Neurology AS

Question 1

Gross anatomy of the spinal cord?

Answer 1

• From Foramen magnum to L1
• Terminates as conus medullaris
• Spinal nerves continue inferiorly as corda equina
• Denticulate ligament and filum terminale are pial extensions that suspend cord in subarachnoid space.

Question 2

What is the blood supply of the spinal cord?

Answer 2

3 longitudinal vessels.

• 2 posterior spinal arteries supply the dorsal 1/3
• 1 anterior spinal artery supplies 2/3
• Reinforced by segmental feeder arteries (artery of Adamkiewicz)
• Longitudinal veins drain into extradural vertebral plexus.

Question 3

What are the tracts of the spinal cord?

Answer 3

Dorsal Columns
Lateral spinothalamic tract
lateral corticiospinal tract
Thalamic nuclei

Question 4

Where are the dorsal columns organised in the spinal cord?

Answer 4

Most posteriorly.

• Composed of the fasciculus gracilis and cuneate fasciculus.
• Cuneate is cervical + thoracic and is positioned less posteriorly than gracile (sacral and lumbar).
• Sensory tracts moving info upwards.

Question 5

What mode of information do the dorsal columns carry?

Answer 5

• Fine touch
• Vibration
• Proprioception

Cell body in the dorsal root ganglion

Question 6

Where is the decussation of the dorsal columns?

Answer 6

In the medulla forming medial lemniscus

Question 7

Where is the lateral spinothalamic tract situated in the spinal cord?

Answer 7

• Organised anterolaterally
  Cervical is medial, whilst sacral is lateral.
• Also known as the anterior white commisure

Question 8

What mode of information does the lateral spinothalamic tract carry?

Answer 8

• Pain and temperature
• Cell body in the DRG

Carrying information upwards

Question 9

Where is the decussation of the lateral spinothalamic tract

Answer 9

In the cord, at the entry level.

Question 10

Where is the lateral corticospinal tract situated in the spinal cord?

Motor Pyramidal tracts

Answer 10

These are the pyramidal tracts

- posterio-laterally but also anterior.

Question 11

What mode of information does the lateral corticospinal tract carry?

Answer 11

• Motor information

- Cell body in the primary motor cortex.

Question 12

Where is the decussation of the lateral corticospinal tract?

Answer 12

Pyramidal decussation in the ventral medulla

Question 13

Other motor tracts of the spinal cord?

Answer 13

Rubrospinal
Reticulospinal
Vestibulospinal
Olivospinal

Question 14

Other sensory tracts?

Answer 14

Spinocerebellar

Question 15

What are the thalamic nuclei?

Answer 15

VPL: Ventral posteriolateral nucleus
VPM: Ventral posteriomedial nucleus
LGN: Lateral Geniculate Nucleus
MGN: Medial Geniculate Nucleus

Question 16

What is the role of the ventral posteriolateral nucleus?

Answer 16

Somatosensory body - Touch

Question 17

What is the role of the ventral posteriomedial nucleus?

Answer 17

Somatosensory head - Touch

Question 18

What is the role of the lateral geniculate nucleus?

Answer 18

Visual

Question 19

What is the role of the medial geniculate nucleus?

Answer 19

Auditory

Question 20

Role of the cerebellum and basal ganglia?

Answer 20

• Output to cortex via thalamus

- Regulation of posture, locomotion, coordination and movement.

Question 21

Role of internal capsule?

Answer 21

White matter carrying axonal fibres from motor cortex to pyramids of medulla

An infarction here –> Contralateral hemiparesis

Question 22

Role of the frontal lobe?

Answer 22

• Cognition and memory
• Executive function
• Motor cortex
• Dominant hemisphere: motor speech (Broca’s Area).

Question 23

Role of the parietal lobe?

Answer 23

Sensory cortex

Body orientation - Visuospatial processing

Question 24

Role of temporal lobe

Answer 24

Memory

Dominant hemisphere: receptive language (Wernicke’s - language comprehension).

Question 25

Homunculus structure?

Answer 25

Medially, the feet, legs, then head. Laterally, hand, nose, upper lip.

Question 26

Anterior cerebral circulation?

Answer 26

Medial top band of brain. Therefore occlusion = paralysis or weakness of foot and lef on the opposite side. Cortical sensory loss in opposite foot and leg

Question 27

Middle cerebral

Answer 27

- Bulk of lateral surface of hemisphere - Superior division of Broca's area = language expression (resulting aphasia) (anterior branch of MCA) - INferior devision supplies lateral temporal lobe (location of Wernicke's areas - Language comprehension (posterior branch of MCA) Lesion is located in the superior temporal gyrus.

Question 28

Posterior cerebral artery

Answer 28

Supplies occipital lobe, cerebellum and brainstem. Vertebral arteries - Basilar artery splits - Can get PICA (posterior inferior cerebellar artery) = Lateral medullary syndrome - Anterior inferior cerebellar artery

Question 29

Long tracts of the motor pathway?

Answer 29

``` Descending motor pathway (UMN) - From motor cortex V - internal capsule V - Midbrain V - Pons V - Medulla V - Decussation of pyramids (cross over) V - Cervical cord - Thoracic cord etc ```

Question 30

Long tracts of the dorsal column pathway? Sensory (proprioception, fine touch, vibration)

Answer 30

``` - Post-central gyrus V - Thalamus (VPL) V - Midbrain V - Pons (becoming the medial lemniscus) V - Medulla (cross over of medial lemniscus (becomes nucleus gracilis, nucleus cuneate) V - Decussation of pyramids (cross over) V - Cervical cord - Thoracic cord etc ```

Question 31

Long tracts of the spinothalamic pathway? Sensory (pain + temperature)

Answer 31

``` - Post-central gyrus V - Thalamus (VPL) V - Midbrain V - Pons (becoming the medial lemniscus) V - Medulla V - Cervical cord - Thoracic cord etc - Lumbar V - CROSS OVER THEN ```

Question 32

12 cranial nerves?

Answer 32

``` I - Olfactory II - Optic III - Oculomotor IV - Trochlear V - Trigeminal VI - Abducens VII - Facial VIII - Vestibulocochlear IX - Glossopharyngeal X - Vagus XI - Accessory XII - Hypoglossal ```

Question 33

Nuclei of the cranial nerves?

Answer 33

All cranial nerves have a nucleus that are present in the brainstem EXCEPT the optic and olfactory (I + II).

Question 34

Mid-brain contains nuclei of which cranial nerves?

Answer 34

Mid- brain houses oculomotor nerve (III) and trochlear nerve (IV).

Question 35

Pons contains nuclei of which cranial nerve?

Answer 35

Trigeminal (V) (M+S) Abducens (VI) Facial nerve (VII) Vestibulocochlear (VIII)

Question 36

Medulla contains nuclei of which cranial nerve?

Answer 36

Glossopharyngeal (XI) Vagus (X) Accessory (XI) Hypoglossal (XII) Rule of S + M

Question 37

What is special about Trigeminal (V)

Answer 37

Sensory and motor nerve fibres from 4 nuclei

Question 38

What is the structure of the NMJ + Stages of synaptic conduction?

Answer 38

1. Presynaptic voltage-gated Ca2+ channels open --> Ca influx 2. ACh vesicles released from presynaptic terminal 3. Ach diffuses across cleft 4. Ach binds to NICOTINIC receptors on post-synaptic terminal 5. --> Na+ influx --> Depolarisation --> Ca2+ release from SR --> Muscle contraction 6. Ach is degraded by acetylcholinesterase and choline is taken up into presynaptic terminal

Question 39

What drug is used to block presynaptic choline uptake?

Answer 39

Hemicholinium

Question 40

What drug blocks ACh vesicle fusion?

Answer 40

Botulinum | Lambert-Eaton Myasthenic Syndrome

Question 41

Which drugs block nicotinic ACh receptors?

Answer 41

Antimuscarinic blocks muscarinic Ach Antinicotonic block nicotonic receptors. Non-depolarising: Atracurium, vecuronium Depolarising: suxamethonium - paralysis therefore short-term paralysis as part of GA.

Question 42

Antimuscarinic agents?

Answer 42

``` Antipsychotics (clozapine) Atropine Tropicamide Scopolamine Atropine ```

Question 43

Antinicotinic agents?

Answer 43

Bupropion | Hexamethonium

Question 44

What are the dopamine pathways of the CNS?

Answer 44

Mesocorticolimbic Nigrostriatal Tuberoinfundibular

Question 45

Role of Mesocorticolimbic in disease?

Answer 45

Schizophrenia

Question 46

Role of Nigrostriatal in disease?

Answer 46

Parkinson

Question 47

Role of tuberoinfundibular?

Answer 47

Hyperprolactinaemia

Question 48

Sympathetic Nervous System structure?

Answer 48

- Autonomic nervous system - Cell Bodies from T1-L2. Response to fight-flight or freeze. - Supplied form the spinal cord, to the left + right ganglia.

Question 49

Where do general visceral efferent fibres synapes to in the sympathetic nervous system?

Answer 49

- Paravertebral ganglia - Prevertebral ganglia - Chromaffin cells of adrenal medulla

Question 50

How are preganglionic fibres different to postganglionic fibres?

Answer 50

``` Pre = Myelinated + release ACh @ nicotinic receptors Post = Unmyelinated + release noradrenaline @ adrenergic receptors (except @ sweat glands where they reelase ACh for muscarinic receptor) ```

Question 51

What are the parasympathetic nerve system cranial nerves?

Answer 51

Rest and digest/ Feed and Breed. Arousal, salivation, lacrimation, urination, digestion, defectation. 3 - Ciliary Ganglion for eye 7 - - Pterygopalatine: mucus membranes of nose, palate + lacrimal gland - Submandibular: submandibular and sublingual glands 9 - Otic: Parotid gland 10 - Vagus (thoracic and abdo viscera) Sacral: Pelvic splanchnic nerves (S2-4) innervate pelvic viscera.

Question 52

What is the difference between preganglionic and post ganglion parasympathetic fibres?

Answer 52

``` Pregang = ACh @ nicotinic receptors Postgang = ACh @ muscarinic receptors ```

Question 53

All nuclei except 4 in Cranial nerves?

Answer 53

All except 4 innervate ipsilateral side. | Fibres from trochlear nucleus decussate in medulla + supply contralateral superior oblique muscle.

Question 54

Vestibulo-ocular pathways?

Answer 54

Vestibulo-ocular reflex (VOR) - Axons from vestibular neurons project via MLF to abducens and oculomotor nuclei. - Head turns L --> Eyes turn R

Question 55

Absent Doll's Eye Sign

Answer 55

Brainstem death

Question 56

Caloric Test physiology?

Answer 56

Warm --> Increasing firing of vestibular nerve --> eye turn to contralateral side with nystagmus to ipsilateral side. - Fast direction of nystagmus COWS Cold: opposite Warm: Same Absence = brainstem damage on side being tested

Question 57

Visual Field Defects? Central Scotoma?

Answer 57

Blind Spot or due to MS

Question 58

Visual Field Defects? Monocular vision loss?

Answer 58

Damage of the optic nerve

Question 59

Bitemporal hemianopia?

Answer 59

Damage at the optic chiasm Upper quadrant defect > lower quadrant defect = inferior chiasmal compression, from pituitary tumour Lower quadrant defect > upper quadrant defect = superior chiasmal compression, commonly a craniopharyngioma. This may cause a diabetic insipidus.

Question 60

Contralateral homonymous hemianopia

Answer 60

Therefore a left contralateral homonymous hemianopia means there is damage to the right hand side. Defect is on the left. Due to damage at the optic tract. = Incongruous defect Also due to damage at the whole of the optic radiation. = congrous defect. Also due to damage of the entire calcarine fissure.

Question 61

Contralateral superior quadrantanopia?

Answer 61

- Damage at the right Meyer's Loop in the right temporal radiation. - Temporal = Superior Superior TEMPO

Question 62

Contralateral inferior quadrantanopia

Answer 62

- Damage at the calcarine fissure at the parietal lobe Inferior quadrantanopia - Remember left inferior quadrantanopia = right parietal lobe lesion.

Question 63

Homonymous hemianopia with central macular sparing?

Answer 63

Lesion at occipital pole - Contralateral. Lesion of the occipital cortex

Question 64

Pupillary light reflex? Optic nerve damage to left?

Answer 64

Left direct reflex is lost. When left eye is stimulated, neither pupil constrict. Right consensual reflex is lost. When left eye is stimulated, right does not constrict. Right direct reflex is intact. Right constricts when signs. Left consensual is intact as it relies on the oculomotor nerve.

Question 65

Schematic diagram for pupillary light reflex?

Answer 65

- Retina on left and right - Travels down optic nerve either side. - Cross overs at retectal N to contralateral and ipsilateral Edinger-Westphal nuclei. - Then travels down CN3 (oculomotor) to the ciliary sphincter.

Question 66

Oculomotor nerve damage on left?

Answer 66

- Left direct is lost - Right consensual reflex is intact - Right direct reflex is intact. - Left consensual reflex is lost.

Question 67

What is a Marcus Gunn Pupil

Answer 67

- Person with abnormal left direct + abnormal right consensual reflex - Afferent pupillary defect.

Question 68

Pattern of Motor Deficits | - Cortical Lesions?

Answer 68

Hyperreflexia proximally in arm or leg

Question 69

Pattern of Motor Deficits | - Internal capsule and corticospinal lesions?

Answer 69

- Contralateral hemiparesis with pyramidal distribution - Lesions with epilepsy, decrease cognition of homonymous hemianopia = In cerebral hemisphere - Lesion with contralateral CN palsy = brainstem lesion on the side of the palsy (e.g Milliard-Gubler syn)

Question 70

Pattern of Motor Deficits | - Cord Lesions?

Answer 70

Quadriparesis/paraparesis | Motor and reflex level: LMN signs at level of lesion and UMN sign below

Question 71

Pattern of Motor Deficits | - Peripheral Neuropathies?

Answer 71

- Usually distal weakness - GBS weakness is proximal (root involvement) - Single nerve = Mononeuropathy: trauma or entrapment - Several nerves = mononeuritis multiplex: Vasculitis or DM. Asymmetrical involvement of individual non-contiguous nerve trunks.

Question 72

What is the UMN lesion pattern?

Answer 72

- increased tone ± clonus - Hyperreflexia - Up-going plantars - pyramidal weakness: extensors in UL (weak extensor) flexors in LL (weak flexor) - No wasting Motor cells in pre-central gyrus to anterior horn cells in the cord.

Question 73

What is the LMN lesion pattern

Answer 73

- Decreased tone/flaccidity - Hyporeflexia - Down-going plantars (normal - Wasting - Fasciculations Anterior horn cells to peripheral nerves

Question 74

Pattern of Motor Deficits | - Primary Muscle Lesions?

Answer 74

- Symmetrical loss - reflexes lost later vs neuropathies - No sensory loss - Fatiguability in myasthenia

Question 75

Patterns of sensory deficits | - Where do sensations travels in the cord?

Answer 75

- Pain + temp travel along spinothalamic tracts | - Touch, joint and vibration travel in large fibres peripherally + dorsal column centrally.

Question 76

Patterns of sensory deficits | - Distal sensory loss?

Answer 76

Neuropathy

Question 77

Sensory level?

Answer 77

Hallmark of cord lesion - Hemi-cord lesion --> Brown-Sequard Syndrome - Ipsilateral loss of proprioception + vibration and UMN weakness with contralateral loss of pain + temp

Question 78

Dissociated sensory loss cause?

Answer 78

- Selective loss of pain and temp with conservation of proprioception and vibration - Occurs in cervical cord lesions e.g syringomyelia

Question 79

What are the specific signs of cerebellar syndrome?

Answer 79

- Dydiadochokinesia - Dysmetria: past-pointing - Ataxia - Nystagmus - Intention Tremor - Speech: slurred, staccato, scanning dysarthria - Hypotonia Head: head tremor (titubation) eye nystagmus and dysarthria (Speech - British Constitution) Arms: rebound pehomenon, intention tremor, past pointing. LEgs: heel-shin, ataxic gait, Romberg's negative. Cerebellar hemisphere - finger-nose ataxia. Cerebellar vermis - Gait ataxia.

Question 80

What are the common causes of cerebellar syndrome?

Answer 80

PASTRIES - Paraneoplastic: e.g from bronchial Ca - Alcohol: thiamine - Sclerosis - Tumour: e.g CPA lesion - Rare: MSA, Friedrich's, Ataxia Telangiectasia - Iatrogenic: phenytoin - Endo: hypothyroidism - Stroke: vertebrobasilar

Question 81

Anterior Cerebral Artery stroke?

Answer 81

- Supplies frontal and medial part of cerebrum - Contralateral motor/sensory loss in the legs >arms - Face is spared - Abulia (pathological laziness)

Question 82

Middle Cerebral Artery?

Answer 82

- Supplies lateral and external part of hemisphere - Contralateral motor/sensory loss in face and arms > legs - Contralateral homonymous hemianopia due to involvement of optic radiation. - Cognitive changes Dominant (L): aphasia (Broca's) Non-dominant (R): neglect, apraxia. ``` Broca's = inferior frontal gyrus. expressive. Comprehension is normal, but speech is non-lfuent, laboured and halting. Wernicke's = receptive aphasia - superior temporal gyrus. Sentences make no sense, speech remains fluient and comprehension is impaired. ``` Dominant is normally left. Therefore the middle cerebral artery supplies both Wernicke's and Broca's area.

Question 83

Posterior cerebral artery?

Answer 83

Supplies occipital lobe | Contralateral homonymous hemianopia with macula sparing

Question 84

Vertebrobasilar Circulation

Answer 84

- Supplies cerebellum, brainstem and occipital lobes. - Combination of symptoms : Visual: hemianopia, cortical blindness - Cerebellar: DANISH - CN Lesions - Hemi-/quadriplegia - Uni/bilateral sensory symptoms.

Question 85

What is lateral medullary syndrome/Wallenberg's syndrome?

Answer 85

PICA: Ipsilateral: facial pain and temperature loss Contralateral: limb/torso pain and temperature loss Ataxia, nystagmus AICA: Symptoms are similar to Wallenberg's (see above), but: Ipsilateral: facial paralysis and deafness It is an important syndrome to be aware of as it is most often due to a stroke affecting the posterior inferior cerebellar artery (PICA). It is the most commonly survived stroke that affects the brainstem and is commonly used as an exam question scenario. Given her symptoms, this would be in keeping with a right-sided posterior inferior cerebellar artery infarct. An anterior inferior cerebellar artery infarct would present in the same way but with the additional symptoms of a same-sided facial weakness and loss of hearing. A basilar artery infarct would result in a locked-in syndrome where the patient is unable to move or communicate but is fully conscious. Both of these are more likely to affect the autonomic centres in the medulla and are associated with a higher mortality.

Question 86

Millard-Gubler Syndrome: Crossed hemiplegia

Answer 86

``` Pontine lesions (e.g infarc) Effects: 6th (can't look laterally) and 7th CN palsy + contralateral hemiplegia. ```

Question 87

Locked in syndrome?

Answer 87

- Pt is aware + cognitively intact but completely paralysed except for eye muscle Causes - Ventral pons infarction: basilar artery. Secondary to hypertension. Reduced GCS, quadriplegia, miosis, absent horizontal eye movement. Pinpoint pupils point to pons. - Central pontine myelinolysis: rapid correction of hyponatreamia

Question 88

Cerebellopontine Angle Syndrome?

Answer 88

Causes: Acoustic neuroma, meningioma, cerebellar astrocytoma, metastasis Leads to a ipsilateral CN5,6,7,8 + cerebellar signs

Question 89

Subclavian Steal Syndrome?

Answer 89

Subclavian A stenossi proximal to origin of vertebral A may_-> blood being stolen from this vertebral artery by retrograde flow - Syncope/presyncope or focal neurology using the arm - BP difference of >20mmHg between arms.

Question 90

What is anterior spinal artery/ Beck's Syndrome

Answer 90

- Infarction of spinal cord in distribution of anterior spinal artery: ventral 2/3 of cord. - Causes: Aortic Aneurysm dissection or repair - Effects Para/Quadriparesis Impaired pain and temperature sensation Preserved touch and proprioception

Question 91

What are the differentials for muscle weakness? Causes in the CNS?

Answer 91

Cerebrum - Vascular: infarct, haemorrhage - Inflammation: MS - SOL - Infection: Encephalitis, abscess Cord - Vascular: Anterior spinal artery infarction - Inflammation: MS - Injury Anterior Horn - MND, polio

Question 92

What are the differentials for muscle weakness? Causes in the PNS?

Answer 92

``` - Motor Nerves Mononeuropathy: compression Polyneuropathy: GBS, CMT - NMJ GB, LEMS, Botulism - Muscle Toxins: steroids Poly/dermatomyositis Inherited: DMD, BMD, FSH ```

Question 93

Gait Disturbance Differential (Motor) - Basal Ganglia: Shuffling gait

Answer 93

Basal: - PD - Parkinsonism: MSA, PSP, Lewy Body Dementia, CBD Hypokinetic (parkinsons) Hyperkinetic (Huntington's)

Question 94

Gait Disturbance Differential (Motor) | UMN Bilateral: Spastic, scissoring

Answer 94

Cord: Compression, trauma, hereditary spastic paraparesis, syringomyelia, transverse myelitis Bihemispheric: CP, MS

Question 95

Gait Disturbance Differential (Motor) | UMN Unilateral: Spastic circumducting

Answer 95

Hemisphere lesion: CVS, MS, SOL | Hemicord: MS, tumour

Question 96

Gait Disturbance Differential (Motor) | LMN bilateral: bilateral foot drop

Answer 96

Polyneuropathy: CMT (charcot-marie tooth), GBS | Corda equina

Question 97

Gait disturbance differential: (Motor) LMN Unilateral: foot drop --> high stepping gait.

Answer 97

Ant horn: Polio Radicular: L5 root lesion Sciatic/common peroneal nerve: trauma, DM. Weakness of hip abduction is L5 radiculopathy.

Question 98

Mixed UMN and LMN: MAST ?

Answer 98

- Motor Neuron Disease - Friedrich's ataxia - Same as SCD but with cerebellar ataxia. - Subacute combined degeneration of the cord = First to go is the dorsal column with joint position and vibration. bilateral spastic paresis (damage to lateral columns) bilateral loss of proprioception and vibration sensation (damage to posterior columns) leading to sensory ataxia and positive romberg's test. Bilateral limb ataxia (damage to peripheral nerve) - absent ankle and knee jerk.

Question 99

What are the differentials for hand wasting?

Answer 99

Cord - Anterior Horn: MND, polio - Syringomyelia Roots - Compression: spondylosis, neurofibroma ``` Brachial Plexus - Compression Cervical rib Tumour: Pancoast's, breast - Avulsion: Klumpke's palsy ``` ``` Neuropathy - Generalised: Charcot Marie Tooth - Mononeuritis multiplex: DM - Compressive mononeuropathy Median: thenar wasting Ulnar: hypothenar and interossei wasting ``` Muscle - Disuse: RA - Compartment syndrome: Volkman's ischaemia - Distal myopathy: myotonic dystrophy - Cachexia

Question 100

Gait disturbance due to sensory impairment? Vestibular causes?

Answer 100

(all Romberg's +ve) Meniere's Viral Labyrinthitis Brainstem Lesion

Question 101

Gait disturbance due to sensory impairment? Cerebellar causes?

Answer 101

Ataxic - ETOH - Infarct Wide-based gait, loss of heel to toe pattern and instability.

Question 102

Gait disturbance due to sensory impairment? Proprioceptive loss (Romberg' +ve)

Answer 102

Dorsal columns: B12 deficiency Peripheral Neuropathy: DM, ETOH, Uraemia Visual Loss

Question 103

What are the cardiac causes of LOC?

Answer 103

Stokes-Adams Attack = collapse without warning and loss of consciousness. - Bradycardia: heart block, sick sinus, Long QT - Tachycardia: SVT, VT - Structural Weak heart: LVF, tamponade Block: AS, HOCM, PE, ACS

Question 104

What are the reflex causes of LOC?

Answer 104

Vagal overactivity - Vasovagal syncope - Situational: cough, effort, micturition - Carotid sinus syncope Sympathetic underactivity= postural hypotension - Salt deficiency: hypovolaemia, Addison's - Toxins Cardiac: ACEi, diuretics, nitrates, a-B Neuro: TCAs, benzos, antipsychotics, L-DOPA - Autonomic neuropathy: DM, Parkinson's, GBS Dialysis Unwell: chronic bed-rest Pooling, venous: varicose veins, prolonged standing (orthostatic hypotension) .

Question 105

What are the arterial causes of LOC?

Answer 105

Vertebrobasilar insufficiency: migraine, TIA, CVA, Subclavian steal Shock HTN: phaeochromocytoma

Question 106

What are the systemic causes of LOC?

Answer 106

Metabolic: decreased glucos Resp: hypoxia, hypercapnoea Blood: anaemia, hypervisocity

Question 107

What are the head causes of LOC?

Answer 107

Epilepsy | Drop Attacks

Question 108

Examination of LOC?

Answer 108

- Postural HTN: difference of >20/10 after standing for 3 mins vs lying down - Orthostatic hypotension - Cardiovascular assessment - Neurological assessment

Question 109

Investigations of LOC?

Answer 109

- ECG ± 24hr ECG - U+E, FBC, Glucose - Tilt table (confirms dysautomomia for neuro) - EEG, Sleep EEG - Echo, CT, MRI brain

Question 110

Presentation of cardiogenic syncope?

Answer 110

Trigger: Exertion, drug, unknown Before: Palpitations, chest pain, dyspnoea During: pale, slow/absent pulse, clonic jerks may occur After: Rapid recovery IX: ECG, 24hr ECG, Echo

Question 111

Presentation of vasovagal syncope?

Answer 111

Trigger: prolonged standing, heat, fatigue, stress, emotional upset Before - Gradual onset: sec--> mins - Nausea, pallor, sweating, tunnel vision, tinnitus. - Cannot occur lying down During - Pale, grey, clammy, brady - Clonic jerks and incontinence can occur, but no tongue biting After: rapid recovery Ix: Tilt-table testing

Question 112

Reflex: Postural hypotension presentation?

Answer 112

Prodrome of sweating, pallor and N+V before a transient LOC are suggestive of a reflex syncope. Most common cause. Defined as SBP fall of at least 20mmHg within 3 mins of standing. Trigger: standing up Before, during and after same as vagal above Ix: Tilt-table testing

Question 113

Presentations of Arterial causes of LOC?

Answer 113

Trigger: Arm elevation (Subclavian steal), migraine Before, during and after same as vasovagal ± brainstem signs (diplopia, nausea, dysarthria Ix: MRA, duplex vertebrobasilar circulation

Question 114

Presentation of systemic causes of LOC?

Answer 114

Hypoglycaemia: tremor, hunger, sweating, light-headedness --> LOC

Question 115

Epileptic presentation of LOC?

Answer 115

Trigger: flashing lights, fatigue, fasting Before: aura in complex partial seizures - feeling strange, epigastric rising, deja/jamais vu, smells, lights, automatisms During: tongue biting, incontinence, stiffness --> Jerking, eyes open, cyanosis, Decreased SpO2. After: headache, confusion, sleeps, Todd's palsy. Ix: EEG, increased SE prolactin at 10-20mins (greater than 2x baseline indicates generalise tonic clonic seizure). Check glucose, WBC, electrolytes.

Question 116

Drop attack? Distinct from syncope?

Answer 116

No trigger. No warning. During: Sudden weakness of legs causes older woman to fall to ground. No post-ictal phase.

Question 117

What is the definition of vertigo?

Answer 117

- The illusion of movement: usually rotatory - Of patients or surrounding - Worse on movement

Question 118

What is not classified as vertigo?

Answer 118

Faintness Light-headedness Lost awareness

Question 119

What is dizziness?

Answer 119

With impaired consciousness = blackout Without impaired consciousness: - Vertigo: Vestibular in nature - Imbalance: vestibular, cerebellar, extrapyramidal

Question 120

What are the causes of Vertigo? Infection?

Answer 120

IMBALANCE Infection/Injury - Labyrinthitis: post-viral severe vertigo, n/v, hearing loss - Ramsay Hunt (shingles of facial nerve) - Trauma: to petrous temporal bone Investigation with audiogram, Rinne's and Weber's test. Will show a sensorineural hearing loss. Previous viral infection.

Question 121

What are the causes of Vertigo? Meniere's

Answer 121

- Recurrent vertigo (~20mins) ± n/v - Fluctuating SNHL (sensorineural hearing loss) - Tinnitis - Aural fullness (ear feeling full)

Question 122

What are the causes of Vertigo? BPPV?

Answer 122

Sudden vertigo proved by head rotation. Short lived experience. Free-floating endolymph particles otoconia). - Episodic vertigo.

Question 123

Other causes of vertigo?

Answer 123

Aminoglycosides/Frusemide Lymph, peri, fistula Path: Connection between inner and middle ears Causes: congenital, truama PC: vertigo, SNHL O/E: tulio's phenomenon - nystagmus evoked by loud sound Arterial - Migraine - TIA/Stroke Nerve - Acoustic Neuroma/Vestibular schwannoma Central lesions - Demyelination, tumour, infarction Epilepsy - Complex partial

Question 124

Causes of hearing loss - Conductive?

Answer 124

WIDENING - Wax or foreign body - Infection: Otitis media, OME - Drum perforation - Extra: ossicle discntinuity - otosclerosis, trauma - Neoplasia: carcinoma - Injury: Barotrauma - Granulomatous: Wegener's, Sarcoid

Question 125

Causes of hearing loss: sensorineural? DIVINITY

Answer 125

Development - Genetic: Alport's - Congenital: TORCH - Perinatal: Anoxia Degenerative - Presbyacusis Infection - VZV, Measles, Mumps, Influenza - Meningitis Vascular - Ischaemia: Interal Auditory Artery - sudden hearing loss and vertigo - Stroke Inflammation - Vasculitis - Sarcoidosis Neoplasia - CPA tumours: acoustic neuroma (commonest cause of unilateral SNHL) Injury - Noise - head trauma Toxins - Gentamicin - Frusemide - Aspirin Lymph - Endolymphatic hydrops = Meniere's (abnormal fluctuation of the fluid in the ear). - Perilymphatic fistula: ruptured round window.

Question 126

Abnormal Involuntary Movements - Dyskinesias. Define Tremor

Answer 126

Regular, rhythmic oscillation Asterixis = rhythmic myoclonus - tremor of the hand when stretched out

Question 127

Types of Tremor? RAPID?

Answer 127

Resting Action/Postural Intention Dystonic

Question 128

What is a resting tremor?

Answer 128

Features - 4-6 Hz, pill rolling - Abolished on voluntary movement - increased with distraction (counting backwards) Causes: Parkinsonism Management: Dopamine agonists (levodopa, cabergoline, bromocriptine), antimuscarinic (procyclidine)

Question 129

What is a postural/action tremor?

Answer 129

Features - 6-12Hz - Absent at rest - Worse with outstretched hands or movement (part of the essential tremors) - Equally bad at all stages of movement - Can also affect the vocal cords. Cause - Benign essential tremor - Endo: thyrotoxicosis, decreased glucose, phaeo - Alcohol withdrawal (caffeine, opioids) - toxins, valproate, theophylline - Sympathetic: physiological tremor may be enhanced e.g in anxiety

Question 130

What is an intention tremor?

Answer 130

Features - >6Hz, irregular, large amplitude - worse at the end of movement - E.g past-pointing Causes: cerebellar damage

Question 131

What is a dystonic tremor

Answer 131

Variable presentations | Mostly idiopathic, as for dystonia

Question 132

What is a benign essential tremor?

Answer 132

- Autosomal dominant - Occurs with action and worse with anxiety, emotion, caffeine - Arms, neck, voice - Doesn't occur during sleep - Better with ETOH. Management: Propranolol Primidone

Question 133

What is myoclonus?

Answer 133

Sudden, involuntary jerks

Question 134

What is myoclonus caused by?

Answer 134

Metabolic = asterixis (L, R, increased CO2) Neurodegenerative disease CJD Myoclonic epilepsies (infantile spasms)

Question 135

What is benign essential myoclonus?

Answer 135

- AD - Childhood onset frequency generalised myoclonus without progression - May respond to valproate

Question 136

What is dystonia?

Answer 136

Prolonged muscle contractures --> Unusual joint posture or repetitive movement

Question 137

What is idiopathic generalised dystonia?

Answer 137

AD | Childhood onset: starts in one leg, spreads on that side of the body over 5-10 years.

Question 138

What is idiopathic focal dystonia

Answer 138

- Commonest form of dystonia - Confined to one part of the body - worsened by stress - Involves rigidity and writhing movements rather than twitching. Types - Spasmodic torticolis - Blepharospasm (eyelids) - Oromandibular

Question 139

What is acute dystonia?

Answer 139

- Torticollis, trismus and or occulogyric crisis - Typically a drug reaction: Antipsychotics Metoclopramide L-Dopa Rx: Procyclidine (antimuscarinics).

Question 140

Chorea?

Answer 140

- Non-rhythmic, purposeless, jerky, flitting movements - Facial grimacing, extending the fingers - Huntington's - Sydenham's - Wilson's - L-Dopa

Question 141

Athetosis?

Answer 141

Slow, sinuous, writhing movements - Causes Cerebral palsy Kernicterus

Question 142

Tardive Syndromes?

Answer 142

Delayed onset following chronic exposure to Da agonists (antipsychotics, antiemetics, L-DOPA). - Dyskinesia: orobuccolingual, truncal - Dystonia: Sustained, sterotyped muscle spasms of twitching or turning - Akathisia: unpleasant sense of inner restlessness ± repetitive movements Manage: Change to atypical or slowly withdraw drug Dyskinesia: Da antagonist Akathisia: B-Blockers.

Question 143

Define Dementia?

Answer 143

Chronically impaired cognition that affects multiple domains: memory, attention, language - No impairment of consciousness - Acquired and progressive

Question 144

What are the most common types of dementia?

Answer 144

Alzheimer's Vascular Lewy Body Frontotemporal Dementia (Pick's)

Question 145

Summary of Alzheimer's?

Answer 145

Epi: 50% Path: neurofibrillary tangles and B amyloid plaques PC: Progressive, global cognitive decline. Memory loss, loss of recent memory first. Misplacing items, apathy, decline in activities, personality change. IADLs. RF: ApoE4, presenillin 1/2 mutation, Down's Ix: MRI - medial temporal lobe atrophy. MMSE, metabolic panel Rx: cholinesterase inhibitor (Donepezil, rivastigmine) if MMSE is 10-20.

Question 146

Summary of Vascular Dementia?

Answer 146

Epi: 20% Path: multiple infarcts PC: sudden onset, stepwise deterioration, patchy deficits, vascular RFs. Ix: MRI - extensive infarcts or small vessel disease Rx: Manage predisposing factors

Question 147

Summary of Lewy Body Dementia

Answer 147

Epi: 20% Path: Lewy body in occipito-parital cortex. PC: Fluctuating cognitive dysfunction, recurrent visual hallucinations, REM sleep behaviour disorder. MAy have a symptom of parkinson's. Distinguished from parkinson's in the onset of dementia first. Rx: Minise antipsychotics, use cholinesterase inhibitors - donepezil/rivastigmine.

Question 148

Summary of Frontotemporal Dementia (Pick's)

Answer 148

<5% - Path: Pick bodies - PC: Disinhibition, personality change, early memory preservation, progressive aphasia - Ix: MRI - frontal or temporal atrophy

Question 149

What are the ameliorable causes of dementia?

Answer 149

Infection - viral: HIV, HSV, PML - Helminth: cysticercosis, toxi Vascular - Chronic subdural haematoma Inflammation - SLE - Sarcoid Neoplasia Nutrition - Thiamine deficiency - B12 and folate deficiency - Pellagra (B3/niacin deficiency) Endocrinology - hypothyroidism - Hypoadrenalism - Hypocalcaemia - Hypocephalus (normal pressure)

Question 150

What is the definition of delirium?

Answer 150

Globally impaired cognition and impaired consciousness

Question 151

Features of delirium?

Answer 151

- Disorientation of person, time and place - Reversal of sleep-wake cycle (hyperactive at night) - Labile mood - illusions, delusions and hallucinations - Cognitive impairment: memory, language, concentration

Question 152

What are the causes of Delirium?

Answer 152

DELIRIUMS - Drugs : opiods, sedatives, L-DOPA - Eyes, ears and other sensory deficit - Low O2 states: MI, stroke, PE - Infection: UTI - Retention: stool or urine - Ictal - under-hydration/nutrition - Metabolic: DM, post-op, sodium, uraemia - Subdural haemorrhage or other intracranial pathology

Question 153

Investigations for delirium

Answer 153

- Bloods: FBC, U+E, LFTs, glucose, ABG - Urine Dip - Septic Screen - ECG, LP Confusion screen = B12/folate, macrocytic anaemia and deficiencies worsen confusion.

Question 154

Management of delirium

Answer 154

ID and Rx underlying cause Surround with familiar people Nurse in moderately lit, quiet room Find glasses, hearing aids Avoid sedatives if possible, but if disruptive: - Haloperidol 0.5-2mg - Chlorpromazine 50-100mg PO/IM (avoid in elderly)

Question 155

What are the differentials for an acute headache?

Answer 155

Common - Acute sinusitis - Otitis media - Menstrual headache - Medication withdrawal/overuse - Migraine - Tension headache - Cerebrovascular incident ``` ACUTE: Vicious - Vascular Haemorrhage: SAH, intracranial, intracerebral, intraventricular Infarction: esp. posterior circulation Venous: Sinus/cortical thrombosis ``` ``` - Infection/Inflammation Meningitis Encephalitis Abscess trigeminal neuralgia ``` - Compression Obstructive hydrocephalus:tumour Pituitary enlargement: apoplexy ICP - Spontaneous intracranial hypotension Acute dural CSF leak Worse on standing initially Ophthalmic - Acute Glaucoma Unknown - Situational: cough, exertion, coitus. - medication overuse/withdrawal - Dental caries/wisdom tooth Systemic - HTN: Phaeo, PET - Infection: sinusitis, tonsillitis, atypical pneumonia - Toxins: CO

Question 156

Chronic headache?

Answer 156

``` MCD TINGS - Migraine - Cluster Headache - Drugs Analgesics Caffeine Vasodilators: Ca2+ antagonists, nitrates ``` Tension headaches ICP increased/decreased - Increased: tumour, aneurysm, AVM, benign intracranial HTn - Decreased: Spontaneous intracranial hypotension Trigeminal Neuralgia GCA Systemic - HTN - Organ failure e.g uraemia

Question 157

What are the investigations for headache?

Answer 157

- Bloods - Urine - Micro Blood cultures Serology: enterovirus (common cause if viral meningitis), HSV, HIV, Syphilis, crypto - CSF - Radiology - Non-contrast CT SAH: blood in sulci, cisterns (white). 90% sensitivity in first 24hr - MRI: MRA - aneurysm - MRV: sinus thrombosis

Question 158

CSF opening pressure for headaches?

Answer 158

Opening pressure (normal = 5-20cm H20): - increased: SAH, meningitis - decreased: spontaneous intracranial hypotension

Question 159

What is xanthochromia?

Answer 159

Yellow appearance of CSF due to bilirubin. Detected by spectrophotometry. Can show evidence of a subarachnoid haemorrhage. If no answer here then cerebral angiography.

Question 160

Bacteria on CSF?

Answer 160

``` Appearance - Turbid Cells - PMN Count - 100-1000 Glucose - decreased (<1/2 plasma) Protein - Increased x2 (>1.5) ```

Question 161

TB on CSF?

Answer 161

``` Appearance - fibrin web Cells - lympho/mononuc Count - 10-1000 Glucose - Decreased (<1/2 plasma) Protein - Very very high (X3) ```

Question 162

Viral of CSF?

Answer 162

``` Appearance - Clear Cells - Lympho-mononuclear Count - 50-1000 Glucose - >1/2 plasma Protein - mild increased (<1) ```

Question 163

Summary of subarachnoid headache?

Answer 163

- Sudden onset, worse ever, occipital headache | - Meningism, focal signs, decreased consciousness

Question 164

Summary of Venous sinus thrombosis?

Answer 164

Rapid onset of symptoms Unilateral. Can be septic or aseptic (trauma, prothrombotic feature) Can have fever, ptosis, reduced corneal reflex, retinal-vein dilatation. Sagittal: headache, vomiting, seizures, decreased vision, papilloedema Transverse: headache ± mastoid pain, focal CNS signs, seizure, papilloedema Need a contrast enhanced high res CT of head. Contrast-enhanced MRI of head Blood cultures Factor V Leiden

Question 165

Summary of Meningitis

Answer 165

- Fever, photophobia, neck stiffness, Kernig's +ve - Purpuric rash - Decreased consciousness

Question 166

Summary of Encephalitis?

Answer 166

- Fever - Odd behaviour/confused - fits - focal neurology (complicated by temporal lobe may give motionless stare or confusion) - Decreased consciousness Investigation CSF: lymphocytosis, elevated protein PCR for HSV CT: medial temporal and inferior frontal changes (e.g. petechial haemorrhages) - normal in one-third of patients MRI is better EEG pattern: lateralised periodic discharges at 2 Hz

Question 167

Summary of acute glaucoma?

Answer 167

- Constant unilateral eye pain, radiating to forehead - Decreased acuity, haloes, n/v - Red eye, cloudy cornea - Dilated non-responsive pupil

Question 168

Summary of tension headache?

Answer 168

- Bilateral/vertex-bitemporal | - Non-pulsatile, bandlike headache.

Question 169

What is a cortical vein thrombosis?

Answer 169

- Thunderclap headache - Stroke-like focal symptoms over days - Focal seizures are common

Question 170

Migraine headache?

Answer 170

Prodrome --> aura --> headache - Unilateral, throbbing - n/v phono/photophobia

Question 171

Cluster headache?

Answer 171

Alcohol may trigger an attack. Occurs in smokers. - Rapid onset very severe pain around/behind eye - Red, watery eye, nasal congestion - Miosis, ptosis - Attacks last 15mins -3hrs, 1-2x a day. - Mostly nocturnal - Clusters last 4-12 weeks, remission lasts 3months - 3yrs. Management: 100% O2 via non-rebreathe mask, sumitriptan Prevention: verapamil, topiramate, Li.

Question 172

What is miosis?

Answer 172

Constriction of eye

Question 173

What is ptosis

Answer 173

Dropping of eyelid

Question 174

What is mydriasis

Answer 174

Dilation of the pupil of eye

Question 175

What is trigeminal neuralgia?

Answer 175

Paroxysms of unilateral intense stabbing pain in trigeminal distribution (usually V2/V3). - triggers: washing area, shaving, eating ,talking - Male >50yrs (refer if less than 50) - 2ndry in 14%: compression of CNV, MS, Zoster, Chiari malformation - Exclude 2nd cause by MRI Management: carbamazepine, lamotrigine, gabapentin Management surgery: microvascular decompression

Question 176

Analgesia overuse?

Answer 176

- Episodic headache becomes daily chronic headache | - Use OTC analgesia on 6 days/month max

Question 177

ICP headache?

Answer 177

Increased ICP: worse in AM, stooping, visual problems (papilloedema), obese women decreased ICP: worse sitting or standing

Question 178

Red flags for headache?

Answer 178

- Worse on lying down - Pain wakes patient up - Present when waking up - Unexplained weight loss - Focal neurological deficit - N/V - Seizures - Vomiting more than once with no cause - New neurological deficit - Reduction in conscious level - Valsalva (coughing or sneezing headache) - Progressive headache with fever) 2 or more red flag are present an urgent CT should be performed as the likelihood of a serious intracranial pathology is high.

Question 179

TMJ dysfunction headache?

Answer 179

Preauricular pain on chewing Associated with crepitus Earache, headache

Question 180

Giant Cell arteritis (>60 yrs, ESR >60, pred 60mg)

Answer 180

- Unilateral temple/scalp pain and tenderness - Thickened, pulseless temporal artery - Jaw claudication - amaurosis fugax, - sudden blindness - Associated with PMR in 50% Ix: ESR very high, platelets raised, ALP raised, HB reduced, temporal artery biopsy Management - High dose prednisolone (60mg) for 5-7 days - guideed by symptoms and ESR - Give PPI + bisphosphonates - Prognosis: 2yr course then complete remission

Question 181

What are the risk factors for migraine?

Answer 181

``` Family history High caffeine intake Obesity Female Stress life event Lack of sleep ```

Question 182

What is the pathophysiology of migraine?

Answer 182

Vascular: cerebrovascular constriction --> aura, dilatation --> headache Brain: spreading cortical depression Inflammation: activation of CN V nerve terminals in meninges and cerebral vessels

Question 183

What are the triggers for migraines?

Answer 183

``` Chocolate Cheese OCP - contraindicated due to increased risk of stroke. Caffeine Alcohol Anxiety Travel Exercise ```

Question 184

Symptoms of a migraine?

Answer 184

Headache- Aura lasting 15-30 mins then unilateral, throbbing headache - Phono/photophobia - N/V - Allodynia (pain in response to touch etc) - Often premenstrual - Prodrome: precedes migraine by hrs - days Yawning Food cravings Changes in sleep, appetite, mood. - Aura: precedes migraine by mins + may persist Visual: distortion, lines, dots, zig-zags, scotoma. Hemianiopic disturbance - spreading scintillating scotoma. Are fully reversible, develop over at least 5 mins, lasts 5-60 minutes. hemianopia Sensory: Paraesthesia (Fingers --> Face) Motor: dysarthria, ataxia, ophthalmoplegia. May have a hemiplegia. Speech: Dysphasia, paraphasia

Question 185

How do you classify migraine?

Answer 185

Migraine with aura (classical migraine) - 25% of patients | Migraine without aura (common migraine)

Question 186

What is the diagnostic criteria for migraine?

Answer 186

- Typical aura + headache or - >5 headaches lasting 4-72hrs with either N/v or photo/phonophobia + >2: - Unilateral - Pulsating - Interferes with normal life - Worsened by routine activity During headache at least one of the following: - 1. nausea and/or vomiting - 2. photophobia and phonophobia

Question 187

What is the differential for a migraine?

Answer 187

- Cluster/tension headache - Cervical spondylosis - HTN - Intracranial pathology - Epilepsy

Question 188

Acute Management of migraine?

Answer 188

Acute episode NICE = oral triptan + NSAID/paracetamol (diclofenac/aspirin) + M/D 2nd: Paracetamol + metoclopramide/domperidone (metoclopramide can cause extrapyramidal SE) 3rd: Rizatriptan (CI: IHD, Uncontrolled HTN, SSRI)

Question 189

Prophylactic management of migraine?

Answer 189

Avoid triggers 1st line: Propranolol, topiramate. Propranolol instead of topiramate in child bearing age. 2ns line: Valproate, pizotifen (increased weight) gabapentin

Question 190

Causes of subarachnoid haemorrhage?

Answer 190

- Rupture of saccular aneurysms (80%) - AVMs - Anticoagulants

Question 191

Risk factors for SAH?

Answer 191

- Smoking - HTN - ETOH - Bleeding diathesis - Mycotic aneurysms (SBE) - FH (close relatives have 3-5x isk)

Question 192

What are the sites of berry aneurysms?

Answer 192

- Junction of the posterior communicating with internal carotid artery - Anterior communicating with anterior cerebral artery - Middle cerebral artery bifurcation

Question 193

Associations of berry aneurysms with other diseases?

Answer 193

Adult Polycystic kidneys CoA Ehler's Danlos

Question 194

Symptoms of SAH?

Answer 194

- Sudden, severe occipital headache - Collapse - Meningism: neck stiffness, n/v, photophobia - Seizures - Drowsiness --> coma

Question 195

Signs of a SAH?

Answer 195

- Kernig's +ve (flex hips, and knee at 90 degree, extension of knee causes back pain) - Retinal or subhyaloid haemorrhage - Focal neuro @presentation suggests aneurysm location Later deficits suggests complications

Question 196

Sentinal headache

Answer 196

Around 6% of patients experience sentinel headache from a small warning bleed

Question 197

Differential for SAH?

Answer 197

In primary care, 25% of those with thunderclap headache have SAH - 50-60% no cause found - Rest: Meningitis, intracerebral bleed, cortical vein thrombosis

Question 198

Investigations for SAH?

Answer 198

Hyponatraemia is very common in these patients and sodium levels are usually closely monitored in the acute period. CT - Detects >90% of SAH within first 48hrs Hyperdense areas in the basal cisterns, sulci + major fissures. 50% of patients have an abnormal ECG LP - If CT -ve and no CIs >12hr after start of headache. - Xanthochromia due to breakdown of bilirubin - May have normal or raised opening pressure. On LP = straw coloured, protein. Refer to Neurosurg as soon as SAH is confirmed Then confirm SAH with intracranial angiogram +/- digital subtraction angiogram

Question 199

What is the management of an SAH?

Answer 199

- Frequent neuro obs: pupils, GCS, BP - Maintain CPP: Keep SBP >160 - CCB vasospasm prophylaxis: Nimodipine 60mg orally every 4hrs for 21 days. - Endovascular coiling (preferable to surgical clipping) If young unruptured aneurysms >7mm, young patients benefit from surgery.

Question 200

Complications of SAH?

Answer 200

- Rebleeding in 20% - Cerebral ischaemia - Due to vasospasm - Hydrocephalus Due to blockage of arachnoid granulations. Suddenly become unresponsive. May require ventricular or lumbar drain - hyponatraemia: common and don't manage with fluid restriction SIADH

Question 201

Define stroke?

Answer 201

Rapid onset, focal neurological deficit due to a vascular lesion lasting >24hr

Question 202

Pathogenesis for a stroke?

Answer 202

Infarction due to ischaemia (80%) or intracerebral haemorrhage (20%)

Question 203

Causes of an ischaemic stroke?

Answer 203

Atheroma (80%) - Large (MCA - Small vessel perforators (lacunar) Embolism - Cardiac (30%) of strokes: AF, endocarditis, MI - Atherothromboembolism: from carotids

Question 204

Causes of a haemorrhagic stroke?

Answer 204

- Increased BP - Trauma - Aneurysm rupture - Anticoagulation - Thrombolysis

Question 205

What are the rarer causes of stroke?

Answer 205

- Watershed stroke: sudden decreased in BP (e.g sepsis) - Carotid artery dissection - Vasculitis: PAN, HIV - Cerebral vasospasm: 2ndry to SAH - Venous sinus thrombosis - Antiphospholipid syndrome, thrombophilia

Question 206

Risk factors for stroke?

Answer 206

``` Hypertension!!! Smoking DM Increased lipids FH Cardiac: AF, valve disease Peripheral vascular disease Previous histroy Ethnicity: Increased in blacks and asians Increased PCV/Hct OCP ```

Question 207

Investigations for HTN induced stroke?

Answer 207

retinopathy nephropathy Big heart of CXR

Question 208

Investigations for cardiac emboli

Answer 208

- ECG± 24hr tape: AF - Echo: mural thrombus, - hypokinesis, valve lesions, ASD, VSD (paradoxical emboli)

Question 209

Investigations for carotid artery stenosis?

Answer 209

Doppler US ± Angio | Endarterectomy beneficial if >70% symptomatic stenosis

Question 210

Bleeding and thrombotic tendency investigations?

Answer 210

'Young' Stroke blood test include thrombophilia and autoimmune screening - performed in those under 55 - ANA, APL, ACL, Lupus anticoagulant, coagulation factors, ESR, homocysteine, syphilis. Thrombophilia screen Autoimmune Thrombocytopenia

Question 211

What is the classification of Stroke?

Answer 211

Oxford/Bamford Classification - Based on clinical localisation of infarct S = Syndrome: prior to imaging I = Infarct: after imaging when atheroembolic infarct confirmed

Question 212

In the Oxford/Bamford classification - what is a TACS?

Answer 212

Total Anterior Circulation Stroke (TACS) - Highest mortality + poor independence - Large infarct in carotid/MCa, ACA territory. Has all 3 of 1) Hemiparesis (contralateral) and or sensory deficit (>2 of face, arm and leg) 2) Homonyzmous hemianopia (contralateral) 3) Higher cortical dysfunction (dysphagia) - Dominant (L usually) dysphasia - Non-dominant: hemispatial neglect

Question 213

In the Oxford/Bamford classification - what is a PACS?

Answer 213

Partial Anterior Circulation Stroke (PACS) - Carotid, MCA and ACA territory. Smaller arteries of anterior circulation (upper/lower division of middle cerebral artery) - 2/3 TACS criteria, usually: 1) Hemiparesis (contralateral) and/or sensory deficit (>2 of face, arm and leg) 2) Higher cortical dysfunction - Dominant: dysphasia - Non-dom: neglect, constructional apraxia Deficit is less dense or incomplete.

Question 214

In the Oxford/Bamford classification - what is a Posterior Circulation Stroke?

Answer 214

- Infarct in the vertebrobasilar territory? - Any of 1. Cerebellar syndrome 2. Brainstem syndrome 3. Contralateral homonymous hemianopia (to the damage). Therefore homonymous hemianopia is on the same side as the paresis. Lesion in the superior cerebellar artery, PICA or AICA. Presetns with vertical nystagmus, and ataxia.

Question 215

In the Oxford/Bamford classification - what is a LACS (lacunar infarct stroke)

Answer 215

Presents with - 1. Unilateral weakness of face and arm, arm and leg or all three 2. pure sensory stroke 3. ataxic hemiparesis ``` Small infarct around the basal ganglia, internal capsule, thalamus and pons. - Absence of Higher cortical dysfunction Homonymous hemianopia Drowsiness Brainstem signs ```

Question 216

What are the 5 syndromes of a LACS?

Answer 216

- Pure motor: Post. limb of internal capsule (commonest) - Pure sensory: Posterior thalamus (VPL) - Mix sensorimotor: internal capsule - Dysarthria/clumsy hand - Ataxic hemiparesis: ant. limb of internal capsule - weakness + dysmetria

Question 217

Other signs of ischaemic stroke?

Answer 217

Carotid bruit AF Past TIA IHD

Question 218

Other signs of haemorrhagic stroke?

Answer 218

Meningism Severe headache Coma

Question 219

Brainstem infarcts - what are the signs for a corticospinal tract damage?

Answer 219

Hemi/quadrparesis

Question 220

Brainstem infarcts - what are the signs for oculomotor system damage

Answer 220

Conjugate gaze palsy (difficulty in moving eyes in the same direction)

Question 221

Brainstem infarcts - what are the signs for a Sympathetic fibres?

Answer 221

Horner's

Question 222

Brainstem infarcts - what are the signs for a CN7 infarct?

Answer 222

Facial weakness

Question 223

Brainstem infarcts - what are the signs for a CN8 infarct?

Answer 223

Nystagmus, Vertigo

Question 224

Brainstem infarcts - what are the signs for CN 9 and 10 infarct?

Answer 224

Dysphagia, dysarthria

Question 225

Brainstem infarcts - what are the signs for cerebellar damage?

Answer 225

Dysarthria, ataxia

Question 226

What is the acute management of a stroke? Step 1 = Resuscitate

Answer 226

Assessment - ROSIER. Exclude hypoglycaemia. LOC = -1 Seizure activity = -1 New acute onset - Asymmetric facial weakness - Asymmetric arm weakness - Asymmetric leg weakness - Speech disturbance - Visual field defect Investigations = Non-contrast CT head scan is first line. ABCDE Ensure patent airway: consider NGT NBM until swallowing assessment by SALT Don't overhydrate: risk of cerebral oedema

Question 227

What is the acute management of a stroke? Step 2 = Monitor

Answer 227

- Glucose: 4-11mM: sliding scale if DM - BP: <185/110 (for thrombolysis) - Rx of HTN can --> decreased cerebral perfusion - Neuro obs

Question 228

What is the acute management of a stroke? Imaging Step 3

Answer 228

Urgent CT/MRI Diffusion-weight MRI is most sensitive for acute infarct. T2 weighted CT will exclude primary haemorrhage (contraindicatons = seizure at onset of stroke, cancer, GI haemorrhage, active bleeding, pregnancy, oesophageal varicies, uncontrolled HTN >200) ``` Carotid Dopplers (>70% stenosis) - don't treat it because it's done. ECG and ECho ``` 24hr tape to identify AF.

Question 229

What is the acute management of a stroke? Step 4 = Medical Management

Answer 229

- Consider thrombolysis if 18-80 yr and <4.5hr since onset of symptoms - Alteplase (tPA) Thrombectomy - pre-stroke status of <3 on Rankin scale. >5 on NIHSS. OFfer thrombectomy within 6hrs + IV thrombolysis IF acute ischaemic stroke + occlusion of the proximal anterior circulation on CTA. Offer thrombectomy ASAP between 6-24hr if confirmed occlusion of proximal anterior circulation and if there is a potential to salvage brain tissue shown on DW MRI. Consider thrombectomy + IV thrombolysis as soon as possible for people last known to be well up to 24hrs. + CT 24hr post-thromboylsis to look for haemorrhage + ASAP Aspirin 24hr (300mg) once haemorrhagic stroke excluded ± PPI. If outside of the window give aspirin (Clopi is a more chronic drug). Clopidogrel if aspirin sensitive. VTE prophylaxis - heparin 5000 units every 12hrs.

Question 230

What is the acute management of a stroke? Step 5 = Neurosurgical opinion if intracranial haemorrhage

Answer 230

May coil bleeding aneurysm Decompressive hemicraniectomy for some forms of MCA infarction. Stroke Unit - Specialist nursing and physio - Early mobilisation - DVT prophylaxis Secondary prevention Rehab

Question 231

What is the primary prevention management of stroke?

Answer 231

- Control RFs: HTN, increased lipids, DM, smoking, cardiac disease. Consider statin is cholesterol >3.5. - Consider life-long anticoagulation in AF (use CHADS2) - Carotid endarterectomy if symptomatic 70% stenosis - Exercise

Question 232

What is the secondary prevention management of stroke?

Answer 232

Risk factor control as above - Start on a statin - Aspirin/Clopi 300mg for 2 weeks after stroke then either - Clopi 75 OD (preferred) - Aspirin 75mg OD Warfarin instead of aspirin/clopi if Cardioembolic stroke or chronic AF - Starts 2 weeks post-stroke (INR 2-3) - Don't use aspirin and warfarin together. Switch to NOAC. Carotid endarterecotmy if good recovery + ipsilateral stenosis >70%

Question 233

What is the rehabilitation for stroke patients?

Answer 233

MDT: Physio, SALT, Dietician, OT, specialist nurses, neurologist, family Eating - Screen swallowing: refer to specialist (consider PEG/NG) - Screen for malnutrition Neurorehab: physio and speech therapy (Botulinum can help) DVT prophylaxis Sores must be avoided. Occupational therapy - Impairment - Disability - Handicap Chronic Risk management - AF start anticoagulation 10-14 days after stroke - HTN - Diabetes - Smoking Carotid artery stenosis> Don't forget carotid dopplers in investigations.

Question 234

What is a TIA?

Answer 234

- Sudden onset focal neurology lasting <24hr due to temporary occlusion of part of the cerebral circulation ~15% of 1st strokes are preceded by a TIA.

Question 235

Symptoms of TIA?

Answer 235

- Symptoms usually brief - Global events (syncope, dizziness) are not typical - Signs mimic those of CVA in the same arterial territory

Question 236

Signs of Causes of TIA?

Answer 236

- Carotid bruits - Increased BP - Heart murmur - AF

Question 237

Causes of TIA?

Answer 237

Atherothromboembolism from carotids is main cause Cardioembolism: post-MI, AF, Valve disease Hyperviscosity: poylcythaemia, SCD, myeloma

Question 238

Differentials for a TIA

Answer 238

Vascular: CVA, migraine, GCA Epilepsy Hyperventilation Hypoglycaemia

Question 239

Investigations for a TIA?

Answer 239

``` Blood glucose: <3.3 = hypo U+E - Na, K, High Ca FBC: usually normal ECG: look for AF CXR Carotid doppler ± angiography Consider diffusion weight MRI ```

Question 240

Management of TIA - Antiplatelet?

Answer 240

In last 7 days = Make urgent assessment within 24hrs by stroke physician. More than a week = refer to specialist assessment as soon as possible within 7 days. Time to intervention is crucial - Avoid driving for 1 month ACAS - Antiplatelet therapy = Aspirin/clopi 300mg/d for 2 weeks then 75mg/d Add dipyridamole MR to aspirin - Warfarin if cardiac emboli: AF, MI, MS After 2 weeks The Royal College of Physicians have published National Clinical Guidelines for Stroke that recommend Carotid endarterectomy for carotid stenosis 50-99% by NASCET criteria, for patients with TIA. The most appropriate initial treatment would therefore be antiplatelet therapy, and a statin would also be indicated. The National Stroke Guidelines suggest patients with suspected TIA who are at high risk of stroke (e.g. an ABCD2 score of 4 or above) should receive aspirin or clopidogrel (each as a 300 mg loading dose and 75 mg thereafter) and a statin, e.g. simvastatin 40 mg started immediately after specialist assessment and investigation within 24 hours of onset of symptoms. Therefore she could be given either aspirin or clopidogrel 300mg (as a one-off dose) then to continue on either aspirin or clopidogrel long-term. Give clopidogrel as first line (aspirin acutely), then aspirin and dipyridamole for patients who cannot tolerate clopidogrel. Give it lifelong. Don't give aspirin if patient has bleeding disorder, taking an anticoagulant, patient is already taking low-dose aspirin regularly. Aspirin is contraindicated. A single TIA patients can start driving if symptom free for 1 month and there is no need for them to inform the DVLA. If multiple TIA 3 months off driving and inform DVLA.

Question 241

Management TIA - Cardiac Risk factor control

Answer 241

BP, lipids, DM Smoking Exercise Diet: decreased salt

Question 242

Management TIA - Assess risk of subsequent stroke

Answer 242

ABCD2

Question 243

Specialist referral to TIA clinic in how long if ABCD >4?

Answer 243

Within 24hr

Question 244

Specialist referral to TIA clinic in how long if ABCD <4?

Answer 244

Within 1 week

Question 245

What does ABCD2 Score stand for?

Answer 245

- Age >60 - BP >140/90 - Clinical Features 1. Unilateral weakness (2 points) 2. Speech distubances w/o weakness - Duration >1hr = 2 points 10-59 mins - DM NB: 7 points max

Question 246

What is a subdural haemorrhage?

Answer 246

- Bleeding from bridging veins between cortex and sinuses - Haematoma between dura and arachnoid - Often due to minor trauma that occured a long time previously - especially deceleration injuries. Acute subdural - Collection of fresh blood within the subdural space and is most commonly caused by high-impact trauma. - CT shows cresentic collection, not limited by suture lines. Appear hyperdense in comparison to brain. Chronic subdural haematoma - Collection of blood in the subdural space that has been present for weeks to months. - Elderly and alcoholic patients are particularly at risk. Taught bridging veins.

Question 247

Risk factors for a subdural haemorrhage?

Answer 247

Elderly: brain atrophy Falls: Epileptics, alcoholics Anticoagulation

Question 248

Symptoms for subdural haemorrhage?

Answer 248

- Headache - Fluctuating GCS, sleepiness that can last for days. - Nausea/Vomiting - Gradual physical or mental slowing - Unsteadiness SUBDURAL cannot cause meningeal irritation.

Question 249

Signs for a subdural haemorrhage?

Answer 249

- Increased ICP (can lead to tentorial herniation) | - Localising signs occur late

Question 250

Imaging for a subdural haemorrhage?

Answer 250

CT-non contrast. Convexity - Crescentic haematoma over one hemisphere - Clot goes from white --> Grey over time (hyperdense to hypodense) - Mid-line shift - Does not respect the suture lines.

Question 251

What is the management of a subdural haemorrhage?

Answer 251

Try ICP lowering techniques = bed to 30 degrees - reverse Trendelenberg. Hyperosmolar with hypertonic saline? Osmotic diuretics mannitol. 1st line: irrigation/evacuation via burr-hole craniostomy. Two holes made, clot is irrigated using saline. 2nd line: craniotomy/hemicraniectomy + duraplasty. Address causes of trauma

Question 252

Differential for Subdural haemorrhage?

Answer 252

Stroke Dementia SOL

Question 253

Extradural Haemorrhage? What is it?

Answer 253

- Often due to fracture of the temporal or parietal bone --> - Laceration of the middle meningeal artery and vein. - Blood between bone and dura. - Suspect if after head injury GCS falls, is slow to improve or there is a lucid interval.

Question 254

Presentation of an extradural haemorrhage?

Answer 254

Lucid Interval! - Deterioration of GCSe after head injury that caused no LOC, or following initial improvement in GCS - Lucid Interval may be hrs or days. ICP increased: - Headache - Vomiting - Confusion --> coma - Fits - Ipsilateral blown pupil (3rd nerve palsy) - ± hemiparesis with upgoing plantars and increased reflexes. Brainstem Compression - Deep irregular breathing (brainstem compression) - Cushing response in response to increased IC Pressure. - increased BP - brain meets perfusion needs by increasing BP. - decreased HR is late. - Irregular breathing (Cheyne Stokes) - Death by cardioresp arrest.

Question 255

What imaging do you use for a extradural haematoma?

Answer 255

CT - will see a lens-shaped haematoma. Skull # (increased risk of extradural haemorrhage). - Limited by suture lines

Question 256

Management of extradural haemorrhage?

Answer 256

- Neuroprotective ventilation (O2 >100, CO2 35-40) - Consider mannitol (1g/kg IV via central line) - Craniectomy for clot evacuation and vessel ligation

Question 257

Dural venous sinus thrombosis - when do symptoms generally come on?

Answer 257

Gradually over days/weeks. Sinus thrombosis may extended to cortical veins. Thrombus formation within the cavernous sinus.

Question 258

Sagittal sinus Intracranial venous thrombosis?

Answer 258

- 45% of IVT - Often co-exists if other sinuses are thrombosed - Headache, vomiting, seizures, decreased vision, papilloedema. - Cushing's reflex

Question 259

Transverse sinus - Intracranial venous thrombosis?

Answer 259

- 35% of IVT | - Headache + mastoid pain, focal neuro, seizures, papilloedema.

Question 260

Sigmoid sinus - intracranial venous thrombosis?

Answer 260

Cerebellar signs, lower CN palsy

Question 261

Inferior Petrosal sinus?

Answer 261

5-6th nerve palsies (Gradenigo's syndrome?)

Question 262

Cavernous sinus syndrome

Answer 262

- Spread from facial pustules or folliculitis - Headache, chemosis, eyelid oedema, proptosis, painful ophthalmoplegia, fever. - Mostly caused cavernous sinus such as a nasopharyngeal malignancy. Lateral wall components - Oculomotor nerve - Trochlear nerve - Ophthalmic nerve - Maxillary nerve

Question 263

Cortical Vein thrombosis?

Answer 263

Often --> venous infarcts with stroke-like focal symptoms that evolve over days Thunderclap headache Focal-seizures

Question 264

Differential for intracranial venous thrombosis ?

Answer 264

``` SAH Meningitis Encephalitis Intracranial abscess Arterial Stroke ```

Question 265

What are the common causes of IVT?

Answer 265

``` Pregnancy/puerperium OCP Head injury Dehydration Intracranial/extracranial malignancy Thrombophilia ```

Question 266

Investigations for IVT?

Answer 266

- Exclude SAH and meningitis - CT/MRI venography: Absence of a sinus/Contrast CT may show an enlarged sinus. LP: increased pressure, may show RBCs and xanthochromia?

Question 267

Management of IVT?

Answer 267

- LMWH --> warfarin (INR 2-3). - Fibrinolytic (streptokinase) can be used via selective catheterisation - Thrombophilia screen

Question 268

What are the meningitic features?

Answer 268

Meningitic - Headache - Neck Stiffness Kernig's: Straightening leg with hip @ 90 Brudzinski's: lifting head --> Lifting of legs - Photophobia - N/V

Question 269

What are the neurological features of meningitis?

Answer 269

Decreased GCS --> Coma Seizures (20%) Focal neuro (20% ): E.g CN palsies

Question 270

What are the septic features of meningitis?

Answer 270

``` Fever Decreased BP, increased HR Increased CRT Purpuric rash DIC ```

Question 271

Causes of Meningitis?

Answer 271

- Neisseria meningitidis (gram negative diplococci) - Strep Pneumo (gram positive diplococci) = 6-60yrs. Listeria Monocytogenes (gram positive rod) Haemophilus influenza (gram negative coccobacilli) Group B strep TB Cryptococcus Virus: Enterovirus (Coxsackie, echovirus), HSV2 0-3 months = GBS, E.coli, Listeria 3months - 6 yrs = Neisseria, Strep pneumonia, Haemophilus 6 yrs - 60 yrs = Neisseria meningitidis, Strep Pneumonia >60 = Strep pneumonia, neisseria meningitidis, listeria monocytogenes.

Question 272

Investigations for meningitis?

Answer 272

LP: MCS, glucose, virology/PCR, lactate/Gram stain. Bloods: FBC, U+E, Clotting, Glucose, ABG BLood cultures

Question 273

Abx Management of meningitis?

Answer 273

Community: benpen 1.2g IV/IM <50: ceftriaxone/cefotaxime 2g IV/IM BD + vancomycin >50: cetriaxone/cefotaxime + ampicillin (cover listeria) If viral suspected: aciclovir.

Question 274

What is the acute management of meningitis?

Answer 274

ABC - O2 15L - SpO2 94-98% - IVI fluid resus with crystalloid If mainly septicaemic - Don't attempt LP - Ceftriaxone 2g IVI - Consider ITU if shocked. If mainly meningitic - If no shock or CIs do LP - Dexamethasone 0.15mg/kg IV QDS - Ceftriaxone 2g IVI post-LP For TB treat for 12 months.

Question 275

What is the continuing management of meningitis?

Answer 275

Ceftriaxone 2g BD IVI - Meningococcus: 7d IV then review - Pneumococcus: 14 d IV then review Maintenance fluids - UO 30ml/h - SBP >80mm Hg Rifampicin prophylaxis for household contacts If response poor, consider !± inotropic support.

Question 276

CIs to LPs: Try LP Unless contraindicated

Answer 276

- Thrombocytopenia - Pressure (signs of raised ICP) - Unstable (Cardio+ resp systems) - Coagulation disorder - Infection at LP site - Neurology (focal neurological signs)

Question 277

Encephalitis presentation?

Answer 277

- Infectious prodrome: fever, rash, LNs, cold sores, conjunctivitis, meningeal signs. - Bizarre behaviour or personality change - Confusion - Decreased GCS --> coma - Fever - Headache - Focal neuro - Seizures - Hx of travel or animal bite

Question 278

Viral Causes of encephalitis?

Answer 278

Usually viral - HSV 1/2 - CMV, EBV, VZV - Arbovirusues - HIV

Question 279

What are the bacterial causes of encephalitis?

Answer 279

Same as meningitis (Strep Pneumo, Neisseria Meningitides, Haemophilus Infuenza, GBS TB Malaria Lyme Disease

Question 280

Investigations of encephalitis?

Answer 280

- Blood: Cultures, viral PCR, malaria film, U+E (rickettsial), LFTs (coxiella, burnetii, rickettsia, tick-borne disase, cytomegalovirus) - Contrast CT: focal bilateral temporal involvement suggests HSV - LP: increased CSF protein, lymphocytes, PCR - EEG: shows diffuse abnormalities, may confirm ddx

Question 281

Management of encephalitis?

Answer 281

- Aciclovir STAT: 10mg.kg/8h IVI over 1h for 14/7. - Supportive measures in HDU/ITU - Phenytoin for seizures If CMV = ganciclovir EBV = aciclovir, ganciclovir, cidofovir

Question 282

Without fever consider encephalopathy due to -

Answer 282

``` hypoglycemia Hepatic DKA Drugs SLE Uraemia Hypoxic brain injury Beri-Beri ```

Question 283

What is a cerebral abscess and what factors predispose to it?

Answer 283

Suppurative collection of microbes within a gliotic capsule occuring within the brain parenchyma. ``` Infection: ear, sinus, dental or peridontal Skull fracture Congenital heart disease Endocarditis Bronchiectasis Immunosuppression ```

Question 284

What organisms cause a cerebral abscess?

Answer 284

- Frontal sinus/teeth: Streptocuccus pyogenes, Strep Milleri, Staph A, oropharyngal anaerobes - Ear: Bacteriodes, other anaerobes

Question 285

Signs for cerebral abscess?

Answer 285

``` Seizures Fever Localising signs Signs of ICP Signs of infection elsewhere ``` Common complication of sinusitis = unilateral facial oedema, photophobia, proptosis, palsies of the cranial nerves which pass through it.

Question 286

Investigations of Cerebral abscess?

Answer 286

CT/MRI: ring-enhancing lesion | Increased WCC, increaseD ESR

Question 287

Management of Cerebral Abscess?

Answer 287

Neurosurgical referral Abx: e.g ceftriaxone Treat increased ICP.

Question 288

What is the definition of epilepsy?

Answer 288

Recurrent tendency to spontaneous, intermittent, abnormal electrical activity in part of the brain, manifest as seizure.

Question 289

What are the causes of epilepsy/ Seizures?

Answer 289

2/3 are idiopathic - 2/3. Mutations in the sodium/potassium channels. Congenital - NF - Tuberous Sclerosis - TORCH - Perinatal anoxia Acquired - Vascular: CVA - Cortical scarring: trauma, infection. - SOL - Other: SLE, PAN, MS, sarcoidosis Non-epileptic/provoked seizures? - Withdrawal: ETOH, opiates, benzos - Metabolic: glucose, Na, Ca, Urea, NH3 - increased ICP: trauma, haemorrhage, encephalitis, cycticerosis, HIV - Eclampsia - Pseudoseizures (pelvic thrusting, family member with epilepsy, common in females, crying after seizure, don't occur when alone, gradual onset). Phenomenon that can mimic true seizures but generally have findings which are not consistent with a seizure. The ability to control location of symptoms is very typical of pseudoseizures and does not fit with any other option.

Question 290

What is a seizure prodrome?

Answer 290

- Prodrome: Pt or others may notice change in mood or behaviour lasting hrs-days. - Not part of seizures.

Question 291

What is a seizure aura?

Answer 291

A simple partial seizure (usually temporal) which may precede other manifestations - Experienced as strange feeling: - Epigastric rising - Deja/jamais vu - Automatism - Smells, lights, sounds

Question 292

What is a partial (focal) seizure?

Answer 292

Isolated to one hemisphere

Question 293

What is a primary generalised seizure?

Answer 293

No warning/aura | Discharge is seen through the cortex and no ascertainable localising features.

Question 294

What is a simple seizure?

Answer 294

Awareness is unimpaired

Question 295

What is a complex seizure

Answer 295

Awareness is impaired

Question 296

What is a secondary generalised seizure?

Answer 296

Focal seizure moving to generalised | Such as an aura moving towards a tonic clonic.

Question 297

What are the diagnostic pointers to epilepsy?

Answer 297

- Aura - Specific trigger e.g flashing lights - Lateral tongue biting (>incontinence) - Typical movements e.g tonic-clonic - Cyanosis - Post-ictal phase

Question 298

What are the presenting features associated with epilepsy? / Types of epilepsy?

Answer 298

``` Simple partial Complex partial Absence (petit mal) Tonic-Clonic Myoclonic seizure Atonic West Syndrome/Infantile spasms ```

Question 299

What is a simple partial seizure?

Answer 299

Focal motor, sensory, autonomic or psychic symptoms. Can present with 2 mins of involuntary twitching movements in their right hand. - Stereotyped movements and quick recovery is consistent with focal aware seizure.

Question 300

What is a complex partial seizure/Focal seizures with impaired awareness.

Answer 300

5As Aura Autonomic: change in skin colour, temperature, palpitations Awareness loss: Motor arrest, motionless stare. Automatisms: lip smacking, fumbling, chewing, swallowing Amnesia Usually arise from temporal lobe. Emotional disturbance and automatism are features of focal seizures.

Question 301

What is an absence seizure?

Answer 301

``` Abrupt onset and offset Short: <10s Eyes: glazed, blank-stare Normal: intelligence, examination, brain-scan Clonus or automatisms may occur EEG: 3Hz spike and wave ``` Stimulated by hyperventilation and photics. Doesnt involve motor aspects.

Question 302

What is a tonic-clonic seizure (Grand Mal)

Answer 302

- LOC - Tonic: limbs stiffen - Clonic: rhythmic jerking of limbs ± cyanosis, incontinence, - tongue biting - Post-ictal confusion and drowsiness. Normally lasts a while.

Question 303

What is a myoclonic seizure?

Answer 303

Sudden jerk of limb, face or trunk

Question 304

what is a atonic seizure?

Answer 304

Sudden loss of muscle tone -- fall | No LOC

Question 305

What is West Syndrome?

Answer 305

Clusters of head nodding and arm jerks | EEG shows hysarrhythrimia

Question 306

What are the localising features of epilepsy? Temporal lobe?

Answer 306

Temporal - Automatisms: lip smacking, chewing, fumbling - Deja vu - Delusional behaviour - Abdominal; rising or n/v - Emotional disturbance: terror, panic, anger, elation - Tastes, smell

Question 307

What are the localising symptoms of frontal lobe epilepsy?

Answer 307

Frontal - Motor features: arrest, Jacksonian march) is a phenomenon where a simple partial seizure spreads from the distal part of the limb toward the ipsilateral face , - Todd's palsy (weakness if part of the body after a seizure). One part of the body after means Todd's Paresis. - Head/leg movement

Question 308

What are the parietal symptoms of epilepsy?

Answer 308

Sensory disturbance: tingling, numbness

Question 309

What are the occipital features of epilepsy?

Answer 309

Visual phenomena: spots, lines, flashes.

Question 310

What are the general management principles for epilepsy?

Answer 310

- After any seizure advise against driving, swimming etc until a Dx is established. - Following first seizure, patients must be seizure free for 6 months before they may reapply to the DVLA for their license to be reissued. - Formal diagnosis means seizure free for 12 months before they apply to DVLA. - For bus drivers - if 2 seizures must be seizure free for 10 yrs. - Don't diagnose epilepsy from a single seizure - Diagnosis should be made by a specialist - After Dx, cannot drive until seizure-free for ?1yr 10yr for HGV (no meds)

Question 311

What are the investigations for epilepsy?

Answer 311

Top investigations - EEG - Used to support Dx (cannot exclude or prove) - helps classification and prognosis (may show a generalised epileptiform activity or focal, localising abnormality). - Use with hyperventilation and photic stimulation Other investigations - FBC, U+E, glucose - Se increased prolactin 10mins after fit (relative to baseline) - indicated a GTCS. - Se AED levels - Urine toxicology - ECG

Question 312

What imaging is used for epilepsy?

Answer 312

- Consider CT head for structural lesions or other process that have caused the seizure. - MRI not routine for idiopathic generalised epilepsy - Indications = Developed epilepsy as an adult or any evidence of focal onset -Seizures continue despite 1st line Rx.

Question 313

What is the management of a tonic-clonic seizure?

Answer 313

1st: Valproate (should not be prescribed to female children or aolescents). 2nd: Lamotrigine, carbamazepine

Question 314

What is the management of an absence seizure?

Answer 314

1st: Valproate/Ethosuximide 2nd: Lamotrigine

Question 315

What is the management of tonic, atonic or myoclonic seizure?

Answer 315

1st: Valproate 2nd: Levetiracetam

Question 316

What is the management of focal ± 2nd gen?

Answer 316

1st: Lamotrigine/Carbamazepine 2nd: Levetiracetam, sodium valproate, oxcarbazepine.

Question 317

What epilepsy drugs should be avoided in pregnancy?

Answer 317

Avoid valproate: take lamotrigine or CBZ. - Ensure you give 5mg folic acid daily if child-bearing age. - CBZ and PHE are enzyme inducers and decrease the effectiveness of the OCP.

Question 318

What other management is there of epilepsy?

Answer 318

Following a first seizure, antiepileptic drug treatment should only be started before specialist review in exceptional circumstances. Only start medication if: 1. Seizure activity observed on EEG 2. Presence of a neurological deficit 3. Presence of a structural brain abnormality 4. Patient, parent or carer considers the risk of a further seizure to be unacceptable - Neurosurgical resection can be an option if single epileptogenic focus is identified - Vagal nerve stimulation can decreased seizure frequency and severity in ~33%. Driving - patients must contact the DVLA - Can drive again after one year of being seizures-free - If a patient has only had a single seizure: Six months if investigations normal. Contraception Pregnancy: valproate. Women considering should take regular folate Safety measures - patients should not bathe or swim

Question 319

Which epilepsy drugs are enzyme inducers?

Answer 319

Carbamazepine Phenytoin Barbiturates

Question 320

Which epilepsy drugs are enzyme inhibitors?

Answer 320

Valproate

Question 321

What are the side-effects of lamotrigine?

Answer 321

- Skin rash --> SJS occurs within 8 weeks. Prodromal illness which resembles a viral URTI. Rapid onset of a painful red skin rash which starts on the trunks and extends abruptly onto the face and limbs. Does not affect scalp, palms or soles. Fluid replacement. - Rash may be associated with hypersensitivity --> fever, increased LFTs and DIC. - Diplopia, blurred vision - Levels affected by enzyme inhibitors/inducers

Question 322

What are the side-effects of valproate?

Answer 322

VALPROATE ``` Vomiting. Alopecia. Liver toxicity. Pancreatitis/ Pancytopenia. Retention of fats (weight gain) Oedema (peripheral) Anorexia. Tremor Enzyme Inhibitor ```

Question 323

What are the side-effects of carbamazepine?

Answer 323

Leukopenia Skin reactions Diplopia, blurred vision SIADH --> hyponatraemia

Question 324

What are the side effects of phenytoin?

Answer 324

``` PHENYTOIN: P: P-450 interactions H: Hirsutism E: Enlarged gums N: Nystagmus Y: Yellow-browning of skin T: Teratogenicity O: Osteomalacia I: Interference with folic acid absorption (hence anemia) N: Neuropathies: vertigo, ataxia, headache ``` Trough levels, immediately before dose should be checked if - adjustment of phenytoin dose - Suspected toxicity - Detection of non-adherence to prescribed medication.

Question 325

What is Status epilepticus?

Answer 325

Generalised convulsive and non-convulsive status epilepticus are neurological and medical emergencies defined as 5 or more minutes of either continuous seizure activity or repetitive seizures with no intervening recovery of consciousness.

Question 326

Investigations of Status epilepticus?

Answer 326

BM Bloods: Glucose, ABG, U+E, FBC, Ca2+ ECG, EEG Consider: AED levels, tox screen, LP, B-HCG, CT. Rule out hypoxia and hypoglycaemia before thinking of other causes. Use the ABCDE approach.

Question 327

What drugs are used in status epilepticus?

Answer 327

``` Lorazepam - 2-4mg IV bolus over 30s - 2nd dose if no response within 2 mins - Alternatives Diazepam 10mg IV/PR (2mg max) Midazolam 10mg buccal ``` If the following does not help - May need phenytoin - 20mg/kg IVI @ 50mg/min - 100mg/6-8hr maintenance - Monitor ECG and BP - CI: bradycardia or heart block

Question 328

Acute management of status epilepticus?

Answer 328

Airway - Oral/nasal airway, intubate/ Suction Breathing: 100% oxygen Check capillary glucose. Gain IV access and take bloods - U+E, LFTs, FBC, Glucose, Ca2+ - AED levels - Tox screen Reverse potential causes - Thiamine 250mg IV if ETOH - 100ml 20% glucose unless glucose known to be normal Then start slow IV bolus phase - Lorazepam IV - IM Midazolam/ Buccal (10mg) - Rectal Diazepam (10mg) Second dose if no response within 2 mins Then - Phenytoin 18mg/kg IV (then 100mg/6-8hr) - Diazepam 100mg in 500ml 5% dex IVI - Phenobarbital if already on regular phenytoin. Remember to use cardiac monitoring when using phenytoin. RSI phase - Rapid sequence induction of anaesthesia. - never spend >20 mins with someone in status w/o getting an anaesthetist. - Propofol/thiopental

Question 329

What is the initial management of a head injury? in the primary survey ?

Answer 329

Primary survey - A: Intubation, immobilisation, C-spine - B: 100% O2, RR - C: IV access, BP, HR - D: GCS, pupils If patient has a GCS less than 8, need immediate review by anaesthetist due to risk of unsecure airway. Treat seizures Lorazepam 2-4mg IV Phenytoin 18mg/kg IVI then 100mg/6-8hr. E: exposure patient and look for other obvious injuries

Question 330

What is the secondary survey management of a patient with head injury?

Answer 330

``` Look for: Lacerations - Obvious facial/skull deformity - CSF leak from nose or eats - Battle's sign, Racoon eyes - Blood behind TM - C-spine tenderness ± deformities ``` To test for CSF - check glucose. Gold standard for CSF is Beta-2-transferrin. Head-to-toe examination for other injuries Fundoscopy Log roll

Question 331

What do you ask in a history of head injury?

Answer 331

How + when GCS and other vitals immediately after injury Headache, fits, vomiting, amnesia, ETOH.

Question 332

Investigations for head injury?

Answer 332

Bloods: FBC (for required blood products) , U+E, glucose, clotting (coagulopathy) , ETOH, ABG (if not breathing), CT head + c-spine. Non-contrast CT - to detect midline shift, subarachnoid haemorrhage. MRI if not clear - immediate CT indicated in all patients with TBI.

Question 333

Management of head injury?

Answer 333

- Neurosurgical opinion if signs of increased ICP, CT evidence of intracranial bleed significant skull #. Admit if - Abnormalities on imaging - Difficulty to assess: ETOH, post-ictal - Not returned to GCS 15 after imaging - CNS signs: vomiting, severe headache Neuro-obs half-hrly until GCS 15 - GCS - Pupils - HR/BP - RR/SpO2 - Temperature

Question 334

What discharge advice do you give someone with a head injury?

Answer 334

``` - Stay with someone for first 48hr Give advice card advising to return on: - Confusion, drowsiness, unconsciousness - Visual problems - Weakness - Deafness - V.painful headache that won't go away - Vomiting - Fit ```

Question 335

When do you intubate someone with a head injury?

Answer 335

- GCS <8 - PaO2 <9kPA on air/ <13 kPA on O2 or PCOs >6 - Spontaneous hyperventilation: PCO2 <4kPa - Respiratory irregularity

Question 336

CT head guidelines for head injury?

Answer 336

CT immediately ``` Break: Open, depressed or base of skull Amnesia >30 mins retrograde Neuro deficit or seizure GCS: <13 @ any time or <15 2hr after injury Sickness: vomited > once ``` Within 8hrs. LOC or any amnesia and any of: - Dangerous mechanism: RTA, great height - Age >65 - Coagulopathy (inc warfarin).

Question 337

Risk of intracranial haematoma in adults?

Answer 337

Fully conscious with no fracture = <1:1000 | Confused with skull fracture = 1:4

Question 338

GCS score for eyes?

Answer 338

Out of 4 ``` Eyes: 4 4 – Spontaneous eye opening 3 – Open to voice 2 – Open to pain 1 – No opening ```

Question 339

GCS score for verbal?

Answer 339

Out of 5 ``` Verbal: 5 5 – Orientated conversation 4 – Confused conversation 3 – Inappropriate speech 2 – Incomprehensible sounds 1 – No speech ```

Question 340

GCS score for motor?

Answer 340

Motor: 6 6 – Obeys commands 5 – Localises pain 4 – Withdraws to pain 3 – Decorticate posturing to pain (flexor) 2 – Decerebrate posturing to pain (extensor) 1 – No movement

Question 341

What is the presentation of a space occupying lesion?

Answer 341

Increased ICP - Headache: worse on walking, lying down, bending forward, coughing, straining - Vomiting - Papilloedema - decreased GCS Seizure - Exclude SOL in adult-onset seizures, especially with localising aura or post-ictal weakness (Todd's). Evolving focal neurology - May be false-localising (esp. CN6 palsy) Subtle personality change

Question 342

What are the causes of SOL?

Answer 342

- Vascular: chronic subdural haematoma, AVM, Aneurysm - Infection: abscess, cyst (cysticercosis) - Neoplasm: primary or secondary - Granuloma: TB, sarcoid

Question 343

What types of tumour cause SOL?

Answer 343

30% are metastatic: breast, lung, melanoma, colorectal. AStrocytoma Glioblastoma multiforme - Glioblastoma is the most common primary tumour in adults and is associated with a poor prognosis (~ 1yr). * On imaging they are solid tumours with central necrosis and a rim that enhances with contrast. Disruption of the blood-brain barrier and therefore are associated with vasogenic oedema. * Histology: Pleomorphic tumour cells border necrotic areas * Treatment is surgical with postoperative chemotherapy and/or radiotherapy. Dexamethasone is used to treat the oedema. - Ependymoma * Commonly seen in the 4th ventricle * May cause hydrocephalus * Histology: perivascular pseudorosettes Meningioma The second most common primary brain tumour in adults * Meningiomas are typically benign, extrinsic tumours of the central nervous system. They arise from the dura mater of the meninges and cause symptoms by compression rather than invasion. * They typically are located at the falx cerebri, superior sagittal sinus, convexity or skull base. * Histology: Spindle cells in concentric whorls and calcified psammoma bodies * Investigation is with CT (will show contrast enhancement) and MRI, and treatment will involve either observation, radiotherapy or surgical resection. Cerebellar haemangioblastoma Vascular tumour of the cerebellum • Associated with von Hippel-Lindau syndrome • Histology: foam cells and high vascularity CNS lymphoma

Question 344

Investigations for SOL?

Answer 344

- CT or MRI (for better post.cranial fossa) | - Consider biopsy

Question 345

What is idiopathic intracranial HTN?

Answer 345

- A syndrome of reduced cerebrospinal fluid absorption Risk factors = Obesity, female, pregnancy, drugs (OCP, steroids, tetracycline, Vit A, Lithium).

Question 346

Presentation of idiopathic intracranial hypertension?

Answer 346

``` Typically obese females As if SOL - Increased ICP - Headache - Papilloedema ``` Visual - Blurred vision - 6th nerve palsy - Enlarged blind spot

Question 347

Investigations of IIH?

Answer 347

High opening pressure on Lumbar puncture Visual field defects testing - looking for enlarged blind spot, inferonasal loss, other nerve fibre bundle.

Question 348

Management of IIH?

Answer 348

- Weight loss - 1st line: Acetazolamide = carbonic anhydrase inhibitor - Topiramate - Lumbar-peritoneal shunt may be necessary if drugs fail and visual loss deteriorates. NB - if it is cerebral oedema = give DEX.

Question 349

What are the types of cerebral oedema?

Answer 349

1. Vasogenic (increased cap permeability): trauma, tumour, ischaemia, infection. 2. Cytotoxic: from hypoxia 3. Interstitial: e.g obstructive hydrocephalus, decreased Na.

Question 350

What are the causes of a raised ICP?

Answer 350

- Haemorrhage - Tumours - Infection: meningitis, encephalitis, abscess - Hydrocephalus - Status - Cerebral oedema

Question 351

Signs and symptoms of raised ICP?

Answer 351

- Headache - N/V - Seizures - Drowsiness --> coma - Cushing reflex --> increased HR, decreased BP, irregular breathing. - 6th CN palsy (may be false localising) - Cheyne-Stokes respiration (longer, deeper breathing, followed by apnoeic episodes). - Pupils: miosis --> mydriasis - Papilloedema, loss of venous - pulsation @ disc.

Question 352

Acute management of raised ICP?

Answer 352

``` ABC - Then treat seizure and correct HTN - Elevate bed to 40 degrees - Neuroprotective ventilation PaO2 >13 PCO2 4.5 Good sedation ± NM blockade - Mannitol or hypertonic saline. Start first then give Burr Hole. - Decreased ICP short-term but may lead to rebound increased ICP later. Mannitol 1g/kg (20% @ 5ml/kg). ```

Question 353

What are the herniation syndromes?

Answer 353

Tonsillar Transtentorial Subfalcine

Question 354

What is a tonsillar hernia (coning)

Answer 354

Increased pressure in posterior fossa --> displacement of cerebellar tonsils through foramen magnum --> compression of brainstem and cardioresp centres in medulla CN6 palsy, upgoing plantars --> irregular breathing --> apnoea

Question 355

Transtentorial/ Uncal Herniation syndrome?

Answer 355

- Lateral supratentorial mass --> compression of ipsilateral inferomedial temporal lobe (uncas) against free margin of tentorium cerebelli. - Ipsilateral CN3 palsy: mydriasis (dilation) then down and out. Parasympathetic fibres of CN3 nerve are arranged around the outside, they are damaged first, leaving a tonic sympathetic input, creating a dilated and fixed pupil. - Ipsilateral corticospinal tract: contralateral hemiparesis - May --> compression of contralateral corticospinal tracts --> Ipsilateral hemiparesis.

Question 356

Subfalcine herniation?

Answer 356

- Frontal mass - Displacement of cingulate gyrus (medial frontal lobe) under falx cerebri - Compression of ACA --> Stroke - Contralateral motor/sensory loss in legs>arms Abulia (pathological laziness)

Question 357

What are the causes of Parkinsonism?

Answer 357

- Parkinson's disease - Parkinson's Plus syndrome (basal ganglia degeneration + other symptoms) - MSA/Shy Drager - Progressive supranuclear palsy - Corticobasilar degeneration - Lewy body dementia

Question 358

What other conditions can cause parkinsonism

Answer 358

``` Infection: Syphilis, HIV, CJD Vascular: Multiple infarcts in SN Drugs: Antipsychotics, metoclopramide Trauma: Dementia pugilistica Genetic: Wilson's ``` Drug induced parkinson's = Symmetrical tremor is rarely caused by idiopathic Parkinson's disease.

Question 359

What are the symptoms of MSA?

Answer 359

- Autonomic dysfunction: postural hypotension, bladder dysfunction - Cerebellar + pyramidal signs - Unilateral symptoms - Rigidity > Tremor - Severe/early onset autonomic dysfunction (postural hypotension/erectile dysfunction)

Question 360

What are the symptoms of progressive supranuclear palsy?

Answer 360

Postural instability --> falls Speech disturbance (+ dementia) Palsy: vertical gaze

Question 361

What are the symptoms of corticobasilar degeneration?

Answer 361

- Aphasia, dysarthria, apraxia - Akinetic rigidity in one limb - Asterognosis (cortical sensory loss) - Alien limb phenomenon

Question 362

Lewy body dementia:

Answer 362

Fluctuating cognition | Visual hallucinations

Question 363

General symptoms of parkinsonism?

Answer 363

Tremor - Worse at rest - Exacerbated by distraction - 4-6Hz, pill rolling - Unilateral resting tremor with bradykinesia. Rigidity - Increased tone in all muscle groups: lead-pipe rigidity - Rigidity + tremor --> cogwheel rigidity Bradykinesia - Slow initiation of movement with reduction of amplitude on repetition - Expressionless face - Monotonous voice - Micrographia Gait - Decreased arm swing - Festinance (Shortened stride quickened gait) - Freezing (esp in doorways

Question 364

Parkinson's Disease epidemiology?

Answer 364

Mean onset 65 yrs | 2% prevalence

Question 365

Pathophysiology of Parkinson's Disease?

Answer 365

Destruction of dopamingeric neurons in pars compacta of substantia nigra? - alpha synuclein - Lewy bodies

Question 366

What are the features of PD?

Answer 366

Asymmetric onst: side of onset remains worse - Resting Tremor: increased by stress, decreased by sleep. - Rigidity: lead-pipe, cogwheel - Bradykinesia: slow initiation, difficulty with repetitive movement, micrographia, monotonous voice, mask-like face. - Postural instability: stooped gait with festingation - Postural hypotension + Other autonomic dysfunction - Sleep disorder: insomnia, excessive daytime sleeping, OSA, RBD - Psychosis: esp visual hallucination - Depression/Dementia.

Question 367

What are the sleep disorders associated with PD?

Answer 367

Affects ~90% of PD patients - Insomnia + frequent waking --> excessive daytime sleeping. Inability to turn, restless legs, early morning dystonia, nocturia, OSA. - REM Behavior sleep disorder Loss of muscle atonia during REM sleep Violent enactment of dreams Da SEs: insomnia, drowsiness, excessive daytime sleeping

Question 368

What are the autonomic dysfunctions associated with PD?

Answer 368

- Combined effects of drugs and neurodegeneration - Postural hypotension - Constipation - Hypersalivation --> Dribbling (decreased ability to swallow saliva) - Urgency, frequency, nocturia - ED - Hyperhidrosis (excessive sweating)

Question 369

What are the side effects of L-Dopa?

Answer 369

DOPAMINE - Dyskinesia - On-Off phenomena = mototr fluctuations - Psychosis - Decreased ABP - Mouth dryness - Insomnia - N/V - EDS (excessive daytime sleeping)

Question 370

Motor fluctuations in Parkinson's caused by?

Answer 370

End-of dose: deterioration as dose wears off with progressively shorter benefit On-Off effect: unpredictable fluctuations in motor performance unrelated to timing of dose.

Question 371

Investigations for Parkinson's Disease?

Answer 371

- Dopaminergic agent trial Mainly diagnosis is made clinically. - Consider MRI brain (mostly normal. May show mild small vessel disease. - DaTscan Bins to dopamingeric neurons and allows visualisation of substantial nigra.

Question 372

General Management of Parkinson's disease?

Answer 372

MDT: neurologist, PD nurse, physio, OT, social worker , GP and carers. Assess disability - UPDRS: unified Parkinson's Disease Rating Scale. - FALLS assessment - Physiotherapy: postural exercises - Depression screening. Medications - Ensure regular medication review to anticipate any difficulties, non-concordance, polypharmacy. - Risk of acute akinesia or neuroleptic malignant syndrome if medication is not taken/absorbed (gastroenteritis). - Advise against giving patients a drug holiday. - Avoid dopamine antagonist like Haloperidol. - Impulse control disorder more common with dopamine agonist therapy, history of previous impulsive behaviours. - Orthostatic hypotension - develops review potential causes. Use Midodrine. - Glycopyrronium bromide for drooling. - If nauseous - prescribe domperidone - does not cross BBB.

Question 373

What is the medical management of Parkinson's Disease?

Answer 373

If GP suspects signs - refer urgently to neurology. Medications is handled by a specialist - and requires careful titration to maximise effect. If young and motor symptoms affecting quality of life 1. Levodopa. If they cannot take levodopa orally, given a dopamine agonist patch to rescue and prevent acute dystonia. If young motor symptoms not affecting quality of life 1. Da agonists: Ropinirole, pramipexole, or levodopa, monoamine oxidase B (MAO-B) inhibitor. Drugs - Da agonist: ropinirole, pramipexole - MOA-B inhibitors: rasagiline, selegiline - L-Dopa: co-careldopa or co-beneldopa. Complications - Falls, cognitive impairment, depression. - SE of medications.

Question 374

What are the special points to consider with Levodopa?

Answer 374

More improvement in motor symptoms. More improvement in ADLs. BUT more motor complications Fewer specified adverse events. Usually combined with a decarboxylase inhibitor (carbidopa) to prevent peripheral metabolism of levodopa to dopamine (Sinemet, Medapar) - reduced effectiveness with time - Unwanted effects: dyskinesia, on-off effect, dry mouth, postural hypotension, psychosis. Normally at a higher dose. - No use in neuroleptic induced parkinsonism - It is important not to acutely stop levodopa. Can be given a dopamine agonist patch as rescue medication to prevent acute dystonia.

Question 375

Dopamine receptor agonists?

Answer 375

Less improvement in motor symptoms, less improvement in ADLs, fewer motor complications, and more specific adverse effects such as hallucinations. Ropinirole, apomorphine (non-ergot) Bromocriptine, cabergoline (ergot derived) associated with pulmonary, retroperitoneal and cardiac fibrosis. Must do a echo, ESR, creatinine + chest x-ray. More likely than levodopa to cause hallucinations in older patients. - Can also cause nasal congestion + postural hypotension.

Question 376

What are the MAO-B inhibitors?

Answer 376

MAO-B = less improvement in motor symptoms, less improvement in ADLs, fewer motor complications, fewer adverse events. - Selegiline - Inhibits the breakdown of dopamine secreted by the dopaminergic neurons.

Question 377

What is amantadine in PD?

Answer 377

Mechanism not understood. Increases dopamine release + inhibits uptake from dopaminergic synapses. - side effects include ataxia, slurred speech, confusion, dizziness, livido reticularis. Management of drug induced dyskinesias

Question 378

COMT inhibitors in PD?

Answer 378

Entacapone, tolcapone | - COMT is an enzyme involved in the breakdown of dopamine + used as an adjunct to levodopa

Question 379

Antimuscarinics in PD?

Answer 379

- Block cholinergic receptors - Now used more to treat drug-induced parkinsonism rather than idiopathic. Help tremor and rigidity - Procyclidine, benzotropine

Question 380

Differential for parkinson's?

Answer 380

``` Parkinson's plus syndrome Multiple infarct Drugs: neuroleptics Inherited: Wilsons Infection: HIV, Syphilis, CJD Dementia pugilistica. ```

Question 381

What is multiple sclerosis?

Answer 381

A chronic inflammatory condition of the CNS characterised by multiple plaques of demyelination disseminated in time and space.

Question 382

Epidemiology of MS?

Answer 382

Common: 1/1000 Age: Mean @ onset = 30 yrs Sex: F>M = 3:1 Race: rare in blacks

Question 383

Aetiology of MS?

Answer 383

Genetic (HLA-DRB1), environmental, viral?

Question 384

What is the pathophysiology of MS?

Answer 384

CD4 cell-mediated destruction of oligodendrocytes --> Demyelination and eventual neuronal death - Initial viral inflammation primes humoral AB responses vs MBP - Plaques of demyelination are hallmark.

Question 385

Classification of MS?

Answer 385

Relapsing-remitting: 80% - acute attacks followed by periods of remission. Secondary Progressive (RR patients who have deteriorated + developed neuro signs + symptoms). Primary Progressive (progressive accumulation) : 10%

Question 386

Presentation of multiple sclerosis?

Answer 386

Female, catheterised, eye signs, cerebellar signs - ATAXIA (unable to heel-toe walk) - UMN signs - pyramidal weakness + brisk reflexes. - Tingling/burning - Eye: optic neuritis (decreased central vision + eye movement pain) - Ataxia + other cerebellar signs - Motor: usually spastic paraparesis (motor walking) - muscle stiffness.

Question 387

Sensory Clinical features of MS?

Answer 387

- Dys/paraesthesia - Decreased vibrations sense - trigeminal neuralgia

Question 388

Motor clinical features of MS?

Answer 388

Spastic weakness Transverse myelitis Foot dragging Fatigue

Question 389

Eye clinical features of MS?

Answer 389

- Diplopia - Visual phenomena - Bilateral INO (internuclear ophthalmoplegia) - due to medial longitudinal fasciculus lesion. - Optic nerve damage - central scotoma, RAPD, colour and VA loss, optic atrophy. - Optic neuritis

Question 390

Cerebellum features of MS?

Answer 390

- Trunk and limb ataxia - Scanning dysarthria (jerky, explosive speech) - Fall - Dorsal column disease - reduced vibration, proprioception, Romberg's +ve.

Question 391

GI features of MS?

Answer 391

Swallowing disorders | Constipation

Question 392

Sexual/GU?

Answer 392

ED + anorgasmia Retention Incontinence

Question 393

What is Lhermitte's Sign?

Answer 393

Neck Flexion --> electric shocks in trunk/limbs

Question 394

What is Optic Neuritis?

Answer 394

- Pain on eye movement, rapid decrease in central vision - Uhthoff's: vision decreased with heat: hot bath, hot meal, exercise. - O/E: decreased acuity, decreased colour vision, white disc, central scotoma, RAPD.

Question 395

What is an internuclear ophthalmoplegia?

Answer 395

- Disruption of Medial Longitudinal Fasciculus connecting CN6 and CN3. - Weak adduction of ipsilateral eye. - Nystagmus of contralateral eye. Convergence preserved.

Question 396

What investigations are needed for MS?

Answer 396

MRI: Gd-enhancing or T2 hyper-intense plaques. Gd-enhancing = active inflammation MRI contrast. Shows dissemination in time and space. -Typically located in periventricular white matter. SAgitall FLAIR = periventricular white matter. LP: IgG oligoclonal bands (not present in serum) - less used Ab: Anti-MBP, NMO-IgG: highly specific for Devic's syndrome (affects the optic nerves + spinal cord). Evoked potentials: delayed auditory, visual, sensory. Don't forget hypothyroidism and B12.

Question 397

Diagnosis of MS?

Answer 397

- Demonstration of lesions disseminated in time and space - May use McDonald's Criteria. Dissemination in space (DIS) - One or more T2-hyperintense lesions in 2 or more of 4 areas of CNS: periventricular, cortical or juxtacortical, infratentorial and spinal cord. Dissemintated in time - Asymptomatic Gd enhancing and non-enhancing lesions at any time - New T2 and/or Gd-enhancing lesion on follow-up MRI.

Question 398

What are the differentials for MS?

Answer 398

Cervical spondylosis - without the cerebellar signs CNS sarcoidosis SLE Devic's Neuromyelitis optica (NMO) - MS variant with transverse myelitis and optic atrophy - Distinguished by presence of NMO-IgG abs. Don't get hemiplegia/spasticity ``` Transverse myelitis (entire width of spinal care) - acute or subacute development of motor weakness, sensory impairment and autonomic dysfunction. Seperate entity to MS - demyelination, autoimmune causes, infectio, Follows a pyramidal pattern. May develop sensory loss. Bladder symptoms Bowel symptoms Lhermitte sign ```

Question 399

General Management of MS?

Answer 399

MDT: Neurologist, radiologist, physio, OT, specialist nurse, GP, family.

Question 400

Medical management of an acute attack of MS?

Answer 400

- Methylprednisolone 1000 mg OD for 3 days. Doesn't influence long-term outcome - Decreased duration and severity of attack. Consider plasma exchange?

Question 401

Medical management to prevent relapse of MS?

Answer 401

DMARDS - IFN-B: decreased relapse by 30% in RR MS - Glatiramer: similar efficacy to IFN-B -Natalizumab, ocrelizumab, cladribine and alemtuzumab are for more aggressive disease. ``` Biologicals - Natalizumab: anti-VLA-4Ab decreases relapses by 2/3 in RRMS - Alemtuzumab (Campath): anti-CD52 2nd line RRMS ```

Question 402

What are the symptomatic treatments of MS?

Answer 402

- Fatigue: amantadine, consider mindfulness training and CBT. - Depression: SSRI - Pain: amitryptylline, gabapentin - Spasticity: physio, baclofen, dantrolene, botulinum. Second line is diazepam, dantrolene, tizanidine. - Oscillopsia (visual fields appear to oscillate). Gabapentin is first-line. - Urgency/frequency: oxybutynin, tolterodine - ED: sildenafil - Tremor: clonazepam

Question 403

What are poor prognostic signs for MS?

Answer 403

``` Older Male Motor signs @onset Many relapses early on Many MRI lesions Axonal loss ```

Question 404

What are better prognostic signs

Answer 404

``` Female <25 Sensory signs @onset Long interval between relapses Few MRI lesions ```

Question 405

Cord compression - What are the symptoms?

Answer 405

- Deep, local spinal pain Stabbing, radicular pain in a dermatomal distribution and LMN weakness @ lesion level. - Progressive UMN weakness and sensory loss below lesion - Bladder hesitancy, frequency --> painless retention. - Faecal incontinence or constipation.

Question 406

What are the signs of cord compression?

Answer 406

- Look for motor, reflex and sensory level. - SHooting, radicular pain @ level, anaesthesia below - LMN signs @ level, UMN below level. - Tone and reflexes are usually reduced in acute cord compression.

Question 407

What are the causes of cord compression?

Answer 407

- Trauma - Infection: epidural abscess, TB - 2ndry to malignancy: breasth, thyroid, bronchus, kidney, prostate. - Disc prolapse - Haematoma: warfarin - Intrinsic cord tumour - Myeloma

Question 408

What investigations would you do for cord compression?

Answer 408

- CXR for primaries (Disc space height, loss of bony detail) - MRI is definitive modality Epidural enhancement, mass effect, T2 cord signal. - Gadolinum-enchanced MRI spine

Question 409

What is the management of cord compression?

Answer 409

This is a neurosurgical emergency - Malignancy Dexamethasone IV Consider chemo radio, decompressive laminectomy - Abscess: abx and surgical decompression.

Question 410

What are the differentials for cord compression?

Answer 410

- Transverse myelitis - MS - Cord vasculitis - Spinal artery thrombosis - Aortic dissection

Question 411

What is cauda equina and conus medullaris lesions?

Answer 411

- Spinal cord tapers to its end at L1 | - Compared with lesions high up the cord, these lesions are - flaccid and areflecix (cf spastic and hyperreflexic)

Question 412

What is conus medullaris lesions?

Answer 412

At the cone itself - Mixed UMN/LMN weakness - **Early constipation and retention** - Back pain - mild pain - Sacral sensory disturbance - Erectile Dysfunction

Question 413

What is the cauda equina lesion?

Answer 413

- Saddle anaesthesia - Back pain - Radicular pain down legs - Bilateral flaccid, areflexic lower limb weakness - Incontinence, retention of faeces, urine. - POOR anal tone.

Question 414

What is the management of cauda equina/conus medullaris?

Answer 414

As for cord compression | These are neurosurgical emergencies and require urgent imaging and surgical decompression

Question 415

What is spondylosis?

Answer 415

- Degeneration due to trauma or ageing - IV disc/vertebral collapse - Osteophytes - May --> central (myelopathy) = cord itself and/or lateral (radiculopathy - nerve root)) pathology.

Question 416

What percentage of men and women are affected by cervical spondylosis? Also called degenerative cervical myelopathy

Answer 416

90% of men >60 | Women >50

Question 417

What is cervical spondylosis?

Answer 417

Specific term for osteoarthritis of the spine, including spontaneous degeneration of either disc or facet joints.

Question 418

What is the presentation of cervical spondylosis?

Answer 418

- Usually asymptomatic - Neck stiffness ± crepitus - Stabbing/dull arm pain (brachialgia) - Upper limb motor and sensory disturbances according to compression level (often C7). - Can --> Myelopathy with quadriparesis and sphincter dysfunction Specific signs - Lhermitte's sign: neck lexion --> tingling down spine - Hoffman reflex: flick to middle finger pulp --> brief pincer flexion of thumb and index finger

Question 419

What is the motor and sensory presentation of a C5 Root (C4/C5 disc) manifestation?

Answer 419

Motor weakness - Deltoid, Supraspinatus, decreased supinator jerk. Sensory abnormality - Numb elbow

Question 420

What is the motor and sensory presentation of a C6 Root (C5/C6 disc) manifestation?

Answer 420

Motor weakness - Biceps (bicep reflex) - Brachioradialis (brachioradialis test) - Decreased biceps jerk Sensory - numb thumb and index finger

Question 421

What is the motor and sensory presentation of a C7 Root (C7/C8 disc) manifestation?

Answer 421

Motor weakness - Triceps (tricep test) - Finger extension - Decreased tricep jerk Sensory - Numb middle finger

Question 422

What is the motor and sensory presentation of a C8 Root (C7/C8 disc) manifestation?

Answer 422

Finger flexors Intrinsic hand Numbness ring and little finger and medial side of hand. C8 exits the spine below the C7 vertebra, only nerve root below a vertebra.

Question 423

What are the investigations for cervical spondylosis?

Answer 423

MRI | Consider X-ray

Question 424

What is the management of cervical spondylosis?

Answer 424

Urgently referred for assessment by specialist spinal services (neurosurgery or orthopaedic spinal surgery). Conservative: stiff collar, analgesia/physiotherapy Medical: Consider NSAIDs, transforaminal steroid injection Most effective treatment - Surgical: decompression, laminectomy or laminoplasty Postoperatively, patients with cervical myelopathy require ongoing follow-up as pathology can recur at adjacent spinal levels. Known as adjacent segment disease.

Question 425

Differential for cervical spondylosis?

Answer 425

- MS - Nerve root neurofibroma - SACD (subacute combined degeneration of the spine) .

Question 426

What is lumbosacral spondylosis?

Answer 426

L5 and S1 roots most commonly compressed by prolapse of L4/L5, L5/S1 disc. - may present as severe pain on sneezing/ coughing a few days after low back strain. - Lumbago - low back pain - Sciatica - shooting radicular pain down buttocks and thigh.

Question 427

What are the signs of lumbosacral spondylosis?

Answer 427

- Limited spinal flexion | - Pain on straight-leg raise

Question 428

What L4/L5 root compression present as?

Answer 428

Weak hallux extension ± foot drop. - In foot drop due to L5 radiculopathy, weak inversion (tibpost) helps distinguish from peroneal N. palsy. - Decreased sensation on inner dorsum of foot. Conservative management - leg crossing, squatting and kneeling should be avoided. Symptoms typically improve over 2-3 months.

Question 429

Wht is L5/S1 --> S1 root compression

Answer 429

- Weak foot plantarflexion and eversion - Loss of ankle-jerk - Calf pain - Decreased sensation over sole of foot and back of calf

Question 430

Management of lumbosacral spondylosis?

Answer 430

- MRI is definitive (emergency if cauda-equina syndrome)

Question 431

Management of lumbosacral spondylosis

Answer 431

- Conservative: rest, analgesia, mobilisation - Medical: transforaminal steroid injection - Surgical: Discectomy or laminectomy may be considered in cauda-equina

Question 432

What is Bell's Palsy?

Answer 432

- Inflammatory oedema from entrapment of CN7 in narrow facial canal. - Probably of viral origin (HSV1) 75% of facial palsy - Pregnant women are 3x more likely to develop Bell's palsy.

Question 433

What are the features of Bell's Palsy?

Answer 433

- Sudden onset: eg overnight Complete, unilateral facial weakness in 24-72hrs - Failure of eye closure --> dryness - Bell's Sign: eyeballs roll up on attempted closure - Smooth of nasolabial folds - Drooling, speech difficulty - Numbness or pain around ear - decreased taste (Ageusia) - Hyperacusis: stapedius palsy (sensitivity to sound) - involvement of all nerve branches Examination - Close eyes, raise eyebrows, frown UMN/LMN - UMN spares the upper fae - presumed evolutionary bicortical innervation to protect eyes. - Loss of corneal reflex (efferent)

Question 434

Investigations for Bell's palsy?

Answer 434

- Mainly clinical - EMG (decreasd in amplitude in muscle action) - Serology for Borrelia Burgdoferi - Examination for Ears (Herpes Zoster Ramsey Hunt). - Must go to ENT - cholesteatoma - Consider MRI: (SOL, stroke, MS), consider LP

Question 435

What is the management of Bell's Palsy?

Answer 435

Give prednisolone w/i 72hrs - 60mg/d PO for 5/7 following by tapering - Valaciclovir if zoster is suspected: Otherwise antiviral don't help - Protect glasses Dark glasses, artificial tears, tape closed at night. - Plastic surgery may help if no recovery.

Question 436

What is the prognosis of Bell's Palsy?

Answer 436

- Incomplete paralysis: recovers completely within weeks | - Complete paralysis: 80% get full recovery: remainder

Question 437

Complications of Bell's Palsy?

Answer 437

Aberrant Neural Connections - Synkinesis: e.g blinking causing up-turning or mouth - Crocodile tears: eating stimulates unilateral lacrimation, not salivation

Question 438

What is Ramsey Hunt Syndrome?

Answer 438

Reactivation of VZV in geniculate ganglion of CNVII

Question 439

Features of Ramsay Hunt Syndrome?

Answer 439

- Preceding ear pain or stiff neck - Vesicular rash in auditory canal ± TM, pinna, tongue, hard palate (no rash = zoster sine herpete) - Normal ear exam goes against RH. - Ipsilateral facial weakness, ageusia, hyeracusis - May affect CN8 --> vertigo, tinnitus, deafness

Question 440

Management of Ramsay Hunt Syndrome?

Answer 440

If Dx suspected give valaciclovir and prednisolone within first 72hrs

Question 441

Prognosis of Ramsay Hunt Syndrome?

Answer 441

Managed within 72hrs: 75% recovery | Otherwise: 1/3 full recovery, 1/3 partial, 1/3 poor.

Question 442

Other causes of facial nerve palsy apart from RH and Bell's?

Answer 442

Bilateral symptoms: consider Lyme, GBS, Leukaemia, Sarcoid, MG. UMN signs: Sparing of frontalis and orbicularis oculi - Due to bilateral cortical representation Other CN palsies Limb weakness Rashes ``` LMN - Bell's palsy Ramsay-Hunt syndrome (due to herpes zoster) acoustic neuroma parotid tumours HIV multiple sclerosis* diabetes mellitus ```

Question 443

Intracranial causes of facial palsy?

Answer 443

SOL, MS, Vascular. - motor cortex --> UMN (assoicated with ipsilateral hemiplegia) - Brainstem nuclei --> LMN Usually associated with CN6 palsy + contralateral hemiplegia - Cerebello-pontine angle: acoustic neuroma, meningioma Both may be accompanied by 5th, 6th and 8th Cn palsies and cerebellar signs - Loss of corneal reflex - Sensorineural deafness, tinnitus, vertigo - DANISH

Question 444

Intra-temporal Facial palsy? - Labrinth to mastoid

Answer 444

- Cholesteatoma - Ramsay Hunt - Otitis Media - Trauma

Question 445

Infra-temporal facial palsy?

Answer 445

Parotid tumours | Trauma

Question 446

Systemic causes of facial palsy?

Answer 446

Peripheral neuropathy - Demyelinating: GBS - Axonal: DM, Lyme, HIV, Sarcoid - Pseudopalsy: MG, Botulism

Question 447

Types of Mononeuropathies?

Answer 447

``` Median Ulnar Radial Brachial Plexus Phrenic Lat Cut N Thigh Sciatic Common Peroneal Tibial ```

Question 448

What is a mononeuropathy?

Answer 448

- Lesions of individual peripheral or cranial nerves. - EMG helps define site of lesions - Mononeuritis multiplex: 2 or more peripheral nerves affects : Usually systemic cause: DM most commonly - Also WAARDS PLC Wegener's AIDS Amyloid RA DM Sarcoidosis PAN Leprosy Carcinomatosis Investigation = Blood (Autoimmune serology: ANA, ANCA, RF, dsDNA. Imaging - XR elbow - US cubital tunnel Special tests - Nerve conduction studies

Question 449

Which dermatomes involved in median nerve palsy?

Answer 449

C6-T1 Wrist: carpal tunnel, trauma (amyloidosis)

Question 450

What are the features (motor + sensory of Median nerve palsy)

Answer 450

Motor features? - LLOAF muscles (lateral 2 lumbricals, Opponens Pollicis, Abductor Pollicis Brevis, Flexor Pollicis Brevis) - Thenar wasting - Sign of Benediction - Pronation of hand Sensory Loss/Features - Radial 3.5 fingers and palm. - Aching pain in hand (decreased 2 point discrimination) - Tinel's and Phalen's +ve. Look for sensation over the thenar eminence - If lost - cannot be carpal tunnel syndroe - PCB arises proximal to the carpal tunnel

Question 451

What are the dermatomes of an ulnar palsy?

Answer 451

- C8-T1 - Mainly caused by Elbow Trauma (e.g supracondylar fracture). BRanches - Muscular branch = flexor carpi ulnaris, medial half of the flexor digitorum profundus. - Palmar cutaneous branch - medial part of the palm - Dorsal cutaneous branch - dorsal surface of medial part of hand.

Question 452

What are the motor and sensory loss features of ulnar palsy?

Answer 452

Motor weakness - most muscles except LOAF. Medial two lumbricals, aDductor pollicis, interossei, abductor digitia minimi, flexor digiti minimi . - Partial claw hand - Hypothenar wasting (first dorsal interosseus) - Can't do good luck sign - Weakness and wasting of 1st dorsal interosseous - Froment's +ve (finger pinch grip) - Loss of thumb adduction Sensory Loss/Features - Ulnar 1.5 fingers - Loss of senation over hypothenar eminence means PCB affect - injury is above wrist. Ulnar paradox - higher lesion causes lesser deforimit - Lower lesions spares FDP - causes flexion at the DIP

Question 453

What are the dermatomes of radial nerve palsy?

Answer 453

If Low: wrist trauma If high: humerus if V high: axilla Fracture of the shaft of the humerus.

Question 454

What are the motor features and sensory loss features of radial nerve palsy?

Answer 454

Motor: Low: finger drop High: wrist drop V.high: triceps paralysis, wrist drop Sensory: Dorsal thumb root (snuff box)

Question 455

What are the presentations of a Brachial plexus injury?

Answer 455

- Caused by Trauma - Radiotherapy (e.g breast) High (C5-C6): Erb's Palsy --> Waiter's tip (Catching from behind). Loss of C5-C6 dermatome. Hand hanging loose, pronated and medially rotated. Low (C8-T1) - Klumpke's --> claw hand. Loss of C8-T1 dermatome. Horner's syndrome. Weakness of hand intrinsic muscle. Root which supplies the thumb adduction and finger abduction is T1. Medial epicondyle is the testing point for the T1 dermatome.

Question 456

Which nerve is at C3-C5?

Answer 456

Phrenic. Damage caused by - Neoplastic: Lung Ca, Myeloma, Thymoma. - Mechanical: Cervical spondylosis, big left atrium. - Infective; C3-C5 zoster, HIV, lyme, TB. Presents with orthopnoea + raised hemidiaphragm.

Question 457

Lateral Cutaneous Nerve Thigh: L2-L3

Answer 457

Entrapment under inguinal ligament. Meralgia paraesthetica --> anterolateral burning thigh pain.

Question 458

Sciatic nerve L4-S3?

Answer 458

Causes of mononeuropathy - Pelvic tumours - Pelvic or femur #s. Motor features - Hamstrings - All muscles below knees weakened. Sensory - Below knee laterally and foot

Question 459

Common peroneal nerve: l4-S1?

Answer 459

Fibular head: trauma, sitting cross legged. Motor: Foot drop: can't walk on heels Weak ankle dorsiflexion, eversion. NB: inversion intact! Sensory loss/Features: Below knee laterally.

Question 460

Tibial damage L4-S3

Answer 460

- Can't plantar flex --> can't stand on tiptoe - Foot inversion - Toe Flexion Loss of sensation sole of foot.

Question 461

What are the features of polyneuropathies?

Answer 461

- Generalised disorders of peripheral or cranial nerves. - Distribution is symmetrical and widespread - Distal weakness and sensory loss (Glove and stocking) Classification of polyneuropathies - Time-course: acute, chronc - Function: motor, sensory, autonomic, mixed - Path: Demyelination, axonal degeneration, both.

Question 462

What are the metabolic causes of polyneuropathies?

Answer 462

Mostly axonal - DM - Renal failure/uraemia - hypothyroidism - decreased B1/B12 (EToH)

Question 463

What are the vasculitic causes of polyneuropathies?

Answer 463

PAN (Polyarteritis Nodosa) RA Wegener's

Question 464

What are the inflammatory causes of polyneuropathies /

Answer 464

- GBS | - Sarcoidosis

Question 465

What are the infective causes of polyneuropathies?

Answer 465

HIV Syphilis Leprosy Lyme

Question 466

What are the inherited causes of polyneuropathies?

Answer 466

Charcot Marie Tooth | Refsum's syndrome

Question 467

What are the toxin causes of polyneuropathies?

Answer 467

Lead Amyloid Paraproteinemias

Question 468

What are the drug causes of polneuropathies

Answer 468

Isoniazid ETOH Phenytoin Vincristine

Question 469

What to ask in a neuro history for polyneuropathy?

Answer 469

``` Time-course Precise symptoms Associated event - D+V: GBS - DecreaseD weight loss: Ca - Arthralgia: connective tissue ``` Travel, ETOH, drugs.

Question 470

What investigations to do in a polyneuropathy station

Answer 470

- LFTs, U+E, Glucose, ESR, B12 - TFTs, B1, ANA, ANCA - Genetic tests: PMP22 in CMt - NErve conduction studies - EMG

Question 471

What are the main causes of a sensory neuropathy?

Answer 471

- Alcohol - B12 - Chronic Renal Failure and Ca (paraneoplastic) - DM - Every vasculitis - Hypothyroidism - HIV

Question 472

General features of a sensory neuropathy

Answer 472

- Gloves and stocking distribution: length dependent - Deep tendon reflexes may be decreased or absent E.g Loss of ankle jerks in diabetic neuropathy - Signs of trauma or joint deformity (Charcot's joints) - Diabetic and alcoholic neuropathies are painful - Some aetiologies favour loss of particular fibres.

Question 473

What are the features of large myelinated fibre damage?

Answer 473

Caused in B12 - Loss of proprioception --> ataia - Pins and needles

Question 474

What are the features of small demyelinated fibre damage?

Answer 474

Caused in alcohol - Loss of pain and temperature sensation - Painful dysaethesia: e.g burning, hyperalgesia

Question 475

What are the main causes of a motor neuropathy?

Answer 475

- Guillan Barre Syndrome - Charcot Marie Tooth, Hereditary Motor and Sensory Neuropathy - Paraneoplastic - Lead poisoning

Question 476

Features of Motor Neuropathy?

Answer 476

Weakness/clumsiness of hands, difficulty walking LMN signs CN: diplopia, Dysarthria, dysphagia Involvement of respiratory muscles --> Decreased FVC.

Question 477

What are the causes of a autonomic neuropathy?

Answer 477

``` Diabetes HIV SLE GBS LEMS ```

Question 478

Features of autonomic neuropathy?

Answer 478

- Postural hypotension - Ejaculatory failure - Decreased sweating - Constipation - Retention - Horner's

Question 479

Autonomic function tests?

Answer 479

BP: Postural drop >20mmHg ECG: variation >10bpm with respiration

Question 480

Primary autonomic failure causes?

Answer 480

Idiopathic or part of MSA/PD.

Question 481

What is Guillain- Barre Syndrome Classification?

Answer 481

AIPD: acute autoimmune demyelinating polyneuropathy AMAN: acute motor (+ sensory) axonal neuropathy Miller-Fisher: (mainly japan) Ophthalmoplegia + ataxia + areflexia. Eyes are affected first.

Question 482

What is the aetiology of GBS?

Answer 482

- 2/3 patients have had infections within 6 weeks of conditions, usually URTI . Immune mediated attack on myelin sheath.

Question 483

Causes of GBS?

Answer 483

Abs cross-react to gangliosides No precipitants found in 40%? Bacteria: C.jejuni, mycoplasma Viruses; CMV, EBV, HSV, HIV, Flu Vaccines: esp rabies.

Question 484

What are the features and investigations for GBS?

Answer 484

GBS = AIDP = acute autoimmune demyelinating polyneuropathy - Presents with GBS (Diarrhoea then weakness). Growing weakness Breathing + bulbar problems Back pain - Sensory disturbances (paraesthesia in extremities + sensory ataxia in Miller-Fisher) Autonomic neuropathy (arrhythmias, decreased HR, Labile BP, sweating, urinary retention)

Question 485

Growing weakness features of GBS?

Answer 485

- Symmetrical, ascending flaccid weakness/paralysis - LMN sign: areflexia, fasciculations may occur - Proximal > distal (trunk, resp, CNS 7) - Progressive phase last <4 weeks.

Question 486

Investigations for GBS?

Answer 486

- Immune - Serology for anti-ganglioside ABs. Evidence of infections - stool sample - Demyelinating nerve conduction studies - slow conduction velocities - isolated raised Protein in CSF - protein often >5.5 g/L. Normal WCC. - Spirometry - Vital Capacity + ABG on air for vent. - Swallow assessment - ECG for arrhythmia and BP for autonomic disturbance.

Question 487

Management of GBS?

Answer 487

Supportive - Airway/ventilation: ITU if FVC <1.5L - Analgesia: NSAIDS, gabapentin - Autonomic: may need inotropes, catheter - Antithrombotic: TEDs, LMWH Immunosuppression - IVIG - Plasma exchange Prognosis - 85% complete recovery - 10% unable to walk alone at 1yr - 5% mortality

Question 488

What is Charcot-Marie-Tooth Syndrome?

Answer 488

- Peroneal muscular atrophy | - Hereditary motor and sensory neuropathy

Question 489

Types of CMT syndrome?

Answer 489

HMSN1/CMT1 - commonest form, demyelinating, AD mutation in the peripheral myelin protein 22 gene HMSN2/CMT2 - second commonest form. Axonal degeneration (therefore near normal conduction studies) CMT4 - AR

Question 490

What are the motor features of CMT?

Answer 490

Typically history of ankle sprains and scoliosis. Motor and sensory loss (sensory milder). - Antero-lateral compartments affected. - Absent reflexes - Pes cavus ``` Onset at puberty? - Nerve = thickened, enlarged nerves - Motor = Foot drop --> high stepping gait, weak ankle dorsiflexion and toe extension, - absent ankle jerks - symmetrical muscle atrophy: Peroneal muscles (loss of muscles) - champagne bottle Hand and arm muscles - Claw hand Pes Cavus (high-arched feet) ``` Papable lateral popliteral nerve - thickened nerves at medial malleolus.

Question 491

What are the sensory features of CMT?

Answer 491

- Variable loss of sensation in a stocking distribution | - Neuropathic pain in some

Question 492

Investigations for CMT?

Answer 492

-Genetic tests: PMP22 gene mutations - Nerve conduction studies: decreased conduction speed in CMT1 B12 DM Alcohol - Physio - Walking aids - Ankle and foot supports

Question 493

Management of CMT?

Answer 493

- Supportive Physio Podiatry Orthoses e.g ankles braces

Question 494

Motor neuron Disease characteristics?

Answer 494

- Cluster of degenerative diseases characterised by axonal degeneration of neurones in the motor cortex, CN nuclei, anterior horn cells. - UM and LN neurons affected (polyneuropathy) - No sensory loss or sphincter disturbances (cf. MS) - Never affects eye movements (compared to MG)

Question 495

Epidemiology of MND?

Answer 495

Prevalence: 6/100,000 Sex: M>F = 3:2 median age @ onset = 60yrs Often fatal in 2-4 yrs

Question 496

Causes of MND?

Answer 496

Unknown Types: - ALS (Amyotrophic lateral sclerosis) = death of both UMN and LMN in motor cortex. LMN signs = flaccid paralysis, weakness, wasting, fasiciultion. UMN = Spastic paralysis, pyramidal weakness, hyper-reflexia, up-going plantars. Primary lateral sclerosis - UMN signs only Progressive muscular atrophy - LMN signs only - Affects distal muscles before proximal - Carries best prognosis Progressive bulbar palsy - Palsy of tongue, muscles of chewing/swallowing and facial muscles due to loss of function of brainstem motor nuclei. - Caries worst prognosis.

Question 497

Investigations for MND?

Answer 497

Primarily Clinical Braincord MRI: exclude structural causes - cervical cord compression (myelopathy) or brainstem lesions). LP: exclude inflammatory cause EMG: shows acute denervation Use Revised EI Escorial Diagnostic Criteria (presence of UMN + LMN of the cranial, cervical, thoracic and lumbosacral segments of neuroaxis.

Question 498

General Management of MND?

Answer 498

MDT: Neurologist, physio, OT, dietician, specialist nurse, GP, family Discussion of end-of-life decision - Advanced directive - DNAR

Question 499

Specific management of MND?

Answer 499

Riluzole: antiglutamatergic that prolongs life by 3 months.

Question 500

What supportive management of MND?

Answer 500

``` Drooling: proantheline or amitriptyline Dysphagia: NG or PEG feeding Respiratory failure: NIV Pain: analgesic ladder Spasticity: Baclofen ```

Question 501

What are the classifications of MND?

Answer 501

- ALS - Loss of Motor neurones in cortex and anterior horn (UMN + LMN + fasciculation) - Progressive Bulbar Palsy (only affects CN9-12 --> bulbar palsy) - Progressive Muscular Atrophy (Anterior horn cell lesions (LMN signs only), distal to proximal. Better prognosis vs ALS) Primary Lateral Sclerosis - Loss of Betz cells in motor cortex --> mainly UMN signs - Marked spastic leg weakness and pseudobulbar palsy - No cognitive decline

Question 502

What is a bulbar palsy?

Answer 502

``` Disease of nuclei 9-12 in the medulla. - LMN lesions of tongue, talking and swallowing. - Signs Flaccid, fasciculating tongue Speech: quiet or nasal (donald duck) Normal/absent jaw jerk Loss of gag reflex ``` Causes - MND - GBS - MG - Central pontine myelinolysis

Question 503

What is a pseudobulbar/corticobulbar palsy?

Answer 503

Commoner than bulbar palsy Bilateral lesions above mid-pons (corticobulbar tracts) --> UMN lesions of swallowing and talking. CN motor nuclei have bilateral cortical representation except lower half of CN7. Signs - Spastic tongue - Slow tongue movements with slow deliberate speech: Hot-potato speech - Brisk jaw jerk - Emotional incontinence Causes - MS - MND - Stroke - CPM

Question 504

How can Polio cause a motor neuron disease?

Answer 504

RNA virus Affects anterior horn cells Fever, sore throat, myalgia. - Asymmetric LMN paralysis - No sensory involvement - May be confined to upper or lower limbs or both - Respiratory muscle paralysis can --> Death

Question 505

How is myopathy different to neuropathy? s for myopathies?

Answer 505

Myopathy - Gradual onset - Symmetrical, proximal weakness: Difficulty combing hair, climbing stairs, getting up from chairs - Dystrophies usually affect specific muscle groups - Preserved tendon reflexes. Neuropathy - Distal weakness - Paraesthesia (tingling) , bladder problems. Other pointers- - Rapid onset: neuropathy, or drug, toxic or metabolic myopathy - Fatigability: MG, LEMS - Spontaneous pain and tenderness @ rest: inflammatory myopathy - Pain on exercise: ischaemia or metabolic myopathy - Oddly firm muscles: pseudohypertrophy in muscular dystrophies - Fasciculations: anterior horn cell or root disease

Question 506

Investigation for myopathies?

Answer 506

- ESR, CK, AST, LDH | - EMG

Question 507

what are the muscular dystrophies?

Answer 507

Group of genetic disease with progressive degeneration and weakness of specific muscle groups.

Question 508

Duchenne's Muscular dystrophy?

Answer 508

3/1000 male births. X-linked recessive --> non-functional dystrophin. - presents at 4 yrs old - Difficulty standing - Calf pseudohypertrophy - Resp failure - increasing lordosis - Diminished muscle tone + Deep tendon reflexes. Investigations: increased CK Some survive >20 yrs. Can use steroids etc.

Question 509

Becker's Muscular dystrophy?

Answer 509

X-linked recessive Partially functioning dystrophin Presents later is less severe and has better prognosis.

Question 510

Landouzy-Dejerine?

Answer 510

``` Almost as common as DMD AD inheritence - Presents @12-14 yrs old Difficulty puffing cheeks and raising arms above heads. Signs - Weakness of face, shoulders, upper arms (asymmetric with deltoids spared) - winging of scapula - Foot drop ```

Question 511

Myotonic dystrophy?

Answer 511

- AD Cl- channelopathy - Onset in 20s - Tonic muscle spasm (myotonia) Lower Motor Neuron. Presentation Face - Myopathic face: Long, thin, expressionless - Wasting of facial muscles and SCM (guttering of the temporalis) - Bilateral Ptosis - Dysarthria: myotonia of tongue and pharynx. Shake hand - squeeze my hand, and told for 3 seconds. try to let go. Percussion myotonia: hypothenar eminence depression visibly fills slowly after percussion. Hands - Myotonia: slow relaxation so inability to release hand after shake. - Wasting and weakness of distal muscles + areflexia --> Wrist drop - Percussion myotonia: percuss thenar eminence --> involuntary thumb flexion. Other signs - Frontal balding - Cataracts - DM - Cardiomyopathy, tachy/bradyarrythmias (pacemaker scar) - Dysphagia - Testicular atrophy Assocations - Cataracts - Dysphagia - Cardiac - cardio + heart block (PPM) - DM - Hypogonasism Invx - LFTs should be checked for NM rsp insufficient - ECG conduction block - Echo for CM - Fasting glucose DM - Slit lamp for cataracts - SALT - EMG: ' Dive bomber' potentials. How to present - The gentleman has evidence of myopathic facies, frontotemporal hair loss with bilateral ptosis, wasting of the facial msucles and sternocleidomastoids. There is also symmetrical wasting of the forearm muscles and small muscles of the hands bilaterally. There is a reduction in power distally in both arm in all muscle groups tested with normal sensation and coordination. The reflexes are reduced. Mr X had difficulty in releasing my hand from a squeeze and opening his eyes when closed firmly - suggesting myotonia. THis is likely to be myoptonic dystrophy> to complete my assessment I owuld like to exaomine the cardiovascular, check bloods, perform a full functional asssessment. Diagnosis can be confirmed with a family history, EMG and geentic testing.

Question 512

What is the management of Myotonic dystrophy?

Answer 512

No Rx for weakness Phenytoin may improve myotonia Caution with GA: high risk of anaesthetic complications.

Question 513

Acquired myopathies of late onset/

Answer 513

Part of systemic disease - Hyperthyroidism, Cushing's increased or decreased Ca. - Drugs: Steroids, Statins, ETOH.

Question 514

What are the inflammatory myopathies?

Answer 514

Inclusion body myositis Polymyositis Dermatomyositis

Question 515

What is the pathophysiology of Myasthenia Gravis?

Answer 515

AI disease mediated by Abs vs nicotinic Ach receptors | - Interferes with NM transmission via deletion of working post-synaptic receptor sites.

Question 516

Presentation of MG?

Answer 516

Increasing muscle fatigue - Extra-ocular: Bilateral ptosis, diplopia - Bulbar: voice deteriorates on counting to 50 - Face: myasthenic snarl on attempt to smile - Neck: head droop - Limb: asymmetric, prox weakness - Normal tendon reflexes - Weakness worsened by: pregnancy, infection, emotion, drugs (B-B, gent, opiates, tetracylines)

Question 517

Investigations for MG?

Answer 517

Tensilon Test - Give edrophonium IV - +ve if power improves within 1 min. Not commonly used due to risk of cardiac arrhythmia. Anti-AChR Abs: Increases in 90%, MuSK abs EMG: decreased response to a train of impulses Respiratory function: Decreased FVC Thymus CT TFTs

Question 518

Differentials for Muscle Fatigability?

Answer 518

Polymyositis SLE Botulism

Question 519

MG associations?

Answer 519

- <50yr MG is commoner in women and asssociated with other AI disease (DM, RA, Graves) and thymic hyperplasia - >50 yrs MG is commoner in men and associated with thymic atrophy or thymic tumour

Question 520

Treatment of MG?

Answer 520

Symptom control: Anticholinesterase: eg. pyridostigmine - Cholingeric SEs= SLUDGEM Immunosuppression - Rx relapse with pred - Steroid may be combined with azathioprine or methotrexate Thymectomy - Consider if young onset and disease not control by anticholinesterases - Remission in 25%, benefit in further 50%.

Question 521

Complications of MG?

Answer 521

Myasthenic Crisis - Weakness of resp muscles during relapse may be lethal - Monitor FVC: vent support if <20ml/kg - Plasmapheresis or IVIg - Manage trigger for relapse (drugs, infection) = Beta-blockers such as bisoprolol are common precipitants of myasthenic crises. ``` Penicillamine Quinidine, procainamide Beta-blockers Lithium Phenytoin Antibitocs: gentamicin, macrolides, quinolones, tetracyclines. ``` For surgery -

Question 522

What is the pathophysiology of Lambert-Eaton Syndrome?

Answer 522

Abs to VGCC decreased influx of Ca2+ during presynaptic excitation --> Decreased presynaptic ACh-vesicle fusion

Question 523

Causes of LEMS?

Answer 523

Paraneoplastic: Eg. SCLC | Autoimmune

Question 524

PResentation of LEMS?

Answer 524

``` Same as MG except: - LEMS LEgs weakness early (before eyes) - Extra: Autonomic and areflexia - Movement improves symptoms - Small response to edrophonium -Anti-VGC abs ```

Question 525

Management of LEMS?

Answer 525

3,4-diaminopyridine (amifampridine) or IVIG Do regular CXR/HRCTs as symptoms may precede Ca by 4 yrs

Question 526

What is Botulism

Answer 526

- Botulinum toxin prevents Ach vesicles release - Descending flaccid paralysis with no sensory signs Anti-cholingeric effects: Mydriasis, cycloplegia, n/v, dry mouth. - Benpen + antiserum

Question 527

Neurofibromatosis 1 features

Answer 527

``` CAFE NOIR - Cafe au lait spots 1st yr of life Increase in size and no with age Adults: >6, >15 mm across ``` - Axillary Freckling Skin folds - Fibromas, neuro- 1) Subcutaneous Small, gelantinous, violaceous nodules Appear at puberty May itch Increased with age 2) Plexiform - Overgrowth of nerve trunk and overlyign tissue - Large cutaneous mass Complications - Sarcomatous change, compression of nerve roots or GI bleeds. - Eye Lisch Nodules (brown/translucent iris hamartomas so use a slit lamp) Optic N. glioma. Neoplasia - CNS (Meningioma, ependyoma, astrocytoma) - Phaemochromocytoma - Chronic or AML Orthopaedic - Kyphoscoliosis - Sphenoid dysplasia Decreased IQ and epilepsy Renal - RAS --> Increased BP

Question 528

Management of NFT Type 1

Answer 528

MDT with GP yearly BP + cutaneous review Excise some neurofibromas Genetic counselling

Question 529

Differential for Cafe Au Lait?

Answer 529

NF Mccune-albright Multiple Lentigenes Urticaria Pigmentosa

Question 530

NF Type 2?

Answer 530

Rarer - AD Chromosome 22 but 50% are de novo.

Question 531

Features of NF type 2?

Answer 531

Cafe-au-Lait (Rare, fewer than NF1) - Bilateral vestibular schwannaomas (Characteristic, symptomatic by 20yrs, SNHL is first sign, then tinnitus, vertgio). - Juvenile Posterior Subcapsular Lenticular Opacity - Form of cataract - Bilateral Complications - Tender schwannomas of cranial and peripheral nerve and spinal nerve roots - Meningiomas, GLiomas.

Question 532

Management of NF Type 2

Answer 532

Hearing Test from puberty | MRI brain if abnormality detected

Question 533

What is Brown-Sequard SYndrome?

Answer 533

- Hemi-cord lesion - Ipsilateral loss of proprioception sense and vibration - Ipsilateral UMN weakness - Contralateral loss of pain sensation

Question 534

What is Syringomyelia?

Answer 534

- Syrinx: tubular cavity in central canal of the cervical cord. Downward displacement or herniation of the cerebellar tonsils through the foramen magnum. Malformation may be congentia. - Onset @ 30 yrs. - Symptoms may be static for years but then worsen fast. e. g on coughing, sneezing as pressure increased. - Commonly located in cervical cord - Syrinx expands ventrally affecting - Decussating spinothalamic neurons - Anterior horn cells - Corticospinal tracts

Question 535

Causes of Syringomyelia?

Answer 535

- Blocked CSF circulation with decreased flow from posterior fossa - Arnold-Chiari malformation (cerebellum herniates through foramen magnum) - Masses Spina bifida 2ndry to cord trauma, myelitis, cord tumours and AVM.

Question 536

What are the cardinal signs of Syringomyelia/

Answer 536

- Dissociated Sensory Loss (absent pain + temp --> Scar from burns). = Cape sign. - Spastic weakness (upper limbs) - Paraesthesia - Neuropathic pain - Upgoing plantars, bowel and bladder dysfunction. Preserved touch proprioception + vibration Root distribution reflects syrinx location. IN a cape distribution (upper limbs + chest). - Wasting/weakness of hand± claw hand - Loss of reflexes in upper limbs - Charcot Joints: shoulder and elbow Other signs - UMN weakness in lower limbs with upgoing plantars - Horner's syndrome - Syringobulbia: cerebellar and lower CN signs - Kyphoscoliosis

Question 537

Investigations of Syringomyelia?

Answer 537

MRI spine

Question 538

Management of Syringomyelia?

Answer 538

Decompression at the foramen magnum for Chiari Mal. Use Shunt.

Question 539

What is Friedrichs Ataxia?

Answer 539

- AR progressive degeneration of DRGs, spinocerebrellar and corticospinal tracts and cerebrellar cells. Mitochondrial disoder Onset in teenage Associated with HOCM and mild dementia

Question 540

What is the presentation of Friedrich's Ataxia?

Answer 540

``` - Pes Cavus and scoliosis Bilateral cerebellar signs (age <25) - Ataxia - Dysarthria - Nystagmus ``` Leg wasting + areflexia but extensor plantar Loss of lower limb proprioception and vibration sense Optic atrophy (paleness of the disc) HOCM --> ESM + 4th heart sound DM --> Hyperglycaemia 20 yr old present with progressive difficulty in walking. Legs are stiff she has been complaining of tripping . UNcle has similar symptoms. Paternal grandfather, also had life long difficulties walking and died of an MI at 59. On examination, she is dysarthrtic. Pes Cavus bilaterall.y Cerebellar signs

Question 541

What is hereditary spastic paraparesis?

Answer 541

Lower limb spasticity Ataxia Extrapyramidal signs

Question 542

HTLV-1?

Answer 542

Retrovirus in Japan and Caribbean? ``` Features - Adult T cell leukaemia/lymphoma - Tropical spastic paraplegia Slowly progressing spastic paraplegia Sensory loss and paraesthesia Bladder dysfunction ```

Question 543

How to present MS?

Answer 543

On inspection Mrs is well There is a right sided pronator drift and psuedoathetosis of the fingers (suggesting loss of proprioception). There is disuse atrophy of the muscles of the right arm. There are pyramidal signs as evidenced by rebound phenomenon and an intention tremor. The combination of cerebellar, dorsal and pyramidal signs suggest a central pathology and the most likely diagnosis is demyelinating disease such as multiple sclerosis. Mrs X is currently using a wheelchair and there is a urinary catheter in place. She needs a full functional assessment. I'd like to examine the fundi to complete my examination. The diagnosis can be confirmed on MRI looking for periventricular white matter lesion and VEPs. A full history would be beneficial to assess.

Question 544

Presenting INO

Answer 544

There is an ataxic nystagmus in the right eye as if fails to adduct. When the abducting eye is covered the other eye is able to adduct normally. This is intranuclear ophthalmoplegia which is most likely related to MS due to lesion in the medial longitudinal fasciculus.

Question 545

Causes of demyelination

Answer 545

``` HIV CIDP Multiple Myeloma MGUS HMSN ```

Question 546

How to present CMT?

Answer 546

On inspection of MR X there is symmetrical wasting of the muscles of the lower limbs distally with evidence of hammer toes with relative preservation of the thigh muscles with pes cavus. THere is also wasting of the distal small muscles of the hands. There is a LMN pattern of weakness in the extensor of the toes and feet and a loss of sensation to light touch in a stocking distribution in both legs. The ankle jerks are absent and the plantar reflexes show no response. The gait is high-stepping. There is a combined sensory and motor peripheral neuropathy - likely hereditary motor and sensory neuropathy. Mr X is currently using foot splints as mobility aids. He needs a full functional assessment. The diagnosis can be confirmed with a family history, nerve conduction studies and genetic testing.

Question 547

Pes Cavus causes?

Answer 547

High Foot arch that does not flatten on weight bearing - Causes: bilateral: Friedrich's ataxia, spinal cord tumours, syringomyelia. - Unilateral: polio, compartment syndrome, spinal trauma/tumour.

Question 548

PCAA

Answer 548

Posterior communicating artery aneurysms | Painful eye to move apart from laterally and downward. Pupil is enlarged and the eyelid drooping.

Question 549

How to present PD?

Answer 549

This gentleman has signs on inspection of a resting pill-rolling tremor, expressionless face and decreased blink rate. The gait is stooped, slow to initiate, and the steps are shuffling with decreased arm swing. On examination of the arms there are asymmetric: UMN signs including increased tone and lead-pipe rigidity in the left compared with right and some loss of muscle power in all groups tested. There is bradykinesia to all movements. There is no sensory involvement. This gentleman has signs consistent with Parkinsonism - he needs a full functional assessment and MMSE. He is currently limited in his mobility as he uses a walkign stick. I would like to take a drug history, look for postural BP drop and examine the cranial nerves for limited upgaze.

Question 550

Incontinence + dementia + shuffling gait

Answer 550

Normal pressure hydrocephalus - Failure to absorb CSF in subarachnoid spcce - LP - Normal pressure - Shunt will treat 70%. - Ventriculoperitoneal shunting. Wet, wobbly and whacky.

Question 551

72 yr old - acute onset dizziness, sensory loss over right side of his face and left arm and leg. On examination, his right pupil is smaller with a mild right ptosis. Which arterial territory is likely to be affected?

Answer 551

Right PICA (same side). Switches below that level.

Question 552

Ophthalmoplegia

Answer 552

Primary Position Max diplopia (outer image) 3rd nerve pupil involvement

Question 553

3rd nerve palsy

Answer 553

On inspection there has a complete right sided ptosis Globe down and out Pupil dilatation - if present means parasympathetic nerve damage, only in surgical causes like tumours/dissection/PCAA (classically painful) - Diabetes spares the pupil classically

Question 554

What muscle for ptosis?

Answer 554

LPS - levator palpebrae superioris

Question 555

Management of 3rd Nerve Palsy

Answer 555

Check the BP and the capillary glucose and examine for a 4th nerve palsy Dilated pupil warrants CT scan + angiography

Question 556

Causes of Medical 3rd nerve palsy

Answer 556

Mononeuritis multiplex, HTN + DM; autoimmune, MS. Additional cause include - Infections: lyme disease, syphillis - Autoimmune disease: SLE,RA, Small vessel vasculitidies - Malignancy: haematological malignancy Consider mass lesion or compression along route of nerve. - Mid-brain - Cavernous sinus - Base of skull.

Question 557

Pupil involvement - 4th nerve palsy

Answer 557

Eye is held adducted and slightly elevated and the patient has a head tilt away from the affect eye. Unable to depress eye in adduction - causes worse diplopia Outer image disappears when the affected eye is covered.

Question 558

Causes of 4th nerve palsy

Answer 558

Vertical diplopia - reading books or climbing stairs Trauma MOnoneuritis mutliplex Congenital III, IV, V1, VI - Cavernous sinus - Tumour, thrombosis, aneurysm

Question 559

6th Nerve palsy?

Answer 559

Longest intracranial nerve - false localising sign May be raised ICP or Cancer. Tumour till proven otherwise. Examine the other cranial nerves; 7th and 8th nerve palsies and cerebellar system. Fundoscopy: papilloedema Palsy results in defective abduction --> Horizontal diplopia.

Question 560

DDx Sixth Nerve Palsy

Answer 560

ICP Helps to be anatomical - so start at the nucleus Nerve itself (infiltrated by heavy metal/sarcoid, demyelinate) - Diabetic neuropathy - Compression by tumour, arterial aneurysm - CPA

Question 561

CPA - cerebello-pontine angle lesion

Answer 561

``` Petrous temporal bone, lateral pons, cerebellar First sign - loss of corneal reflex - Failure of Abduct eye - SNHL - Facial sensation loss - Cerebellar sign ``` -Which nerves? 69 Nooooo try 58.

Question 562

Weber's Syndrome

Answer 562

Midbrain: ipsilateral III CN and contralateral hemiparesis. Involves the oculomotor nerve resulting in an ipsilateral CN III palsy.

Question 563

Rule of S+M

Answer 563

Lateral (Sensory + sympathetic + pain) - Pons = 5,7,8 - MEdulla = 9,10,11 Medial (motor) - 3,4 (midbrain) - Pons (6) - Medulla (12)

Question 564

Causes of Bilateral Ptosis

Answer 564

MG Myotonic dystrophy Bilateral Horner's and 3rd Nerve palsy Congenital

Question 565

Dilated pupil?

Answer 565

Compressive 3rd nerve | Holmes Adie Pupil

Question 566

Compressed pupil?

Answer 566

Miosis Argyll-Robertson, Horner's

Question 567

Holmes Adie Pupil

Answer 567

Mainly in women Benign Associated with Sjorgens Sluggish pupil constriction to light, normal to accommodation. May be associated with reduced/absent reflexes and autonomic neuropathy.

Question 568

Argyll- Robertson

Answer 568

Small, irregularly shaped pupils Neurosyphillis Diabetes Accommodates but doesn;t react

Question 569

Wasting of hand muscle

Answer 569

Dorsal guttering - first to be affected in ulnar lesion.

Question 570

Presentation of stroke

Answer 570

This elderly lady is well on inspection and hold her right hand in a flexed position at the elbow with her right leg in extension. The gait is hemiplegic. On examination of the legs a pyramidal pattern of weakness is evident with UMN sign on the right including increased tone, reduced power to at least grade 4 (with relatively greater weakness in the flexors) and brisk reflexes. Coordinations is intact but sensations is impaired to light touch with no clearly demonstrable sensory level or dermatome. Those signs suggest a hemiparesis and the commonest cause of this would be a CVA. The patient is currently wheelchair bound. This lady needs a full functional assessment. To complete my exam i would like to fully examine the neurology in the arms and cranial nerves, look at an ECG for AF, the BP chart and dipstick the urine to aggressively control her secondary risk factors. Image the brain with a stroke protocol MRI.

Question 571

Wernicke's Encephalopathy

Answer 571

Thiamine Deficiency - chronic alcohol use or repeated vomiting Triad: Delirium, ataxia and an eye movement disorder (most common nystagmus, could be 6th nerve or INO) . Can also have peripheral neuropathy. Bilateral lateral rectus palsy. - Mamillary bodies - classically involved on MRI. IV thiamine for 2 days, then tablets. Irreversible damage = amnesic syndrome (Korsakoff psychosis). Addition of antero-retrograde amnesia and confabulation.

Question 572

Fundoscopy

Answer 572

Red reflex (loss in cataract, retinoblasta, vitreous haemorrhage) Disc Follow each vessel to periphery Look at the light - macula 3 C of disc - Colour, cup and contour

Question 573

Sudden visual loss

Answer 573

Vitreous - DM Retina (RA/RV occlusion, hemorrhagic macular degeneration) Optic nerve (ischaemia) Cortex Headaches? GCA? Unilateral - Compressive - Ischaemic - Demyelination Bilateral - Inherited - Toxic - Nutritional - Vitamin A

Question 574

Retinitis Pigmentosa?

Answer 574

Blind Patient (white stick) ABsent red reflex - associated cataract Peripheral retina - bone spickle pigmentation Optic atrophy (pale disc) 50% is sporadic Friedrich's ataxia Deafness (hearing-ad/white stick with red stripes): Kearns-Sayre syndrome. Discussion - blind by age 40, first sign - reduction in night vision Retinal degeneration Vitamin A - slow progression.

Question 575

Syndromes with RP?

Answer 575

Lawrence-Moon-Bardet- Diedl: polydactyl Usher: deafness Kearns-Sayre: ophthalmoplegia - can't see. Refsum: cerebellar ataxia

Question 576

Gradual Visual Loss

Answer 576

Cataract ARMD Diabetic maculopathy Glaucoma

Question 577

Diabetic Retinopathy - Made worse with pregnancy

Answer 577

Retinopathy - Need photocoagulation (reduce rate of progression) - Tunnel vision (peripheral vision worse). Should have a full assessment. - Aneurysm - Hard exudates - Cotton wool spots Maculopathy - Symptomatic loss of central vision (treated with laser).

Question 578

Neuroleptic malignant syndrome?

Answer 578

- Dopamine blockage by antipsychotics trigger massive glutamate release and subsequent neurotoxicity and muscle damage. - Presents with pyrexia, muscle rigidity, autonomic lability: HTN, Tachy, tachypnoea, agitated delirium with confusion. CK present in most cases. AKI secondary to rhabdo may develop in severe cases - leading to deranged U+E. Management - Stop antipsychotic - IV fluid s - Dantrolene in some cases. - Mainly dopamine agonist like bromocriptine.

Question 579

Motor, Sensory or both cranial nerves?

Answer 579

Some Say Marry Money But My Brother Says Big Brains Matter Most

Question 580

FLAIR MRI

Answer 580

Estimating onset of acute ischaemic stroke within 6 hours enabling more patients to receive thrombolytic therapy. T2 is more sensitive than T1 weighted imaging in detecting ischaemic changes.

Question 581

Diffusion weighted MRI?

Answer 581

Early changes after stroke event and diagnose vascular strokes highlighting the early presence of hypoxic oedematous changes.

Question 582

CT head with contrast?

Answer 582

Detecting cerebral mets and abscesses.

Question 583

Tuberous sclerosis?

Answer 583

Genetic condition of autosomal dominant inheritance. Neurocutaneous feature: - Depigmented ash-leaf spots which fluoresce under UV light. - Roughened patches of skin over lumbar spine. - Adenoma sebaceum (angiofibromas): butterfly distribution over nose. - Fibromata beneath nails - Cafe-au-lait spots may be seen. Neurological features - Developmental delay - Epilepsy - Intellectual impairment Also - Retinal hamartomas - Rhabodymoyomas - Gliomatous changes in brain - PKD

Question 584

Lennox-Gastaut syndrome

Answer 584

Severe, complex, childhood onset epilepsy. Associated with West Syndrome

Question 585

Neuropathic pain management?

Answer 585

Damage to nervous system - often difficult to treat and responds poorly to standard analgesia. Examples - diabetic neuropathy, post-herpetic neuralgia, trigeminal neuralgia, prolapsed intervertebral disc. First line - Amitriptyline, duloxetine, gabapentin or pregabalin - if the first-line drug treatment does not work try one of the other 3 drugs. - Tramadol may be used as rescue therapy for exacerbation. Topical capsaicin may be used for localised neuropathic pain

Question 586

Hoover sign

Answer 586

Push down with your right heel and lift left lef up against resistance. Sign of leg paresis is a specific manouever to distinguish organic and non-organic paresis. This is based on the concept of synergistic contraction. If a patient is genuinely making an effort, the examiner would feel the 'normal' limb pushing downwards against their hand as the patient tries to lift the 'weak' leg. Noticing this is indicative of an underlying organic cause of the paresis. If the examiner, however, fails to feel the 'normal' limb pushing downwards as the patient tries to raise their 'weak' leg, then this is suggestive of an underlying functional weakness, also known as 'conversion disorder'.

Question 587

Jendrassik Maneouvre

Answer 587

Compares a reflex with/without distraction.

Question 588

Hoffman's sign

Answer 588

Reflex test to investigation corticospinal tract lesion. This patient is likely to have degenerative cervical myelopathy [DCM], which is associated with upper motor neuron signs. Hoffmans sign is elicited by flicking the distal phalaynx of the middle finger to cause momentary flexion. A positive result is exaggerated flexion of the terminal phalanyx of the thumb. Patients with DCM often have subtle signs that are easily missed [1], but as a progressive condition, these are likely to get worse [2]. Whilst the sensitivity of signs is low (i.e. their absence does not rule out a problem), their specificity is high (i.e. there will be a problem). Therefore, in order to diagnose early DCM and improve patient outcomes, a high index of suspicion, alongside a comprehensive neurological examination and monitoring for progression is required.

Question 589

Psychogenic non-epilectic seizure

Answer 589

Remains conscious during whole-body convulsions, has no post-ictal state and can remember what happened. Focal seizures do NOT involve whole-body convulsions.

Question 590

MRC grading?

Answer 590

Grade 0 = No movement Grade 1 = Trace of contraction Grad 2 = Movement at the joint with gravity eliminated Grade 3 = Movement against gravity, but not against added resistance Grade 4 = Movement against an external resistance with reduced strength Grade 5 = Normal strength

Question 591

Brain abscess?

Answer 591

May result from a number of causes: CNS abscesses may result from a number of causes including, extension of sepsis from middle ear or sinuses, trauma or surgery to the scalp, penetrating head injuries and embolic events from endocarditis The presenting symptoms will depend upon the site of the abscess (those in critical areas e.g.motor cortex) will present earlier. Abscesses have a considerable mass effect in the brain and raised intra cranial pressure is common. Although fever, headache and focal neurology are highly suggestive of a brain abscess the absence of one or more of these does not exclude the diagnosis, fever may be absent and even if present, is usually not the swinging pyrexia seen with abscesses at other sites. Assessment of the patient includes imaging with CT scanning. Treatment is usually surgical, a craniotomy is performed and the abscess cavity debrided. The abscess may reform because the head is closed following abscess drainage.

Question 592

Intercostobrachial

Answer 592

Injured during axillary dissection. Armpit numbness.

Question 593

Cataplexy

Answer 593

Sudden and transient loss of muscular tone caused by strong emotion (laughter, being frightened). Around 2/3 patients with narcolepsy have cataplexy. Ranges from buckling knees to collapse.

Question 594

5-HT3 antagonists

Answer 594

Antiemetics used in the management of chemotherapy related nausea. Mainly act in the chemoreceptor trigger zone area of the medulla oblongata. Examples - ondansetron, granisetron. Constipation and prolonged QT interval are common SE.

Question 595

Reflexes?

Answer 595

Ankle - S1-S2 Button my shoe Knee - L3-L4 Kick the door Bicep - C5-C6 Pick up sticks Tricep - C7-C8 open the gate

Question 596

Carbamazepine

Answer 596

Carbamazepine is chemically similar to the tricyclic antidepressant drugs. It is most commonly used in the treatment of epilepsy, particularly partial seizures, where carbamazepine remains a first-line medication. Other uses include trigeminal neuralgia bipolar disorder ``` Adverse effects P450 enzyme inducer dizziness and ataxia drowsiness headache visual disturbances (especially diplopia) Steven-Johnson syndrome leucopenia and agranulocytosis hyponatraemia secondary to syndrome of inappropriate ADH secretion ```

Question 597

What is autonomic dysreflexia.

Answer 597

Can only occur if the spinal cord injury occurs above the T6 level. - Combination of severe HTN, flushing, sweating without congruent response in HR in the context of spinal cord injury. - Indicates autonomic dysreflexia - Indicates a discontinuity between nocioreceptors on the visera and brainstem autonomic centres due to cord injury. Afferent signals cause a sympathetic spina lreflex via thoracolumbar outflow. Usually centrally mediated, parasympathetic response is prevented by the cord lesion.

Question 598

What is a low pressure headache?

Answer 598

Commonly develops after a lumbar puncture Caffeine and fluids used to treat low pressure headache. Small volume of cerebrospinal fluid is removed, which reduced pressure around the brain. Second line: blood patch - small volume of the patients blood in to the epidural space a the site of the original lumbar puncture. The blood clots and in effect patches up the meningeal leak. usually develops within 24-48 hours following LP but may occur up to one week later may last several days worsens with upright position improves with recumbent position Factors contributing to headache - Increased needle size - Direction of bevel - Not replacing the stylet - Increased number of LP attempts Factors which do not contribute to headache - Increased volume of CSF removed - Bed rest following procedure - Increased fluid intake post procedure - Opening pressure of CSF - Position of patient

Question 599

Axillary nerve

Answer 599

Winds around the bone at the neck of the humerus. Also at risk during shoulder dislocation.

Question 600

Restless Leg syndrome?

Answer 600

Restless legs syndrome (RLS) is a syndrome of spontaneous, continuous lower limb movements that may be associated with paraesthesia. It is extremely common, affecting between 2-10% of the general population. Males and females are equally affected and a family history may be present Clinical features uncontrollable urge to move legs (akathisia). Symptoms initially occur at night but as condition progresses may occur during the day. Symptoms are worse at rest paraesthesias e.g. 'crawling' or 'throbbing' sensations movements during sleep may be noted by the partner - periodic limb movements of sleeps (PLMS) Causes and associations - there is a positive family history in 50% of patients with - idiopathic RLS - iron deficiency anaemia - uraemia - diabetes mellitus - pregnancy Mangement simple measures: walking,stretching, massaging affected limbs treat any iron deficiency dopamine agonists are first-line treatment (e.g. Pramipexole, ropinirole) benzodiazepines gabapentin Ropinirole

Question 601

Spontaneous intracranial hypotension

Answer 601

Spontaneous intracranial hypotension is a very rare cause of headaches that results from a CSF leak. The leak is typically from the thoracic nerve root sleeves. Risk factors include connective tissue disorders such as Marfan's syndrome. Key features strong postural relationship with the headache generally much worse when upright. Patients may, therefore, be bed-bound Investigations MRI with gadolinium: typically shows pachymeningeal enhancement Management usually conservative if this fails an epidural blood patch may be tried

Question 602

Bacterial vaginosis?

Answer 602

Anaerobic organisms = Gardnerella vaginalis. Fall in lactic acid - raised vaginal pH. Fishy, offensive odour. Amsel criteria - Thin, white homogenous discharge. - Clue cells on microscopy - Vaginal pH >4.5 - positive whiff test. Manage with oral metronidazole

Question 603

Epidural spinal abscess investigation for confirmation?

Answer 603

Full spine MRI to search for skip lesions. SEA is commonly caused by Staph A. Due to IVDU or direct inoculation. Presents with fever, back pain, focal neurological deficits.

Question 604

Pressure Sores?

Answer 604

``` Pressure ulcers develop in patients who are unable to move parts of their body due to illness, paralysis or advancing age. They typically develop over bony prominences such as the sacrum or heel. The following factors predispose to the development of pressure ulcers: malnourishment incontinence lack of mobility pain (leads to a reduction in mobility) ``` Waterlow score used to screen for patients who are at risk of developing pressure area.

Question 605

Head injury ATLS - patient comes in with cerebral contusion what is the management?

Answer 605

Insert an intracranial pressure monitoring device. For those with GCS 3-8 with normal CT. Mandatory for patients with GCS 3-8 with abnormal CT can.

Question 606

Bilaterally dilated pupils?

Answer 606

Poor CNS Perfusion

Question 607

Unilaterally dilated pupils?

Answer 607

3rd nerve compression secondary to tentorial herniation

Question 608

Bilaterally constricted pupils?

Answer 608

Opiates Pontine lesions Metabolic encephalopathy

Question 609

Unilateral constricted pupils

Answer 609

Sympathetic pathway disruption

Question 610

Brain stem death?

Answer 610

Criteria for brain stem death testing - Deep coma of known aetiology - reversible cause excluded - No sedation - Normal electrolytes.

Question 611

Testing for brain death?

Answer 611

- Fixed pupils which do not respond to sharp changes in the intensity of incident light - No corneal reflex - Absent oculo-vesibular reflex - No response to supraorbital pressure - No cough reflex to bronchial stimulation or gagging response - No observed respiratory effort in response to disconnection of ventilator.

Question 612

When is an urgent neurosurgical review warranted before CT?

Answer 612

GCS <8 or = 8 with open fracture and depressed skull fracture.

Question 613

When should a patient with a +ve Battle's sign have a CT?

Answer 613

Within 1 hr.

Question 614

What are the clinical suspicions of cervical spine injury?

Answer 614

Age 65 and older Danger mechanism of injury - fall from height, axial load to head like diving. Focal peripheral neurological deficit Paraesthesia in the upper or lower limbs Provisional written radiology report should be made within 1hr of scan being performed.

Question 615

What is binocular vision post-facial trauma and pain on opening mouth suggest?

Answer 615

Depressed fracture of the zygoma.

Question 616

Infants presenting with hydrocephalus?

Answer 616

Present with increased head circumference, a bulging fontanelle and sunsetting of the eyes (pressure on the tectal plate)

Question 617

Hydrocephalus definition?

Answer 617

Hydrocephalus is defined as a condition in which there is an excessive volume of cerebrospinal (CSF) fluid within the ventricular system of the brain and is caused by an imbalance between CSF production and absorption.

Question 618

Symptoms of hydrocephalus?

Answer 618

Headache (typically worse in the morning, when lying down and during valsalva) Nausea and vomiting Papilloedema Coma (in severe cases)

Question 619

Types of hydrocephalus

Answer 619

Obstructive (‘non-communicating’) hydrocephalus - due to the structural pathology blocking the cerebrospinal fluid. Non-obstructive (‘communicating’) hydrocephalus - increased production or failure of absorption - post-haemorrhagic.

Question 620

Normal pressure hydrocephalus triad?

Answer 620

Dementia Incontinence Disturbed gait

Question 621

Diffuse axonal injury?

Answer 621

Head is rapidly accelerated or decelerated. Multiple haemorrhages Diffuse axonal damage in white matter.