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MEDICINE NEW > Neurology > Flashcards

Neurology Flashcards

1
Q

Causes of bilateral facial palsy

A

Lyme’s disease
Guillain Barré
Sarcoidosis

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2
Q

What is synkinesia?

A

In Parkinson’s exam, whilst examining tone, getting them to tap their leg and it accentuating the cogwheel rigidity

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3
Q

What are the causes of a combined upper and lower motor deficit

A

Fred’s Tabby Cat Seeks Mice

Freidrich's Ataxia
Taboparesis (syphillis)
Cervical spondylosis
Subacute degeneration of the cord
Motor neurone disease
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4
Q

If a nystagmus is worse when looking to the left side, where is the lesion site if:
A. It is caused by a cerebellar lesion
B. It is caused by vestibular nerve/nuclear lesion (CN VIII)

A

A. Left (ipsilateral)

B. Right (contralateral)

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5
Q

Patient has ataxic gait and trunk but limbs have normal tone, coordination and no dysmetria evident. Where is the site of the lesion?

A 
Cerebellar vermis (a central part)
(Often alcohol may causes vermis atrophy)
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6
Q

Causes of unilateral cerebellar syndrome (DASHING SYMPTOMS)

A

Demyelination (MS) or brain stem stroke on ipsilateral side

Rarely: posterior fossa tumour, abscess

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7
Q

Causes of bilateral cerebellar syndrome

A 
DADS HAR
Drugs (anticonvulsants)
Alcohol
Demyelination (MS)
Stroke (brain stem)

Hypothyroid
Antineuronal antibodies (paraneoplastic syndrome)
Rare- Freidrich’s, Ataxic telangiectasia

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8
Q

What is internuclear opthalmaplegia and which condition does bilateral opthalmaplegia occur in?

A

Inability to adduct eye when looking to opposite side, contralateral eye gets a nystagmus.

In MS due to demyelinating lesion of the medial longitudinal fasciculus

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9
Q

Young woman has pain on eye movement and rapid reduction in central vision, with tingling in her right arm. What is the diagnosis?

A

Multiple sclerosis- unilateral optic neuritis is often the first sign
Ishihara plates might show a reduction in red colour vision

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10
Q

What objective imaging or tests support a clinical diagnosis of MS?

A

Based on the McDonald criteria:
MRI plaques disseminated in time and space
Oligoclonal IgG bands in CSF (not serum)
Delayed evoked potentials- normal amplitude

Neuromyelitis Optica IgG antibodies (Devic’s syndrome)

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11
Q

Medications used in MS:

A

All the medications reduce relapses in relapsing and remitting MS but do not alter progression of the disease ultimately.

Relapse reducing:
Immunomodulation- IFN B + Glatiramer
Monoclonal antibodies: Alemtuzamab (anti-T cell) + Natalizumab (anti VLA-4 R that allows Abs to cross the BBB)

Symptomatic:
Methylprednisolone reduces length of short relapses
Baclofen- spasticity
Botox- tremors
Carbamezepine- seizures
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12
Q

How can Devic’s syndrome be distinguished from MS?

A

Devic’s syndrome- Anti-aquaporin 4 antibodies in CSF (60%)
Also known as neuromyelitis optica antibodies

Both may get transverse myelitis- loss of motor, sensory, autonomic, reflex + sphincter function below lesion
Both may get optic atrophy (pale disc, altered acuity)

Rx: for Devic’s is plasma exchange

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13
Q

Difference between decorticate and decerebrate posturing and their cause?

A

No-one celebrates in decerebrate posturing (hands by sides, no clapping) and means brain stem is affected ?vegetative state
If somone goes from decorticate to decerebrate = pontine tonsils at risk of herniation

In decorticate posturing, they look meek like they’re in court, arms bent up (cerebrum, internal capsule and thalamus may be involved)

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14
Q

In a stroke patient with decorticate posturing, which muscle groups would you expect to be stronger in upper and lower limbs?

A

Decorticate (not decerebrate where no one is celebrating because brain stem is involved)
Is extended legs and flexed arms, so on examination

Flexors stronger in upper limb
Extensors stronger in lower limb

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15
Q 
Young patient (in 30s) presents with stroke-like findings, acute onset of focal neurological deficit.
What other causes of stroke need to be considered?
A

Blood perfusion:
Sudden BP drop (ie sepsis, affects watershed zone)
Carotid artery dissection
Subarachnoid haemorrhage

Vessel changes:
Vasculitis (check ESR)

Blood components:
Venous sinus thrombosis
Thrombophilia (like antiphospholipid syndrome)
Inherited- Fabry’s (lysosomal storage), CADASIL

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16
Q

In Fabry disease, which parts of the body may there be problems with and what are the problems?

A 
X linked lysosomal storage disease due to a-galactosidase A
Skin- angiokeratoma (burgundy moles)
Eyes- lens opacities
Heart- MI, syncope, arrhythmia
Kidneys- failure
CNS- stroke
Nerves- neuropathy
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17
Q

What is CADASIL?

A

Cerebral Autosomal Dominant Arteriopathy with Subcortical Infarcts + Leucoencephalopathy

Main genetic cause of strokes due to Notch3 gene mutation (19q) affecting vascular smooth muscle
PC: Migrane, TIA, mood disorders, dementia ± psuedobulbar palsy
IHx: MRI

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18
Q

Nme 5 types of lacunar infarct:

A
  1. Pure motor
  2. Ataxic hemiparesis (cerebellar signs + weakness)
  3. Pure motor
  4. Dysarthria/clumsy hand
  5. Mixed sensorimotor
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19
Q

What are the 3 H’s of a total anterior circulation stroke?

A

Hemiparesis
Homonymous hemianopia
High cortical deficit (dysphasia, visual inattention, dyspraxia)

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20
Q

When would a UMN lesion mimic a LMN lesion?

A

In the first few hours, before the spasticity and hyper-reflexia develop. This occurs from ‘spinal shock’- not well understood

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21
Q

Patient has hemiparesis of the right leg and reduced cognition- broadly where is the site of the lesion?

A

Left cerebral hemisphere

If hemiparesis with epilepsy, reduced cognition or a homonymous hemianopia it is in the cerebral hemispheres

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22
Q

Cranial nerve palsy in CN 3-8 with contralateral hemiplegia means the site of the stroke is where?

A

Brainstem on the side of the cranial nerve deficit

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23
Q

Where does pain, temperature, proprioception and vibration sense travel in the spinal cord?

A

Pain + Temp- raise ALert = Anterolateral (immediate decussation to get away from danger)

Vibration + Proprioception = Dorsal columns (ring the DOORbell, open the door)

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24
Q

How does the side of sensory loss differ if the lesion is in the brainstem or above it?

A

In the brainstem- lesion is ipsilateral to cranial nerve sensory loss and contralateral to arm + leg
Above- contralateral for both (sensory nerves have all decussated by then)

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25
Q

Which artery predominantly supplies the motor cortex that controls the leg?

A

The anterior cerebral artery- think of the leg hanging over the sulcus edge.

Middle cerebral- arm + face

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26
Q

Where does the vertebrobasilar arteries supply and what symptoms occur from occlusion?

A

Brainstem, cerebellum + occipital lobes

Any symptoms of
Hemi/quadraplegia + hemisensory loss
Hemianopia, cortical blindness, diplopia
Vertigo, nystagmus, ataxia, dysarthria, dysphasia

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27
Q

Which 2 parts of the brain may be involved in lateral medullary syndrome and symptoms?

A

Lateral medulla or inferior cerebellum
Vertebral artery occlusion of posterior inferior cerebellar artery

Vertigo, dysphagia, nystagmus, ipsilateral ataxia, vomiting
Ipsilateral Horner’s, crossed sensory loss (ipsilateral facial, contralateral to trunk + limbs)

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28
Q

Locked in syndrome is caused by damage to which structure because of which artery?

A

Ventral pons

Pontine artery

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29
Q

Where is Wernicke’s area that if damaged may cause Wernicke’s aphasia?

A

Supramarginal gyrus of parietal lobe and upper part of the temporal lobe

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30
Q

Where is Broca’s area, that if damaged may cause Broca’s aphasia?

A

Inferior frontal gyrus

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31
Q

If a patient can’t repeat ‘no ifs, ands or buts’ what type of aphasia do they have and where might the lesion be?

A

Conductive aphasia- arcuate fasciculus

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32
Q

On the speech exam, the speech is slurred and the patient barely opens their mouth. What are the causes of a spastic dysarthria?

A

Bilateral UMN weakness:
Pseudobulbar palsy (brainstem lesion, cerebrovascular disease of vertebrobasilar circulation)
Motor neurone disease

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33
Q

How can the cause of dysphonia be distinguished during an exam using a simple request?

A

Normal cough- laryngitis
Fatiguable- myaesthenia gravis

Others: Guillain Barre (ascending weakness)
CN X damage

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34
Q

3 causes of slurred staccato speech dysarthria:

A

Cerebellar lesions:
Alcohol intoxication
Multiple sclerosis
Phenytoin toxicity

Rarely inherited ataxias

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35
Q

Common causes of spastic hemiparesis (seen as scissoring gait)

A

Cerebral palsy
Multiple sclerosis
Cord compression

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36
Q

Causes of apraxic gait (patient looks like they have forgotten how to walk)- uncoordinated, dithering at attempts to lift leg

A 
Cortical integration of movement is impaired
Normal pressure hydrocephalus
Cerebrovascular disease (often frontal lobes)
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37
Q

Causes of high stepping gait:

A

Foot drop due to:
Common peroneal nerve lesion (wraps around the fibular bone)
L5 radiculopathy (root compression)
Bilateral: Cerebrovascular event

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38
Q

Where is the site of the lesion if L hemiplegia with R-sided drooping eyelid, fixed dilated pupil, looking down and out

A

A) Right midbrain- third nerve palsy

Posterior cerebral artery branches

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39
Q

Where is the lesion: R sided hemiparesis of arm + leg with double vision, on examination the L eye can’t look towards the left

A

Contralateral hemiparesis with ipsilateral 6th nerve palsy, may be 7th nerve involvement in these cases (facial muscle weakness with no sparing of the forehead)

= Pontine lesion
(3-4 midbrain, 5-8 pons, 9-12 medulla)

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40
Q

Patient has L sided weakness of arm and on sticking their tongue out, it deviates to the R. Where is the lesion?

A

Isolated R sided CN 12 weakness with L sided hemiparesis:

Medulla

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41
Q

Which cranial nerves may be implicated in a tumour in the cerebellopontine angle?

A

5, 7, 8

5- corneal reflex absent, numbness, weak muscles of mastication
7- facial muscle paralysis
8- hearing problem + balance

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42
Q

Which cranial nerves would be affected in a cavernous sinus lesion?

A

3, 6, 5a

Down + out eye, wide pupil, droopy lid
Difficulty abducting
Numbness over the forehead and nose

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43
Q

Which nerves are affected in jugular foramen syndrome?

A

9, 10 + 11

Impaired gag reflex
Weak sternocleidomastoid

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44
Q

Which autonomic nerves control the light reflex and accommodation reflex?

A

Parasympathetic nerves

Constrict

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45
Q

Cause of complete compared to a partial ptosis:

A

Complete- 3rd nerve palsy

Partial- Horner’s syndrome (symp nerves), age-related ptosis (weakening of levator muscles)

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46
Q

What is Argyll Robertson pupil and 3 causes?

A

Like the prostitute: reacts but does not accommodate + small pupil

Syphilis, diabetes mellitus, MS

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47
Q

Central and peripheral causes of Horner’s syndrome

A

Partial ptosis, meiosis, anhydrosis + enopthalmus

Central: hypothalamus, medulla, cervical cord (exits at T1)
Stroke- lateral medullary syndrome, demyelination

Peripheral: Pancoast’s, carotid dissection (travels with carotid)

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48
Q

Causes of reduced acuity, not correctable with pinhole test:

A

Corneal lesion: ulcer or oedema
Cataract
Age-related macular degeneration
Retinal haemorrhage
Optic neuropathy (MS, ischaemic, compressive)
Optic tract, medial longitudinal fasciculus, occipital cortex

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49
Q

Patient has a homonymous quadrantanopia, how do you know if the lesion is in the parietal or temporal lobe?

A

Lower quadrant missing in vision- parietal

Upper quadrant unseen- temporal

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50
Q

Loss of peripheral vision (constricted visual fields)

A

Glaucoma
Chronic papilloedema

Retinitis pigmentosa

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51
Q

In a patient with a CN 3 palsy, what feature would make you consider it was more likely to be due to diabetes than a posterior circulation aneurysm?

A 
The constrictor (parasympathetic) fibres of the nerve are superficial, so compressing forces will affect them (= dilated)
Whereas diabetic and ischaemic forces seem to affect the axon worst with sparing of the outer constrictor fibres
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52
Q

Top causes of isolated CN 3, 4 or 6 palsy

A

Diabetes mellitus
Atherosclerosis

Rarely Vasculitis, Guillain Barré

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53
Q

What is internuclear opthalmoplegia and where is the lesion located?

A

In a INO, on abduction there is a nystagmus looking temporally, but can adduct nasally slowly without nystagmus.

Affects medial longitudinal fasciculus which joins CN 3-4 in midbrain with CN 6 in the pons
Affected in MS

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54
Q

Describe the full function of cranial nerve VII:

A

Face, ear, taste, tear

Muscles of facial expression
Stapedius (dampen sound)
Anterior 2/3rds of tongue
Parasympathetic lacrimal gland (+)

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55
Q

Branches of the trigeminal nerve, which mediates the corneal reflex?

A

Ophthalmic does

Maxillary
Mandibular

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56
Q

On asking the patient to close their eyes what will you observe if they have a LMN seventh nerve palsy?

A

Bell’s sign: eyes roll back into head on that side

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57
Q

Causes of one sided CN 7 palsy, no forehead sparing:

A

Unilateral LMN CN VII palsy:

Bell’s palsy
Pontine vascular accident
Ramsay Hunt syndrome- vesicles in external auditory meatus

Parotid tumours, Lyme disease

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58
Q

Causes of bilateral CN VII weakness, no sparing of forehead:

A

Sarcoid
Guillain Barré

Myaesthenia gravis
Lyme disease

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59
Q

Causes of one-sided CN VII palsy, sparing of the forehead:

A

UMN CN 7 palsy
Cerebrovascular accidents
MS

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60
Q

Causes of bilateral CN 7 weakness, forehead sparing:

A

Bilateral UMN:
Pseudobulbar palsy- lower brainstem
MND

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61
Q

Which cranial nerves mediate the jaw jerk?

A

Sensory branches of V and the motor branches of V

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62
Q

You test the corneal reflex on a patient, how does the site of the lesion differ depending on whether one eye or both eyes blink?

A

If neither eye closes on touch, then the eye didn’t feel it (CN Va lesion)
If one eye doesn’t close there’s a CN 7 lesion

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63
Q

What type of tuning fork is used for Weber’s + Rinne’s compared to testing vibration sense?

A

Weber’s- 516Hz (got to add 5 + 1 to find your solution-6)

Vibration- 128Hz (got to prepare the patient, 1, 2..8!)

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64
Q

Which antiepileptic causes gum hypertrophy?

A

Phenytoin

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65
Q

In a patient with a R sided cerebrovascular accident in a hemisphere controlling CN 11, how would trapezius and sternocleidomastoid be affected?

A

L sided trapezius weakness

R sided sternocleidomastoid weakness (decussates twice so is ipsilateral to cerebral hemisphere)

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66
Q

In a patient with weak shoulder shrugging and sternocleidomastoid on the same side, what else should be tested?

A

CN 9 + 10 palsies- suggests jugular foramen lesion (like a glomus tumour or neurofibroma)

Test by ‘Ahhh’ (10) + gag reflex + making ‘gah’ sound (10)
Gag reflex 9 = afferent, 10 = efferent

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67
Q

Which nerve supplies:

  1. Arm extensors
  2. Intrinsic muscles of the hand mostly
A
  1. Radial nerve

2. Ulnar nerve (T1 supply)

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68
Q

Which intrinsic hand muscles does the median nerve supply?

A 
LOAF
Lateral two lumbricals
Opponens pollicis
Abductor pollicis brevis
Flexor pollicis brevis
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69
Q

How can an UMN and LMN lesion of the accessory nerve (CN 11) be differentiated?

A

UMN- ipsilateral sternocleidomastoid weakness + contralateral trapezius weakness

(Sternoicleidomastoid nerves decussate twice)

LMN- weakness on the same side

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70
Q

Describe the nerve roots responsible for different actions in the arm:

A 
Shoulder abduction: C5
Elbow flexion: C5, C6
Elbow + wrist + finger extension: C7
Finger flexion: C8
Intrinsic muscles hand: T1
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71
Q

Describe the muscle + nerves responsible for the movements of shoulder abduction:

A

Deltoid
Axillary nerve
C5

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72
Q

Describe the muscle + nerves responsible for the movement of elbow flexion

A

Biceps brachii
Musculocutaneous nerve
C5,C6

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73
Q

Describe the muscle + nerves responsible for the movements of elbow extension

A

Triceps
Radial nerve
C7

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74
Q

Describe the muscle + nerves responsible for the movements of finger extension

A

Extensor digitorum
Posterior interosseous nerve (radial branch)
C7

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75
Q

Describe the muscle + nerves responsible for the movements of finger flexion

A

Flexor digitorum superficialis + profundus
Ulnar nerve mostly
C8

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76
Q

Which nerve roots are responsible for the leg movements:

A

Hip flexion: L1, L2
Knee extension: L3, L4
Dorsiflexion + extension of big toe: L5
Hip extension, knee flexion, plantarflexion: S1

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77
Q

Describe the muscle + nerves responsible for the movements of hip flexion

A

Iliopsoas
Lumbar sacral plexus
L1-L2

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78
Q

Describe the muscle + nerves responsible for the movements of hip extension

A

Gluteus maximus
Inferior gluteal nerve
L5, S1

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79
Q

Describe the muscle + nerves responsible for the movements of knee flexion

A

Quadriceps femoris
Femoral nerve
L3, L4

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80
Q

Describe the muscle + nerves responsible for the movements of knee extension

A

Hamstrings (semitendonosis, semimembranosis, biceps femoris)
Sciatic nerve
L5, S1

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81
Q

Describe the muscle + nerves responsible for the movements of foot dorsiflexion

A

Tibialis anterior
Deep peroneal nerve
L4, L5

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82
Q

Describe the muscle + nerves responsible for the movements of planarflexion of the foot

A

Gastrocnemius
Posterior tibial nerve
S1

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83
Q

Describe the muscle + nerves responsible for the movements of big toe flexion

A

Extensor hallucis longus
Deep peroneal nerve
L5

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84
Q

For the reflexes of the body, which nerves mediate them?

A

Biceps- musculocutaneous
Triceps- radial
Supinator- radial (watch brachioradialis)

Knee- femoral
Ankle- tibial

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85
Q

Weak in arms and legs, brisk reflexes, positive Babinski sign
Where is the lesion?

A

Cervical cord or bilateral pyramidal tracts (go from cerebral hemispheres to brainstem/spinal cord)

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86
Q

Patient is weak in all 4 limbs, with absent reflexes, how can a myopathy be discriminated from a polyradiculopathy or peripheral neuropathy?

A

In myopathies, sensation should be normal

87
Q

L sided arm + leg weakness, with R sided pain and temperature loss indicate which type of lesion?

A

Brown Sequard- L sided half cervical cord lesion

88
Q

5 categories of myopathy causes

A

Inherited: dystrophies (Duchenne’s, Becker’s, myotonic)
Inflammatory: polymyositis, dermatomyositis, polymyalgia rheumatica
Endocrine: steroids, high or low thyroid
Metabolic: glycogen storage
Toxic: alcohols, statins, chloroquine

89
Q

What commonly causes radiculopathies?

A 
Disc protrusion:
Commonly C6 (affects elbow flexion, biceps reflex)
or C7 (affects elbow, wrist + finger extension)
Commonly L5 (affects dorsiflexion, big toe extension)
Or S1 (affects plantarflexion, ankle reflex)

Rarely tumours, neurofibromas

90
Q

Common cause of mostly motor peripheral neuropathy

A

Guillain Barré (polyradiculopathy, proximal weakness)

Rarely porphyria
Lead poisoning

91
Q

Cause of peripheral sensorimotor neuropathies

LMN signs + sensory loss

A

EACH MET
Endocrine- diabetes mellitus, hypothyroidism
Amyloidosis
Charcot Marie tooth

Metabolic- vitamin B1 + B12 deficiency, uraemia, metal toxicity

92
Q

Causes of mononeuritis multiplex:
WARDS PLC

(On wards please look c the underlying link)

A 
Wegeners
AIDs/amyloid
Rheumatoid arthritis
Diabetes mellitus
Sarcoid
PAN
Leprosy
Carcinomatosis
93
Q

Causes of peripheral neuropathies (affecting long nerves- glove + stocking)

A

Diabetes mellitus
Alcohol-related B1 deficiency
Drugs- vincristine, pyrazinamide

94
Q

Features + cause of a proximal myopathy to find on examination

A

Proximal muscle weakness, distal sparing
Absent reflexes, muscle wasting, waddling gait
No sensory change

Guillain Barré- acute, Genetic- muscular dystrophy, metabolic storage
Endo- Thyroid, parathyroid, Addison’s, Cushing’s
Metabolic- K+ high or low
Steroids, statins

95
Q

Signs indicative of a peripheral neuropathy on a lower limb assessment + causes

A

Skin dryness, trauma, joint deformation
Loss of all sensory modalities in a glove and stocking distribution
Absent/ hypoactive reflexes
Preserved motor ability often (heel toe ability impaired)

Diabetes mellitus
Deficiency of B1 (alcohol related)
Drugs- vicristine, pyrazinamide

96
Q

Signs indicative of multiple sclerosis on a neuro lower limb exam

A 
Spastic weakness (UMN)
Increased tone, hyper-reflexic

Gait: spastic scizzoring
ataxic (cerebellar involvement)
hemiplegia (wheelchair)

Sensory: Complete loss of autonomic, sensory + reflexes (transverse myelitis)
or milder dysaesthesia (pins + needles)
Or loss of vibration

97
Q

Patient has spastic legs, with sensory loss, but preserved vibration and proprioception. What has happened?

A

Anterior spinal artery occlusion- preservation of dorsal columns

If in the upper limbs with LMN wasting of muscles could be syringomyelia

98
Q

Patient has bilateral
Reduced tone, power, reflexes
With muscle wasting

No pain or temperature sense, but vibration and proprioception.
What is the likely cause?

A

Syringomyelia- fluid filled cavity that spreads within the spinal cord

Other signs that may be present:
UMN signs in legs (Babinski’s ++reflexes)
Horner’s
Cerebellar signs if extending into the brainstem (syringobulbia)

99
Q

Causes of syncope/blackouts

A

Vascular:
Vasovagal- faint (bradycardia + peripheral vasodilation)
Orthostatic hypotension- (inadequate vasomotor reflexes)

Cardiac:
Stoke-Adams attacks- transient arrhythmias (heart block)
Effort syncope- syncope on exertion = cardiac origin (AS, HCM)

Neurogenic:
Carotid sinus syncope- hypersensitive baroreceptors (shaving, head turning)
Epilepsy- may occur when lying down

Metabolic:
Hypoglycaemia

100
Q

In a patient who has a blackout, how does the speed of recovery indicate potential cause?

A

Slowest in epilepsy, post-ictal confusion
Then vasovagal
Fastest is a arrhythmic Stokes-Adams attack

NB: vasovagal can’t occur when a patient is lying down

101
Q

A patient falls to the ground as their legs give way, they don’t lose consciousness. How would you determine if it was due to a drop attack or due to hydrocephalus?

A

Drop attack- resolves spontaneously
Hydrocephalus- takes hours to get up again, also has the following triad
(1. Gait disturbance of wide-based, shuffling
2. urinary incontinence
3. dementia)

102
Q

What is tilt table testing and why is it done?

A

To differentiate between reflex syncope (vasovagal) and orthostatic hypotension

Bradycardia + syncope = reflex syncope
Low BP = orthostatic hypotension

103
Q

Investigations to consider if a patient comes in with an acute confusional state (delirium)?

A

FBC- infection or high or low Hb
U+E- glucose, Na+, uraemia
LFTs- alcohol withdrawal, liver failure, encephalitis
Blood glucose
ABG- hypoxia
Septic screen- urine dip, CXR, blood cultures
ECG- MI

Others: MRI/CT, malaria films, EEG (Epilepsy)

104
Q

Which haematological conditions can cause a TIA (transient focal neuro deficit lasting < 24 hours)

A 
Hyperviscosity syndromes:
Polycythaemia (^ platelets)
Sickle cell anaemia
Leukostasis (^ WCC)
Myeloma

Commonest TIA cause is carotid thromboembolism, then thrombus post MI or in AF or in valve disease

105
Q

Mimics of a TIA

A

Migrane aura, focial epilepsy
Hypoglycaemia
Hyperventilation

106
Q

Investigations to do if a patient comes in with a TIA?

A

FBC- (hyper-viscosity mimics: leukostasis, myeloma)
ESR- vasculitidies can cause
U+Es- may impact choice of therapy
Glucose- increases in stroke, hypoglycaemia mimics
Lipids
ECG- AF
Carotid doppler

107
Q

Rx for a TIA

A

Aspirin 300mg OD within 24 hours

Then
Clopidogrel 75mg OD
+ 20-80mg Statin

Will need a 300mg Clopidogrel loading dose
impacts ADP receptors on platelets preventing aggregation

108
Q

When would you treat a TIA with warfarin rather than antiplatelet drugs?

A

If it suspected to originate from cardiac emboli, secondary to AF, MI or mitral stenosis

109
Q

How long do patients have to avoid driving for, once they’ve had a TIA?

A

1 month

Have to inform DVLA if getting multiple attacks in short time or residual deficit

110
Q

How do you decide which patients with a TIA need to see a specialist within 24 hours rather than the routine 7 days time?

A

A score of 4 or more:

Age over 60 = 1
Blood pressure >140/90 = 1
Clinical features of 
     Speech disturbance without weakness = 1
     Unilateral weakness = 2
Duration of Sx
      10-59 mins = 1
      >1 hour = 2
Diabetes = 1
111
Q

Where do lacunar infarcts occur?

A

Basal ganglia, thalamus, pons or internal capsule

112
Q

5 outcomes of lacunar infarct

A 
Ataxic hemiparesis
Pure motor
Pure sensory
Sensorimotor
Dysarthria + clumsy hand
113
Q

Aside from when a patient will need thrombolysis within 4.5 hours, what are the other indications for urgen tCT/MRI rather than in 24 hours?

A
  1. Cerebellar stroke (haematoma there may need urgent evacuation)
  2. High risk of haemorrhage- GCS, ICP up, anticoagulated, headache severe, meningism
114
Q

What medical treatment should be given within 24 hours of a stroke, aside from thrombolysis

A

Aspirin 300mg for 2 weeks

Then clopidogrel 75mg afterwards

115
Q

CI to thrombolysis in stroke, aside from haemorrhage seen on CT

A
  1. Lumbar puncture or liver biopsy in last 24 hours
  2. Major trauma, surgery, head injury, birth in last 3 weeks
  3. Cerebral AV malformation, liver disease, portal hypertension
  4. Cerebral malignancy, seizures at presentation
  5. Bleeding disorder, previous CNS bleed, GI bleed in last month
  6. Anticoagulated, platelets <100
116
Q

Name the risk factors for stroke:

A 
Hypertension
Diabetes
Hyperlipidaemia, Hypercholesterolaemia
Smoking, drinking
The pill
AF
Syphilis
117
Q

What INR is the target in a patient who is taking Warfarin, has AF and has had a stroke

A

2.5-3.5

118
Q

Investigations for a patient after their stroke?

A

BP
Echocardiogram- look for post-MI hypokinetic region or AF
ECG
Carotid doppler
Glucose, lipids, cholesterol, U+Es, FBC (hyperviscosity)
ESR, ANA (vasculitis as a cause)
Clotting

119
Q

Patient is being treated for their stroke, but you notice they have a fever and a murmur. What may be the stroke’s aetiology?

A

Infective endocarditis

120
Q

In a long history, what 10 things need to be asked about to assess disability?

A

Barthel’s index of ADL

In order of starting the day:

  1. Transfer (bed to commode, sit up)
  2. Mobility (wheelchair, walks with help)
  3. Bladder (incontinent, occasional accident in 24 hours)
  4. Bowels
  5. Toilet use (need some help, can wipe/dress/transfer)
  6. Dressing (half unaided, buttons/zips/laces)
  7. Bath or shower
  8. Grooming (face, hair, teeth, shaving)
  9. Stairs (unable, needs some help)
  10. Feeding (help cutting, spreading butter)
121
Q

Differential of thunderclap headache

A

Subarachnoid haemorrhage
Sinus venous thrombosis (or cortical vein thrombosis)
Meningitis, encephalitis, brain abscess
Arterial infarction

122
Q

Between which layers does a haematoma form in subdural and extradural haemorrhage?

A

Subdural- dura and arachnoid mata (as veins bridge between cortex and venous sinuses)

Extradural- between dura and bone, often fractured temporal/parietal bone causing middle meningeal artery laceration

123
Q

How do myaesthenia gravis, lambert eaton syndrome, Botox and aminoglycosides affect excitation contraction coupling at the neuromuscular junction?

A

Affecting the presynaptic nerve:
Lambert Eaton acts on VG-calcium channels preventing depolarisation needed for ACh release
Aminoglycosides (gentamicin) also block the VG calcium channel
Botox prevents cleavage of the snare protein needed for exocytosis of ACh

Postsynaptic muscle fibre:
Myaesthenia gravis= autoantibodies against the AChR on the muscle fibre needed to allow depolarisation and thus calcium influx into the muscle

124
Q

Treatment for Alzheimer’s disease?

A

AcetylcholineEsterase Inhibitors- MMSE is 10-20
Donepezil, Rivastigmine, Galantamine

Antiglutamatergic, NMDA antagonist- MMSE <10 severe
Memantine

Antipsychotics in severe non-cognitive symptoms (psychosis, extreme agitation), increases risk of death and progression

125
Q

Patients may be given anticholinesterases for Alzheimer’s, what side effects should be expected

A

Increased ACh =
^ parasympathetic system
(preganglionic= nAChR, postganglionic = mAChR)
^ muscle contraction (except in blood vessels, dilation)

Diarrhoea + incontinence (muscarinic R’s mediate bladder contraction)
Blurred vision (increased constriction)
Dizziness (vessel dilation)
Peptic ulcers (activates ECL cells to produce histamine, more acid)
Heart block (slowed heart)

126
Q

Anticholinergic drug side effects:

A

Can’t see, can’t pee, can’t shit, can’t spit

Parasympathetics- pupil constriction, bowel muscle contraction, salivation
mAChR- bladder contraction, heart slowing

127
Q

Name some uses of anti-cholinergic drugs:

A

Tricyclic antidepressants (amitriptyline)
Anti-emetics (cyclizine)
Anti-Parkinson’s tremor meds (benzhexol)
Anti-psychotics (olanzepine, clozapine)
Antispasmodics (baclofen)
Anti- urge incontinence (oxybutamine, tolteradine)

ACh causes muscles to contract at NMJ (except in blood vessels)
ACh promotes gut motility and acid production (through ECL cells producing histamine)
ACh causes bladder contraction

128
Q

Which vitamin deficiencies can mimic dementia?

A

Vit B12/folate (due to pernicious anaemia, veganism, causes subacute combined degeneration of the cord + megaloblastic anaemia) = hydrocobalamin

Vit B1 (thiamine > Wernicke’s, Korsakoff, dry (neuronal) or wet (oedematous) beriberi = Pabrinex

Vit B3 nicotinic acid (causes pellagra, dementa, diarrhoea, dermatitis)

[also hypothyroidism]

129
Q

Which infections mimic dementia and how can they be investigated for?

A

Syphilis (serology)
CNS cysticercosis- pork tapeworm (CT/MRI head)
HIV (antibody test)
Wipple’s disease (G+ve bacteria)

130
Q

How does fronto-temporal dementia differ from Alzheimer’s?

A

Histology- Alzheimers (b-amyloid plaques, tau fibrils)
Fronto-temporal (may have Pick’s inclusion bodies)

Alzheimer's- global domains affected
Fronto-temporal- spatial orientation + episodic memory preserved
Frontal changes in :
Executive impairment (planning)
Personality change
Disinhibition
131
Q

Which drugs have Parkinsonian effects?

A

Neuroleptics
Metoclopramide (dopamine antiemetics)
Prochlorperazine (typical antipsychotic)

132
Q

Which cause of chronic liver disease is associated with Parkinson’s?

A

Wilson’s disease- copper acculumate
Liver enzyme that gets rid of copper by binding it to ceruloplasmin to enter the bloodstream and be excreted into bile is impaired

= Low ceruloplasmin

133
Q

Medical treatments of Parkinson’s

A

Early: Dopamine agonists (ropinirole, pramipexole, IV apomorphine)
Anticholinergics for tremor (benzhexol)
MAO-B inhibitors (selegiline, rasagiline)

Dopa replacement with peripheral decarboxylase inhibitor
COMT inhibitors (entacapone- reduce 'off' time)
134
Q

Treatment for Alzheimer’s disease?

A

AcetylcholineEsterase Inhibitors- MMSE is 10-20
Donepezil, Rivastigmine, Galantamine

Antiglutamatergic, NMDA antagonist- MMSE <10 severe
Memantine

Antipsychotics in severe non-cognitive symptoms (psychosis, extreme agitation), increases risk of death and progression

135
Q

Patients may be given anticholinesterases for Alzheimer’s, what side effects should be expected

A

Increased ACh =
^ parasympathetic system
(preganglionic= nAChR, postganglionic = mAChR)
^ muscle contraction (except in blood vessels, dilation)

Diarrhoea + incontinence (muscarinic R’s mediate bladder contraction)
Blurred vision (increased constriction)
Dizziness (vessel dilation)
Peptic ulcers (activates ECL cells to produce histamine, more acid)
Heart block (slowed heart)

136
Q

Anticholinergic drug side effects:

A

Can’t see, can’t pee, can’t shit, can’t spit

Parasympathetics- pupil constriction, bowel muscle contraction, salivation
mAChR- bladder contraction, heart slowing

137
Q

Name some uses of anti-cholinergic drugs:

A

Tricyclic antidepressants (amitriptyline)
Anti-emetics (cyclizine)
Anti-Parkinson’s tremor meds (benzhexol)
Anti-psychotics (olanzepine, clozapine)
Antispasmodics (baclofen)
Anti- urge incontinence (oxybutamine, tolteradine)

ACh causes muscles to contract at NMJ (except in blood vessels)
ACh promotes gut motility and acid production (through ECL cells producing histamine)
ACh causes bladder contraction

138
Q

Which vitamin deficiencies can mimic dementia?

A

Vit B12/folate (due to pernicious anaemia, veganism, causes subacute combined degeneration of the cord + megaloblastic anaemia) = hydrocobalamin

Vit B1 (thiamine > Wernicke’s, Korsakoff, dry (neuronal) or wet (oedematous) beriberi = Pabrinex

Vit B3 nicotinic acid (causes pellagra, dementa, diarrhoea, dermatitis)

[also hypothyroidism]

139
Q

Which infections mimic dementia and how can they be investigated for?

A

Syphilis (serology)
CNS cysticercosis- pork tapeworm (CT/MRI head)
HIV (antibody test)
Wipple’s disease (G+ve bacteria)

140
Q

How does fronto-temporal dementia differ from Alzheimer’s?

A

Histology- Alzheimers (b-amyloid plaques, tau fibrils)
Fronto-temporal (may have Pick’s inclusion bodies)

Alzheimer's- global domains affected
Fronto-temporal- spatial orientation + episodic memory preserved
Frontal changes in :
Executive impairment (planning)
Personality change
Disinhibition
141
Q

Which drugs have Parkinsonian effects?

A

Neuroleptics
Metoclopramide (dopamine antiemetics)
Prochlorperazine (typical antipsychotic)

142
Q

Which cause of chronic liver disease is associated with Parkinson’s?

A

Wilson’s disease- copper acculumate
Liver enzyme that gets rid of copper by binding it to ceruloplasmin to enter the bloodstream and be excreted into bile is impaired

= Low ceruloplasmin

143
Q

Medical treatments of Parkinson’s

A

Early: Dopamine agonists (ropinirole, pramipexole, IV apomorphine)
Anticholinergics for tremor (benzhexol)
MAO-B inhibitors (selegiline, rasagiline)

Dopa replacement with peripheral decarboxylase inhibitor
COMT inhibitors (entacapone- reduce 'off' time)
144
Q

Side effects of dopaminergic drugs

A

Vomiting- DA inhibits motility in upper gut

Chorea, dystonia, psychosis

145
Q

5 types of Parkinson’s plus syndromes:

A
  1. Progressive supranuclear palsy- postural instability, vertical gaze palsy, symmetrical onset
  2. Multiple systemi atrophy- autonomic signs (postural BP drop, incontinence, rigidity) + cerebellar
  3. Lewy Body dementia- cognitive symptoms within 1 year of motor
  4. Cortico-basal degeneration- alien limb or unable to identify objects with touch (asteroagnosia)
  5. Vascular
146
Q

Which infections can trigger Guillain Barré?

A 
Campylobacter jejuni (diarrhoea)
CMV (lymph nodes, sore throat, myalgia)
Herpes zoster (shingles)
HIV
EBV
Mycoplasma (pneumonia, haemolytic anaemia)
147
Q

What tests should be performed if suspecting Guillain Barré?

A

Ascending symmetrical muscle weakness, affecting the proximal muscles especially

Raised CSF protein
Normal CSF WCC
Forced vital capacity- every 4 hours

148
Q

Guillain Barré Rx?

A

IV immunoglobulin
Plasma exchange

10% are still unable to walk at 1 year

149
Q

What 4 types of symptoms can people experience in an aura preceeding a migrane?

A

Aura: lasts 15-30 minutes followed by a unilateral throbbing headache within an hour

Visual- scotomata, hemianopia, distortions
Somatosensory- paraesthesia (abnormal sensation, pins + needles)
Motor- dysarthria, ataxia, opthalmoplegia, hemiparesis
Speech- dysphasia

150
Q

Criteria to diagnose migrane if there is no aura

A

5 headaches lasting 4-72 hours
+ nausea and vomiting/phonophobia/photophobia

With 2 of
Unilateral
Pulsating
Impairs routine activity

151
Q

Acute treatment of migranes:

A

NSAIDs + 5-HT agonists (triptans)

CI to triptans: IHD, coronary spasm, uncontrolled BP
Lithium, SSRIs

Last line: ergotamines, botox type A injections

152
Q

CI to sumitriptan for migranes:

A

Triptans work by causing vascular vasoconstriction, so not suitable for

PMH: IHD, coronary spasm, uncontrolled BP
DHx: Lithium
SSRIs (already enough 5-HT)

153
Q

Prophylactic Rx for migranes:

A

If more than 2 migranes a month or not responding to drugs

1st: propranolol
amitriptyline (anticholinergic)
topiramate (teratogenic)
Ca2+ blockers

154
Q

What things will be bright on a diffusion weighted MRI?

A 
Shows where movement of water is restricted, so when ischaemia prevents na/k/atp pumps working
Ie
Acute infarct
Some tumours
Abscess
155
Q

When are patients most at risk of mass effect following infarct?

A

3-5 days due to oedema or haemorrhage

156
Q

Name 3 anticholinesterases used in Alzheimers disease?

A
  1. Donezepil
  2. Rivastigmine
  3. Galantamine
157
Q

What is the most obvious way to delineate motor neuron disease from myaesthenia gravis in a neuro exam?

A

MND never affects eye movement, unlike myaesthenia which affects them early.

Also myaesthenia gravis demonstrates fatiguable movements

158
Q

What are the 4 clinical patterns of motor neuron disease?

A
  1. Amyotrophic lateral sclerosis- motor cortex + anterior horn cells so UMN and LMN signs
  2. Progressive bulbar palsy- CN 9-12
  3. Progressive muscular atrophy- anterior horn cells only (distal LMN)
  4. Primary lateral sclerosis- Betz cells in motor cortex
159
Q

Which form of MND do you get pseudobulbar palsy in?

A

Primary lateral sclerosis particularly

Progressive bulbar palsy = bulbar palsy moreso (CN 9-12)
Progressive muscular atrophy is LMN mostly
Amyotrophic lateral sclerosis = more motor cortex + anterior horn

160
Q

How is motor neuron disease diagnosed?

A

Clinical diagnosis:
Definite if LMN + UMN signs in 3 regions

Exclude other causes: MRI for space occupying lesion, LP for inflammatory causes, neurophysiology for denervation

Caused by neuron apoptosis

161
Q

Where is the lesion in bulbar palsy compared to pseudobulbar palsy?

A

Bulbar is Below- in the medulla affecting CN 9-12

Pseudobulbar is above the mid Pons (corticobulbar tracts)

162
Q

Top causes of pseudobulbar palsy compared to bulbar palsy?

A

Bulbar- LMN: MND, Guillain Barré, Polio, myaesthenia gravis

Pseudobulbar- UMN: MS, MND, stroke

Both can occur in central pontine myelinolysis (change in Na)

163
Q

What Rx is given for motor neuron disease?

A

Symptomatic mostly

Antiglutaminergic drugs prolong life by 3 months (riluzole)
Amitriptyline for drooling (anti-ACh effects on salivary gland)
NIV for respiratory failure

164
Q

In MS, how does the course of the disease and healing or neuronal damage affect whether a patient has relapsing and remitting symptoms or progressive?

A

After demyelination, if myelin heals well, patient will be in remission with full recovery. If healing poorly, remission is incomplete and disability accumulates, if demyelination lasts a long time, axonal death will occur with permanent loss (progressive)

165
Q

What symptoms are typical of optic neuritis?

A

Pain on eye movement and rapid reduction in central vision

Usually unilateral

166
Q

In a patient with suspected demyelinating disease, how does the CSF findings influence likely diagnosis?

A

Oligoclonal IgG- suggests MS (not present in Devic’s syndrome)

Raised WCC + protein in CSF suggests:
vasculitis (PAN)
rheumatological (SLE, Sjögren’s)
or sarcoid causation rather than MS

167
Q

What is Lhermitte’s sign?

A

Neck flexion causes electric shock spasms in trunk or limbs

Seen in MS, subacute combined degeneration of the cord (low B12), cord tumours, cervical spondylosis

168
Q

What is Uhthoff’s phenomena?

A

Reduced vision with hot baths, hot meals or exercise

Occurs in optic neuritis

169
Q

Which muscle groups are affected first in myaesthenia gravis?

A 
Eyes
Bulbar- chewing + swallowing
Face
Neck
Limb girdle
Trunk
170
Q

In a patient with myasthenia gravis, what would you expect to find on examination of their reflexes?

A

Normal

In first activation of muscle sufficient muscular nAChR are available for activation of the muscle, as the receptors become occupied and saturated, the muscle fatigues.

171
Q

Tests for myaesthenia gravis?

A 
Anti-AChR antibodies
MuSK antibodies (muscle specific tyrosine kinase Abs)

Neurophysiology: decremental muscle response to repetitive nerve stimulation
Imaging: CT of thymus

Exam: look up for a number of minutes or apply ice and ptosis improves by 2mm

172
Q

Rx for myaesthenia gravis

A

Symptom control- anticholinesterase (pyridostigmine)
Immunosupression- prednisolone, azathiprine/methotrexate
Thymectomy- often hyperplastic, seems to be involved in the pathology of the disease

Myaesthenic crisis- IV Ig or plasmapheresis (ventilatory collapse)

173
Q

Difference between Lambert Eaton syndrome and myaesthenia gravis

A

Pathophysiology: in Lambert Eaton antibodies are against the presynaptic VG Ca channels, rather than the muscular AChRs
As well as being autoimmune, Lambert Eaton may be paraneoplastic (small cell lung cancer)

Symptoms: Lambert- gait before eye signs, autonomic involvement, Sx improve after exercise

Exam: Lambert- hyporeflexic, myaesthenia- normal reflexes

IHx: in MG do CT to look for thymus hyperplasia, in LE look for small cell lung cancer

174
Q

How do symptoms differ between the different causes of myopathy?

A

Pain at rest and local tenderness- suggests inflammatory cause
(Ie inclusion body myositis of tau proteins or polymyositis etc)

Pain on exercise- ischaemic or metabolic cause (glycogen storage disease)

175
Q

Commonest primary (genetic) muscular dystrophy

A

Sex-linked recessive Duchenne’s
Dystrophin protein is non-functional- onset age 4

Less common is Becker’s muscular dystrophy
Partly functioning dystrophin- better prognosis

Dystrophin is a protein that connects the muscles cytoskeleton to extracellular matrix around the muscle, via the cell membrane

176
Q

Features of facioscapulohumeral muscular dystrophy

A

Almost as common as Duchenne’s- autosomal dominant

Facio- unable to puff out cheeks, weakness of face
Scapulo- winging scapula, difficulty raising arms above head
Humeral- weak shoulders and upper arms

Also scoliosis, horizontal clavicles, foot drop

177
Q

How are myotonic disorders different to muscular dystrophy?

A

Both cause muscle wasting and weakness
Dystrophy = more proximal, myotonic disorders = distal

In dystrophia myotonica, patient experiences tonic muscle spasms from chloride channelopathies (rather than dystrophin protein abnormality)
On histology in myotonica can see central nuclei in the middle of the muscle fibre rather than around the outside.

178
Q

What investigations may be used to rule out an infectious cause of cord compression (ie extradural abscess)

A

Obs: Temp raised
Ex: tender spine
IHx: WCC, ESR + CRP raised

179
Q

Commonest cause of cord compression:

A

Secondary metastases- gland tissue: breast, lung, kidney, prostate, thyroid

Rarer- infectious abscess, cervical disc prolapse, hematoma (warfarin), myeloma

180
Q

Investigations of cord compression

A 
Whole spine MRI
Biopsy of any mass
FBC (infection), U+E (kidney mets), ESR, B12 (Subacute degen)
Syphilis serology
Serum electrophoresis (myeloma)
CXR- TB, lung cancer
181
Q

Management of cord compression

A

Dexamethasone IV

Radiotherapy or chemotherapy

182
Q

Difference in examination findings between cauda equina lesion and cord compression?

A

Cauda equina- LMN flaccid and areflexic

Cord- UMN spastic and hyperreflexic

183
Q

Different presentations of tertiary syphilis:

A

Tabes dorsalis- afferent pathways from muscle spindles are lost (reduced tone and reflexes), no weakness

Taboparesis- spastic paraparesis with extensor plantars (taboparesis) and absent tendon reflexes (tabes dorsalis)

184
Q

What’s the difference between partial and generalised seizures and simple and complex?

A

If the seizure begins focal then spreads it is still considered partial, if there is simultaneous onset of electric discharge throughout both cortices without localising features referable to one hemisphere is it considered generalised.

NB it is possible to have a partial seizure with secondary generalisation

Simple = unimpaired awareness
Complex = impaired awareness
185
Q

In what circumstances would you consider giving someone with a seizure (presumed epileptic) antiepileptics after only one fit?

A

High risk of recurrence:
Structural brain lesion
Unequivocal epileptiform EEG

Otherwise wait for 2nd fit to start

186
Q

Rx for a generalised tonic-clonic seizure:

A

1st: Sodium valproate

Lamotrigine (often better tolerated)

187
Q

Rx for absence seziures

A

Sodium valproate
Or lamotrigine
Or ethosuximide

188
Q

Treatment for myoclonic or atonic (drop attack) seizures?

A

Valproate

Or lamotrigine

189
Q

Rx for partial seizures ± secondary generalisation

A

1: carbamazepine
2: valproate, lamotrigine

190
Q

What factors might make a non-epileptic attack disorder (psychogenic seizures) more likely?

A

Uncontrollable symptoms
No learning disabilities
Normal CT, MRI, CNS exam, EEG

191
Q

Potential SEs of the first line drug for partial seizures?

A

Carbamazepine- also used in trigeminal neuralgia
Blocks VG Na+ channels and agonises GABA R

FBC- leucopenia
Dizzy, drowsy, diplopia
CYP inducer (CRAP GPS)

192
Q

Potential side effects of the first line treatments for generalised epilepsy?

A

Sodium valproate + lamotrigine (L for generLised)

VALPROATE 
Appetite up
Liver failure
Pancreatitis
Reversible hair loss
Oedema
Ataxia
Teratogenic/Tremor/Thrombocytopenia
Extrapyramidal effects

Cyt P450 inhibitor

Lamotrigine: Stephen Johnson syndrome, aplastic anaemia, vomiting

193
Q

Preferential drug Rx for a 30 year old woman with myotonic epilepsy?

A

Normally between valproate and lamotrigine, as she is of child bearing age:
Lamotrigine and folic acid 5mg

Also pills may be affected by cytp450 inducers (carbamazepine, phenytoin) or inhibitors (valproate)

194
Q

What is an Arnold Chiari malformation?

A

Cerebellum herniates through the foramen magnum

Can block CSF flowing from 4th ventricle to the cord, so syringomyelia occurs (fluid filled cavity forms of CSF)

195
Q

Which sensation is affected in syringomyelia?

A

Pain and temperature, as the anterolateral tract is closer to the central canal of CSF

Vibration + proprioception + light touch are unaffected

196
Q

What signs of deficits may be present in a space occupying lesion affecting the parietal lobe?

A

Hemisensory loss
Reduced 2 point discrimination
Astereognosis (unable to discriminate objects with touch alone)
Sensory inattention- when both sides touched at same time
Gerstmann’s syndrome (agraphia, acalcula, left right disorientation, finger agnosia)

197
Q

Signs of cerebellar disease

A 
Dysdiadokinesis (impaired rapidly alternating movements)
Dysmetria
Ataxia (truncal and limb)
Slurred speech (dysarthria)
Hypotonia/hyporeflexia
Intention tremor
Nystagmus (multi-directional, non-fatiguing)
Gait abnormality
198
Q

A patient has truncal ataxia, how can you determine if this is due to a cerebellar lesion or a loss of proprioception (dorsal column damage)?

A

Ask the patient to close their eyes, if it gets much worse = due to dorsal column damage

199
Q

Drug causes of peripheral neuropathy

A

I’M PN (peripheral neuropathy)

Isoniazid
Metronidazole
Phenytoin
Nitrofurantoin

200
Q

Damage to which epicondyle risks damage of the ulnar nerve?

A

Medial epicondyle

201
Q

Muscles innervated by the radial nerve
Clue 1: not just the extensors
Clue 2: BEST

A

Brachioradialis
Extensors
Supinator
Triceps

202
Q

How do the signs differ depending on whether the ulnar nerve is damaged at the wrist Vs the elbow?

A

Claw hand is more marked in lesions at the wrist unlike the elbow, as flexor digitorum profundus is intact to flex the interphalangeal joints

203
Q

How can you test for autonomic nerve function?

A

Postural drop > 20mmHg/10mmHg
ECG rate change greater than 10bpm
Cystoscopy- Bladder pressure studies (may get urinary retention)
Pupils- dilating eye drops (cocaine, abnormal if pupil doesn’t dilate)

204
Q

Tests that can be done to delineate cause of LMN palsy of the 7th nerve?

A

Borrelia antibodies in Lyme disease (may be indistinguishable from Bell’s clinically)
Varicella Zoster viral antibodies in Ramsay Hunt syndrome

If considering UMN cause then MRI can look for stroke, MS or space occupying lesion

205
Q

Rx for Bell’s palsy

A

Corticosteroids: prenisolone- if presenting within 72 hours of onset

Lubricating eye drops, taping eye closed at night.
No antivirals.

For longterm failure of eye closure, surgery may be tried (lid-to-lid suturing or lid loading)

206
Q

How is ramsay hunt syndrome distinguished from Bell’s palsy?

A

Ramsay Hunt due to reactivation of latent varicella zoster in geniculate ganglion, so patient may have painful vesicular rash in auditory canal whereas Bell’s shouldn’t be painful.

May get deafness, dry mouth and eyes in Ramsay Hunt, vertigo

Rx: Ramsay Hunt = aciclovir PO within 72 hours of onset

207
Q

What is the pathophysiology of cervical spondylosis?

A

Degeneration of the annulus fibrosus of cervical intervertebral discs ± osteophytes narrow the spinal cord + intervertebral foramina, damaging the cord

208
Q

Patient has neck stiffness, stabbing arm pain, dull reflexes and numbness in the hands, what imaging modality is warranted?

A

Motor and sensory affected
LMN suggested by reflexes
Pain in neck will occurs if C3 or C4 nerve roots are affected

MRI ?cervical spondylosis (degeneration of vertebral discs) or tumour
B12 level ?subacute combined degeneration
Calcium- spinal sarcoidosis

209
Q

Surgical treatment for cervical spondylosis?

A

Surgical root decompression- laminectomy or laminoplasty

Laminectomy- a portion of the lamina on the vertebrae is removed to make more space for the cord

Laminoplasty- once the lamina is removed, screws and plates are attached to take over the function of the lamina and provide structural support. May have greater reduction of pain but more neck stiffness

210
Q

What’s the difference in symptoms between an occlusion of the anterior inferior cerebellar artery and the posterior inferior cerebellar artery?

A

AICA (aaggh? Can’t hear) = deaf and dizzy
PICA (all the P’s) = dysPhagia + dysPhonia + dizzy

SCA= dizzy

211
Q

Commonest primary brain tumour?

A

Gliomas, which includes:

Astrocytomas (astrocytoma, glioblastoma)
Oligodendrocytomas
Ependyoma
Primitive neuroepithelial tumours

212
Q

Commonest bacterial cause of meningitis in south east asia?

A

Strep Suis

213
Q

Which bacteria and protozoa can cause meningo-encephalitis?

A

Bacteria- spirochaetes (leptospira, treponema pallidum, borrelia)

Protozoa- amoeba, toxoplasma

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