure
b) Clonic Seizure generalised seizure
c) Tonic-Clonic generalised seizure
d) Absence generalised seizure
e) Atonic generalised seizure

A

a) Tonic seizure generalised seizure

311
Q

A 15 year old girl presents to you in A&E with her mum after having a “fit”. The mum shows you a video of her “fitting”. In the video, you see high legs for stiff and she falls to the floor. Her memory of the episode is completely missing and she was unconscious during the episode. According to her mum, this is the second such episode in about 3 months.

You refer the girl to neurology and they start her on preventative therapy.

What is the most appropriate medication to start her on?

a) Ethosuxide
b) Sodium Valproate
c) Carbamazepine
d) Topiramate
e) Lamotrigine

A

e) Lamotrigine

312
Q

You are a GP who has been seeing a patient who has been complaining of her hands shaking when she watches TV. She is 60 years old and currently takes amlodipine, ramipril, furosemide and clozepine. Whilst she is talking to you, you notice her movements are slow and she seems to have impaired dexterity. You ask how she has been feeling lately and she say quite down, and she doesn’t want to do much during the day. How would you manage this lady?

A) Do nothing, there’s nothing to worry about

B) Start her on levodopa

C) Start her on prednisolone

D) Stop her clozepine

E) Start her on a MAO-B inhibitor

A

D) Stop her clozepine. This is drug induced Parkinsonism. Bradykinesia and a resting tremor are present, however the dopamine antagonist should be stopped before starting her on any other treatments.

313
Q

You see an eldery gentleman in you clinic who has attended with his wife. She tells you that his memory is getting much worse and he has started to become withdrawn. You also learn that 5 years ago he had a stroke. You ask the patient about how he is feeling and he tells you that he has been okay, but about a month ago he got worse, and hasn’t recovered yet. What would you diagnose this man with?

A) Alzheimer’s

B) Vascular dementia

C) Frontotemporal dementia

D) Dementia with Lewy Bodies

E) This is not dementia

A

B) Vascular dementia. This is classic of vascular dementia. The patient is showing memory problems and behavioural disturbance. He also had a stroke and the history is indicating a stepwise progression

314
Q

You are working in A&E and you get told that a stabbing victim is on their way in. The patient is an 18-year-old male with no significant history and no drug history. Upon arrival, you hear the patient panicking as he can’t feel his right leg. You test his pain sensation and it is intact on the right, but missing on the left. What test would you order for this patient?

A) FBC

B) MRI

C) X-ray

D) CT

E) LFTs

A

C) X-ray. This is Brown-Sequard syndrome. The patient needs a pain radiograph (X-ray) to assess the damage of the penetrating wound. An MRI might be useful after the initial results, but would not be first-line

315
Q

A 28-year-old pregnant woman comes to see you complaining of pins and needles in the fingers of her right hand. She tells you that she is also having difficulty picking up some objects around the house and over the last week, she has been woken up by pain in her wrist. What treatment plan would you follow for this woman?

A) Splint the wrist and prescribe naproxen

B) Offer a steroid injection

C) Nothing is needed here

D) Refer for surgical intervention

E) Advise she rest the wrist and avoid gripping objects

A

E) Advise she rest the wrist and avoid gripping objects. This is a case of Carpal Tunnel Syndrome. As the patient is pregnant, it is very likely that the condition will resolve itself postpartum. For the time being, she should rest the affected wrist

316
Q

What type of dementia would you be concerned about with this:

A) Alzheimer’s

B) Vascular

C) Dementia with Lewy Bodies

D) Frontotemporal

E) Combination dementia

A

C) Dementia with Lewy Bodies

317
Q

You have a patient with confirmed Huntington’s Disease. As this is an inherited condition, what genetic change would you expect to see?

A) Increased CAG repeats

B) Decreased CAG repeats

C) Increased GAC repeats

D) Decreased GAC repeats

E) Increased CCA repeats

A

A) Increased CAG repeats. Huntington’s Disease is an autosomal dominant condition that results in the increase of CAG repeats on the Huntington gene on chromosome 4p16.3

318
Q

You see a 37-year-old lady in A&E who is complaining of bowel problems. She is having trouble controlling her bowel movements, and this has only been a problem for 1 day. She also has lower back pain. Upon examination you find she has loss of anal tone and anal sensation and an absent ankle reflex. What is the management for this patient?

A) Analgesia

B) MRI

C) Antibiotics

D) Physiotherapy

E) Surgical decompression

A

E) Surgical decompression. This is a classic presentation of Cauda Equina syndrome. This is a medical emergency that requires immediate surgical decompression. The other options are all possible treatments if required post-operatively

319
Q

You see a 30 year old woman in your clinic who is complaining of intermittent fatigue and numbness in her arms and hands. She tells you that it is so much worse after a hot shower and she is really very confused by this. After some more testing, you diagnose her with multiple sclerosis. What pattern does this lady suffer from?

A) Relapsing-remitting

B) Secondary progressive

C) Primary progressive

D) Primary continuous

E) Secondary continuous

A

A) Relapsing-remitting. This patient has symptoms that come and go - this is relapsing-remitting MS

320
Q

A young man present to A&E with numbness in his toes and legs. He tells you that he is really worried as the numbness has climbed upward in the last few days. On examination you find that he has absent reflexes. To confirm your diagnosis you take a history and find that the patient had a stomach bug 5 weeks ago. He didn’t think much of it and he recovered quickly. What is your diagnosis?

A) Multiple sclerosis

B) Lambert-Eaton Syndrome

C) MND

D) Guillain-Barre Syndrome

E) Peripheral neuropathy

A

D) Guillain-Barre syndrome. The patient has the classic ‘toe to nose’ weakness, and had a GI infection less than 6 weeks ago. He also has absent reflexes, which is another sign of GBS

321
Q

You are on placement and see a 60 year old lady with muscle weakness, fasciculations, wasting in the small muscles of her hands and excessive fatigue. She tells you that this started 1 year ago on her right side, but has now progressed to the left as well. Recently she has been struggling with dysarthria and dysphagia. What medication would you expect this patient to be on?

A) Gabapentin

B) Aspirin

C) Riluzole

D) Natalizumab

E) Interferon beta

A

C) Riluzole. This patient is suffering from ALS. The symptoms are a mixture of upper and lower motor neuron signs, and the onset was asymmetrical. Riluzole is the life-prolonging drug for MND patients. Natalizumab and interferon beta are multiple sclerosis treatments

322
Q

You see a patient who has presented with muscle weakness that gets better with rest, weakness in the small muscles of her hands and triceps, but no muscle wasting. Based on her presentation and history you suspect myasthenia gravis. Which of these investigations would be inappropriate?

A) ACh receptor antibody test

B) Crushed ice test

C) TFTs

D) Lactate

E) All of these are appropriate

A

D) Lactate

323
Q

You see a 3 year old child and his mother in A&E. She tells you that her son has a fever and has been vomiting for the last 2 days. He’s also been shying away from the light. On examination you find a non-blanching rash and immediately start treatment for meningitis. You send off CSF for analysis so that you can tailor the treatment and the results show a cloudy CSF with elevated pressure and increased WBC and protein. What is the cause of this child’s meningitis?

A) Bacterial

B) Viral

C) Fungal

D) Parasitic

E) Non-infective

A

A) Bacterial. There are 2 clues here. First there is a non-blanching rash, which only occurs with bacterial infection. Secondly, the results of the CSF analysis indicate a bacterial cause. It is cloudy, with raised pressure and high WBCs

324
Q

What is the mechanism behind Lambert-Eaton Syndrome?

A) Impared post-synaptic release of acetylcholine

B) Impared presynaptic release of acetylcholine

C) Impaired post-synaptic release of glutamate

D) Impared presynaptic release of glutamate

E) Impared post-synaptic release of GABA

A

B) Impaired presynaptic release of acetylcholine. Lambert-Eaton Syndrome is caused by impared presynaptic release of acetylcholine due to damage of voltage-gated calcium channels

325
Q

Which of the following is not a diagnostic criteria for giant cell arteritis?

A) Elevated ESR >50 mm/hour

B) New headache

C) Abnormal temporal artery biopsy

D) Abnormal temporal artery

E) Over 60 years old

A

E) Over 60 years old. The correct criteria is over 50 years old. All of the others are part of the American College of Rheumatology Classification

326
Q

On your GP placement you see a 55 year-old man who has come in due to a painful rash on his chest. You take a look and see fluid-filled blister contained to just the upper right section of his anterior chest. He has a mild fever and had chickenpox as a child. Based on this, the GP makes a diagnosis of shingles and prescribed antiviral treatment. What is the mechanism of shingles?

A) He was infected by someone else

B) Reactivation of VZV that was dormant in the dorsal root ganglia

C) Reactivation of CMV that was dormant in the dorsal root ganglia

D) Reactivation of VZV that was dormant in the ventral root ganglia

E) Reactivation of EBV that was dormant in the ventral root ganglia

A

B) Reactivation of VZV that was dormant in the dorsal root ganglia. Shingles is caused by the reactivation of the varicella-zoster virus (VZV) that has been dormant in the dorsal root ganglia since the primary infection. CMV = Cytomegalovirus EBV = Epstein-Barr Virus

327
Q

Describe the management for:

a) migraine
b) tension headaches
c) cluster headaches
d) trigeminal neuralgia
e) temporal arteritis

A
328
Q

A 70-year-old female presents to you in the GO practice with increasing fatigue and proximal weakness. He reports several episodes of left-sided headache and scalp-tenderness. What is the most appropriate management?

a) 10mg prednisolone PO for 14 days
b) Immediate 70mg prednisolone
c) Immediate 70mg prednisolone and urgent referral to rheumatology
d) Immediate 70mg prednisolone and same-day referral to ophthalmology

A

C) Immediate 70mg prednisolone and urgent referral to rheumatology.

D not unreasonable but no indication of eye involvement (yet)

If there is any indication of current or previous eye-involvement then they need to go straight to an ophthalmologist but that isn’t the case here. In reality the most important thing is to get them started on high dose pred and get them into hospital (which specialists need to do what and when can then be sorted)

329
Q

A 16-year-old female with known epilepsy has been having a generalized seizure for 15 minutes. Buccal midazolam has failed to terminate the seizure. What is the next most appropriate management option?

a) Buccal diazepam
b) Induction of GA with propofol
c) IV phenytoin
d) Repeat midazolam

A

c) IV phenytoin

330
Q

Alice is a 6 month old baby. She presents to A+E with a high fever and rashes on her legs. The mom explained that when she pressed a glass on the rashes, the rashes did not seem to disappear. She has been crying all day and clearly seems very unwell and in pain. She keeps putting her hands above his eyes. She is passing stool normally but is not eating and drinking well. On examination, Alice’s HR and RR were high. What is the most likely diagnosis?

A. Guillan Barre

B. Encephalitis

C. Meningitis

D. Bacterial Pneumonia

E. Infective endocarditis

A

C. Meningitis

331
Q

Alice is diagnosed to have meningitis caused by a fungal infection and is given a lumbar puncture. What findings are most appropriate with this diagnosis?

A. Granulocytes present; protein high; glucose low

B. Lymphocytes present; protein high; glucose low

C. Lymphocytes present; protein high; glucose normal

D. Granulocytes present; protein low; glucose high

Which one is bacterial?

Which one is TB?

Which one is viral?

A

A. Bacterial

B. Fungal and TB

C. Viral

332
Q

Josh is 19 y.o. man presenting to the clinic with a headache. The headaches comes and goes. He has his exams coming up and so he’s barely been sleeping and studying all night. He has pain around his whole forehead. He has no cough, cold, fever. What is the most likely diagnosis?

A. Tension Headaches

B. Cluster headaches

C. Migraines

D. Sinusitis

E. Temporal Arteritis

A

A. Tension headaches

333
Q

John is a 23 yo man that has come into the clinic complaining of unilateral headache that has lasted for 3 years but it comes and goes. He has noticed that sometimes he sees weird visual zig zags and lines before getting her headaches. Her father explained that he’s had this problem before too. He had also been diagnosed with asthma 2 years ago and is worried that might be causing the headaches. What is the prophylactic treatment for this diagnosis for John?

A. Verapamil

B. Sumatriptan

C. Propranolol

D. Ibuprofen

E. Topiramate

A

E. Topiramate

334
Q

Mary comes to the clinic with severe pain on one side of her head that comes and goes. It feels very tender over the area and explains that sometimes when she chews her jaw hurts.

A. What is the diagnosis?

B. What is the first line investigation for her?

C. What is the gold standard investigation?

D. What is the treatment for this?

E. What is the most dangerous complication to look out for?

A

A. Giant cell arteritis

B. CRP/ESR for inflammation

C. Temporal artery biopsy

D. Prednisolone

E. Blindness if the inflammation spreads to the optic arteries

335
Q

Sarah is presenting at the A+E seizuring after collapsing at the mall. Her husband explained that she had collapsed with her arms and legs flailing and jaw clenching. She lost all consciousness and has been continuing her seizure since. She is also 12 weeks pregnant. On the way to the hospital, EMT gave Sarah diazepam but did not help. At A+E she was given a dose of lorazepam but did not work.

A. What type of seizure is this?

B. As lorazepam has not worked what is the next course of action to stop her seizure?

C. Does this patient have epilepsy?

D. If she is confirmed to have epilepsy then what treatment course should she be started on now?

A

A. Generalised seizure

B. Another course of IV lorazepam 10 to 20 minutes after the first; if this doesn’t work give phenytoin

C. No. Patient needs to be investigated for all other causes first. If she is found to have TWO seizures of unknown cause = epilepsy

D. Lamotrigine. She is pregnant

336
Q

Josh, a 19 y.o. boy, comes to the clinic complaining of weird jerks that happens to him while he is just walking around. Yesterday while he was with his girlfriend, his arm first jerked punching his girlfriend, then he lost his structure and almost fell then his leg suddenly just jerked and kicked his girlfriend. This has happened a few times and he is worried if it keeps happening then his gf will break up with him. What is the most likely diagnosis?

A. Huntington’s Chorea

B. Parkinson’s

C. Guillan Barre

D. Focal Seizure

E. Petit Mal Seizure

A

D. Focal seizure

337
Q

Jack is a 59 y.o gentleman presenting to the A&E with stroke-like symptoms. He describes himself gardening 5 hrs ago, when he started having headaches, feeling dizzy and nauseous and not able to see out from the right half of both eyes. He also describes feeling weak across his arms and you notice his gait to be unsteady.

He has hypertension, hypercholesterolemia and diabetes.

Based on the most likely diagnosis, what should be your next step in management.

A. Order a CT scan

B. Order MRI scan

C. Start IV Alteplase & Aspirin

D. Insert an endotracheal tube

E. Mechanical thrombectomy

A

A. Order a CT scan

338
Q

Dharshan is a 72 y.o gentleman who presents to the A&E department with unusual features of hemiparesis. He is unable to lift his left arm and left leg, however he is still able to feel people touching him. He complains of no other symptoms. His symptom has lasted for more than a day now.

Based on the above, which of the following fits best with what he is having?

A. Total anterior circulation stroke

B. Partial anterior circulation stroke

C. Posterior circulation stroke

D. Lacunar stroke

E. Transient ischaemic stroke

Name some aetiological causes of TIA/Stroke?

A

D. Lacunar stroke

Aetiological causes of TIA/stroke: large artery atherosclerosis, cardioaortic embolism, small vessel occlusion, undetermined

339
Q

Jane comes into A&E with severe sudden onset headache an hour ago. The pain was at its worst in the first 3 minutes and the pain is still present. He describes soreness around his neck and shoulders and was begging for the nurses to off the lights. He has tried taking painkillers but it has not helped at all.

He has a past medical history of migraine and is not on any medications for it.

What is your next best step in management?

A. Urgent non-contrast CT head

B. Do a lumbar puncture

C. Start rescue therapy with Sumatriptan

D. Start high-flow-rate oxygen at 100%, 15L/min

E. Start oral prednisolone

Name 5 complications of the pathology in question?

A

A. Urgent non-contrast CT head

5 complications: hydrocephalus, vasospasm, seizures, rebleeding, electrolyte abnormalities

340
Q

Jane is a 67 y.o lady coming in to the A&E with confusion in the last 2 days. She is unable to give a complete history but her daughter is present. From the conversation, you found out that Jane was a victim of a snatch theft 2 weeks ago where she might have received a traumatic blow to the head. However, she did not come into the hospital as she recovered quickly.

Past medical history of MI, hypertension and high cholesterol

CT scan: Crescent shape haematoma on left side with midline shift

Based on the aetiology of the disease, which is the most common cause for this disease?

A. Cerebral hypotension

B. Malignancy

C. Rupture of cerebral aneurysms

D. Rupture of bridging veins

E. Rupture of middle meningeal artery

Name 4 risk factors for the above pathology.

A

D. Rupture of bridging veins

4 risk factors: alcoholism, old age, trauma, anticoagulants use or bleeding disorders

341
Q

Joe is a 59 y.o gentleman who has been detained under section 2 of the Mental Health Act. His wife said that he was acting oddly telling them to get off the car in the middle of the motorway and to walk across to the other side of the road. The wife said that he has been acting strangely for the last 2 months and seems to make rude comments or behave without restraint. He once took a strip of bacon off a stranger’s plate while dining in a Michelin-starred restaurant.

A series of tests were ordered. His Addenbrooke’s test was normal across all categories.

MRI showed atrophy of the right frontal lobe.

Based on the above, which is the most likely diagnosis?

A. Frontotemporal dementia

B. Alzheimer’s dementia

C. Depression

D. Vascular dementia

E. Lewy body dementia

What can found in the histopathology of AD?

A

A. Frontotemporal dementia

Histopathlogy of AD: amyloid/senile plaque, neurofibrillary tangles, cortical atrophy, loss of Ach production

342
Q

Jane is a 30 y.o lady with an acute onset of pain in her left eye. She says that she sees double and has difficulty telling colours apart. She remembers having a similar episode 3 months ago but did not see the doctor for it. She has also been feeling more tired and has noticed her foot dragging off the floor sometimes.

MRI shows presence of lesions in the white matter.

Based on the most likely diagnosis, how would you manage this patient?

A. Methylprednisolone

B. Dimethyl fumarate

C. Baclofen

D. Propranolol

E. Gabapentin

Name 3 types of MS.

A

A. Methylprednisolone

3 types of MS: relapsing-remitting, primary progressive, secondary progressive

343
Q

George has a brain tumour.

  1. Name 4 cardinal presenting symptoms of a brain tumour.
  2. Name 4 places where a lung tumour could metastasize to.
  3. Name 4 primary sites which a lung tumour could have metastasized from.
  4. Name 5 places where a prostate cancer can metastasize to.
A
  1. Symptoms of raised ICP, progressive neurological deficit, epilepsy, lethargy
  2. Brain, liver, adrenal, bone
  3. Bowel, bladder, breast, renal cell carcinoma
  4. Prostate, kidney, breast, thyroid, bone
344
Q
A

C. Forced Vital Capacity

345
Q
A

B. Antibodies to post-synaptic acetylcholine receptors (Anti-ACh)

346
Q

Regarding the previous case:

a) what bedside test would you do?
b) what scan would you order for her and why?

A

a) Upward gaze fatigability
b) CT neck scan - thymoma

347
Q
A

A. Median neuropathy

348
Q
A

e) Common peroneal nerve palsy - most common cause of foot drop

349
Q
A

A. DAT scan. You would expect to see degeneration of substantia nigra

B. Lewy bodies

C. Bradykinesia, rigidity

D. Drug-induced, multiple system atrophy

E. Levodopa: postural hypotension, dyskinesia (involuntary movements), dry mouth, drowsiness

Dopamine agonist (ropinirole, cabergoline, bromocriptine): compulsive gambling (impulsivity), drowsiness, associated with pulmonary fibrosis

Monoamine Oxidase B inhibitor (MOA-B inhibitor), e.g. selegiline

F. Essential tremor

Phase 2a (13 decks)

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