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Medicine > Neurology > Flashcards

Neurology Flashcards

1
Q

Where can the motor cortex be found? What is also at this location?

A

Precentral gyrus in frontal lobe - also has Broca’s area

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2
Q

Where can the sensory cortex be found?

A

The postcentral gyrus in the parietal lobe

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3
Q

Where can Wernicke’s area be found?

A

The dominant temporal lobe.

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4
Q

Where does the corticospinal tract cross?

A

At the level of the medulla

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5
Q

Where does the spinothalamic tract cross?

A

Crosses at same level of entry of S.C.

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6
Q

What does the spinothalamic tract carry?

A

Coarse touch, pain and temperature

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7
Q

What happens in syringomyelia?

A

Dilated central canal presses on spinothalamic tract –> impairment of temperature and scars due to burns

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8
Q

What info does the dorsal column carry?

A

Fine touch and vibration and position.

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9
Q

Where does the dorsal column cross?

A

Medulla

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10
Q

When is spectrophotometry used?

A

It is used on CSF to look for blood breakdown products in suspected subarachnoid haemorrhage.

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11
Q

What is aphonia?

A

Problem with phonation (sound and volume)

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12
Q

What is dysarthria?

A

Problem with articulation of speech

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13
Q

What is aphasia?

A

Problem with comprehension and production of language.

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14
Q

A patient just has a problem with repeating things. What is this called and what is likely to have been damaged?

A

Conductive aphasia. Usually due to lesion in the arcuate fasciculus.

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15
Q

What is the afferent and efferent in the pupillary reflex?

A 
Afferent = II
Efferent = III
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16
Q

Name 3 symptoms of optic neuritis

A
  • Visual loss
  • Retro-orbital pain
  • RAPD
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17
Q

What does absent venous pulsation and blurring of optic disc margins suggest?

A

Optic disc swelling

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18
Q

How would the optic disc look if it is atrophied?

A

Pale optic disc with sharp edges

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19
Q

When nerve innervates the superior oblique muscle?

A

Trochlear nerve (4th)

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20
Q

How would the eye look like in a cranial nerve III palsy?

A

Ptosis, down + out, impaired accommodation (CN III is efferent nerve)

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21
Q

How would the eye look like in a cranial nerve IV palsy?

A

Incomplete depression in adducted position, vertical diplopia. Tilting head towards opposite shoulder.

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22
Q

How would the eye look like in a cranial nerve VI palsy?

A

Horizontally separated double vision on looking to the side, with limitation of abduction of eye

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23
Q

What is the afferent and efferent nerves involved in the corneal reflex?

A 
Afferent = V1 
Efferent = VII (facial)
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24
Q

Which nerves are carried in the internal acoustic meatus?

A

VII and VIII

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25
Q

What is Bell’s phenomenon?

A

The upward and outward movement of the eye when attempting to close the eye - occurs in a CN VII palsy

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26
Q

In terms of the nerves affected, what differentiates bulbar from pseudobulbar palsy?

A 
Bulbar = LMN lesion 
Pseudobulbar = UMN lesion
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27
Q

What features can be seen in a pt with bulbar palsy?

A

Wasted & atrophic tongue w/ fasciculation, depressed jaw reflex, nasal speech

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28
Q

What features can be seen in a pt with pseudobulbar palsy?

A

Small, slow-moving spastic tongue. Brisk jaw reflex, spastic, slurring speech, emotional lability, increased gag reflex

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29
Q

What would happen to the uvula in a vagus lesion?

A

The uvula deviates away from the side of the lesion (away to Vegas)

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30
Q

What are the afferent and efferent nerves involved in the gag reflex?

A 
Afferent = CN IX (Glossopharyngeal)
Efferent = CN X (Vagus)
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31
Q

What happens to the tongue in a hypoglossal nerve lesion?

A

Unilateral wasting and fasciculation of tongue - deviates towards the side of the lesion

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32
Q

How would acute labyrinthitis present?

A

Sudden onset rotatory vertigo, vomiting and loss of balance

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33
Q

How does Meniere’s disease present?

A

Deafness, tinnitus, episodic vertigo, vomiting

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34
Q

A patient struggles to turn their head to the right - lesion of what cranial nerve could have caused this?

A

Lesion of the left CN XI has lead to weakness of the left SCM

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35
Q

What is Jugular foramen syndrome?

A

Unilateral lower CNs palsy –> deviation of uvula, weakness in twisting head and shrugging shoulders

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36
Q

How does Horner’s syndrome present?

A

Unilateral ptosis, small pupil, enopthalmos (posterior displacement of eye in orbit), lack of sweating

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37
Q

What happens in internuclear ophthalmoplegia?

A

When a patient looks to right/left, there is ataxic nystagmus in abducted eye + failure to adduct other eye.

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38
Q

What causes internuclear ophthalmoplegia?

A

Due to lesion in medial longitudinal fasciculus (connects CN III nucleus to 1 side to CN VI nucleus on other side)

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39
Q

What is pseudoathetosis? What causes it?

A

Continuous involuntary movements of outstretched hands and fingers when eyes are closed
Caused by failure of proprioception

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40
Q

How does someone with Friedreich’s ataxia body look like?

A

Pes cavus (claw foot), absent ankle jerks, upgoing planters, scoliosis

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41
Q

What would you find when doing an CSF analysis for someone with demyelinating neuropathy?

A

High protein

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42
Q

What nerve has been lesioned in a pt with claw hand?

A

Ulnar nerve

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43
Q

How does a common peroneal nerve lesion present?

A
  • Weakness in dorsiflexion of ankle and big toe
  • Eversion of foot
  • Foot drop –> high steppage gait
  • Possible decrease in pinprick sensation over lateral calf and dorsum of foot
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44
Q

What happens to ankle jerk in a common peroneal nerve lesion?

A

It is preserved

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45
Q

How does a L5 root lesion present?

A
  • Foot drop
  • Inversion of ankle
  • Usually painful
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46
Q

How does sciatic nerve lesion present?

A
  • Foot drop
  • Weakness of toe plantarflexion
  • Loss of ankle jerk
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47
Q

Which type of headache is typically described as a “tight band” around the head?

A

Tension headache

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48
Q

What is the main treatment used in tension headaches?

A

Amitriptyline

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49
Q

What treatment options can be used for acute migraine attacks?

A

Simple analgesics, +/- antiemetics, triptans

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50
Q

What treatment options are available to prevent migraines in patients?

A
  • Propanolol
  • Amitriptyline
  • Pizotifen
  • Topiramate
  • Botox injections
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51
Q

What medication can be introduced to those suffering from medication overuse headaches?

A

Amitriptyline

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52
Q

At what point during the day do cluster headaches occur?

A

Mainly at night, same time of the day usually.

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53
Q

Other than excruciating pain around the eye, what are the other symptoms of cluster headaches?

A

Watering and redness of the eye and nasal blockage.

Occasionally Horner’s syndrome.

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54
Q

What are the 2 treatment options for acute cluster headaches?

A

Sumatriptan subcut injection or high-flow oxygen

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55
Q

What are the treatment options to prevent cluster headaches?

A

Pizotifen, verapamil, topiramate and steroids

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56
Q

Where is the pain felt in trigeminal neuralgia?

A

Pain is felt over area supplied by 1 branch of CN 5.

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57
Q

What is the first line treatment for trigeminal neuralgia and what other treatments are available?

A

1st line = Carbamazepine
Others: Phenytoin, Lamotrigine, Gabapentin
Surgery - glycerol injection of 5th nerve and microvascular decompression.

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58
Q

How does concussion syndrome present?

A

Lack of concentration, struggling to stay awake, poor memory, dizziness, vomiting. persistent headache

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59
Q

What is the treatment for concussion syndrome?

A

Amitriptyline

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60
Q

What must be excluded in patients presenting with suspect IIH and how would you do this?

A

Must exclude cerebral venous sinus thrombosis - would do CTV/MRV to exclude this.

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61
Q

Which lobe is most commonly involved in a partial seizure?

A

Temporal lobe

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62
Q

How does a temporal lobe seizure present?

A

Epigastric sensation rises up the throat

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63
Q

How does a frontal lobe seizure present?

A

Deviation of head and eyes to 1 side. Jerking of arm. Paralysis of arm (Todd’s paralysis).

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64
Q

How does a parietal lobe seizure present?

A

Sensory symptoms

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65
Q

What happens during the tonic phase of a seizure?

A

Pt goes rigid, froth, lasts for seconds

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66
Q

What happens during the clonic phase of a seizure?

A

Rhythmic jerking, tongue biting, urinary incontinence, lasts for minutes.

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67
Q

How do myoclonic seizures present?

A

Sudden, brief jerks that affect the upper limb. May precede a generalised tonic-clonic seizure. Often occur in the morning, and in late childhood.

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68
Q

In whom do psychogenic attacks tend to occur in and how do they look?

A

Females, starts in early adolescence/adulthood. Linked with emotional trauma. Pt falls down with coarse alternating movements and pelvic thrusting.

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69
Q

Define status epilepticus

A

A single epileptic seizure lasting over 5 minutes or 2 or more seizures within a 5 minute period without the person returning to normal between them.

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70
Q

What are the general side effects associated with taking anticonvulsants?

A

Nausea, sedation, irritability, headache and depression.

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71
Q

What is the first line medication used for partial-onset seizures?

A

Carbamazepine (Tegretol)

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72
Q

What is the 1st line medications used for generalised epilepsy?

A

Sodium valproate

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73
Q

What 2 seizure types is Carbamazepine (Tegretol) NOT used in?

A

Absence and myoclonic seizures

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74
Q

Name 2 side effects specific to Carbamazepine (Tegretol)

A

Skin rash and hyponatraemia

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75
Q

Name some side effects specific to sodium valproate

A

Tremor, weight gain,, hair loss, amenorrhoea

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76
Q

Phenytoin is an anticonvulsant drug that requires monitoring of its blood levels. Name a few of its side effects.

A

Rash, hepatotoxicity, blood dyscrasias, drowsiness, tremor, gum hyperplasia, ataxia.

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77
Q

In what type of epilepsy is Ethosuximide only used in?

A

Only used in children with absence seizures

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78
Q

Which anticonvulsant is an enzyme inducer?

A

Carbamazepine

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79
Q

Which anticonvulsant is an enzyme inhibitor?

A

Sodium valproate

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80
Q

When can you consider stopping anticonvulsants in someone?

A

If they have been seizure free for at least 2 years

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81
Q

What is the treatment of status epilepticus?

A

lorazepam as IV bolus, IV phenytoin infusion

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82
Q

A pt with a history of epilepsy wants to know how long it will take before they are allowed to drive their family car - what do you tell them?

A

they have to be seizure free for at least 1 year or had attacks only during their sleep for 3 years

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83
Q

A lorry driver with epilepsy asks how long it will take before he is allowed to drive his lorry again - what do you tell him?

A

He would have to be seizure free for 10 years without taking AEDs

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84
Q

A patient has experienced their first seizure. They want to know how long it will be until they are allowed to drive again - what do you tell her?

A

6 months

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85
Q

what should women on anti-epileptic drugs be taking during their pregnancy?

A

5mg folic acid daily

86
Q

Are women on anti-epileptic drugs allowed to breastfeed?

A

Yes as the amount of AEDs in breastmilk is v small

87
Q

What should be given to babies born to women taking anti-epileptic drugs and why?

A

1 mg of vitamin K IM @ birth to reduced the risk of haemorrhagic disease of newborn.

88
Q

A tremor affects the arms, head and voice - diagnosis?

A

Essential tremor

89
Q

What form of parkinsonism tends to present with early gait changes?

A

Vascular parkinsonism

90
Q

How does progressive supranuclear palsy present?

A

Limitation in their gaze, especially downwards. Axial and symmetrical rigidity w/ v little tremor - they develop dementia and falls early

91
Q

How does a patient with multiple system atrophy look like?

A

In a wheelchair, urinary bladder issues, impotence, brisk reflexes, upgoing planters, rigidity

92
Q

What time of imaging can be used to diagnose parkinsonism?

A

SPECT (CT) assesses dopamine transporter availability PD less bright on scan.

93
Q

What drugs may make up the treatment for someone with PD?

A
  • L-DOPA
  • Decarboxylase inhibitor (e.g. Benserazide)
  • COMT inhibitors (e.g. Entacapone, opicapone)
  • MAO-B inhibitors (e.g. Selegiline, Rasagiline)
  • Dopamine agonists (Ropinirole, Pramipexole)
94
Q

List some side effects and effectiveness problems with Levodopa

A

N&V, efficacy decreases with time
Long term: Dyskinesias, painful dystonias, unpredictable ‘off’ freezing, pronounced end-of-dose reduced response, psychosis, visual hallucinations

95
Q

List some side effects of dopamine agonists

A

Drowsy, nausea, hallucinations, compulsive behaviour (gambling, hyper-sexuality)

96
Q

What medication can be used for drug-induced dyskinesias in late PD?

A

Amantadine

97
Q

Name 2 side effects of MAO-B inhibitors?

A

Postural hypotension and AF

98
Q

In a patient with PD - what will you give them to treat their symptoms of cognitive impairment?

A

Rivastigmine - an acetylcholinesterase inhibitor used to treat dementia

99
Q

In a patient with PD - what will you give them to treat their symptoms of hallucinations and psychosis?

A

Modify anti-PD drugs and Quetiapine (atypical antipsychotics)

100
Q

In a patient with PD - what will you give them to treat their symptoms of lack of sleep/XS sleepiness/ parasomnias (bad dreams)?

A

Clonazepam (a benzo)

101
Q

In a patient with PD - what will you give them to treat their symptoms of orthostatic/ postural hypotension?

A

Fludrocortisone (steroid)

102
Q

Which part of the circulation may be affected in a patient with diplopia/ cortical blindness (due to damage to occipital cortex)?

A

Posterior (vertebrobasilar) circulation ischaemia

103
Q

How would a subarachnoid haemorrhage present?

A

Sudden onset severe headache that peaks in seconds, with vomiting and neck stiffness

104
Q

What is the most common cause of subarachnoid haemorrhages? How can they be treated surgically?

A

Rupture of intracranial (Berry) aneurysm on the Circle of Willis. Coil/surgical clipping.

105
Q

What 3 main investigations should you do for a patient with subarachnoid haemorrhages?

A

Brain CT then LP (look for xanthochromia and do spectrophotometry to confirm), CTA/MRA or cerebral angiogram

106
Q

What are the complications of subarachnoid haemorrhages? How can you reduced these risks?

A

Rebleeding, secondary ischaemia due to vasospasm - give nimodipine and IV fluids to reduce this risk.

107
Q

What should you do if you suspect a cardiac source of emboli is involved in an ischaemic stroke?

A

TTE/TOE & 24 hour ECG

108
Q

What should you do if a patient with a suspected ischaemic stroke presents within 4 and half hours from onset of symptoms?

A

Urgent brain CT, Thrombolysis w/ IV alteplase

109
Q

What should you do if a patient with a suspected ischaemic stroke presents over 4 and half hours from onset of symptoms?

A

Brain CT ASAP then 300mg of aspirin

110
Q

How may cerebral venous sinus thrombosis present?

A

headache, seizure, focal neuro signs, maybe papilledema

111
Q

What may cerebral venous sinus thrombosis be linked to?

A

Pregnancy and OCP

Otitis media and mastoiditis.

112
Q

What investigation must you do to exclude hypercoagulability disorders in a patient with cerebral venous sinus thrombosis?

A

Full thrombophilia screen

113
Q

What imaging should you do in a patient with suspected cerebral venous sinus thrombosis?

A

Brain CT - may identify venous infarction

CTV/MRV is diagnostic

114
Q

What is the main treatment for a patient with cerebral venous sinus thrombosis?

A

Anticoagulation

115
Q

How does optic neuritis present?

A

Pain worse on moving eyes and visual impairment. Central scotoma. Loss of colour vision. RAPD.

116
Q

What are the 2 types of optic neuritis? In which type does the optic disc look abnormal?

A
  • Retrobulbar (posterior): common, optic disc looks normal

- Papillitis (anterior): less common, optic disc is usually red and swollen w/ exudates and haemorrhages

117
Q

Name the 4 types of MS

A

Relapsing-remitting (most common)
Primary progressive
Secondary progressive
Progressive-relapsing

118
Q

Name 2 things you can find on investigations of someone to diagnose them with MS

A

1) Lesions which are disseminated in time and place on brain MRI
2) Oligoclonal bands that are positive in CSF but not in the blood (indicates intrathecal Ig synthesis)

119
Q

What 2 medications can you give to a patient with MS who is suffering from spasticity?

A

1) Baclofen (a CNS depressant and skeletal muscle relaxant)

2) Tizanidine (Central a z adrenergic agonist)

120
Q

Name 2 medications you can offer someone with MS who is in pain?

A

Amitriptyline or gabapentin

121
Q

When might you recommend anticholinergics (e.g. oxybutynin) to someone with MS?

A

If they have bladder instability

122
Q

What medication is used to treat the relapses of MS?

A

IV methylprednisolone (1g daily for 3 days) to shorten the duration of relapses (NB: They have NO influence on long-term outcome)

123
Q

What would show up on a Brain MRI of someone with neuromyelitis optica?

A

Normal!

124
Q

What would show up on a spinal MRI of someone with neuromyelitis optica?

A

Demyelination lesions over 3 or more vertebral segments

125
Q

Would oligoclonal bands be present in someone with neuromyelitis optica?

A

No

126
Q

Which antibodies may be discovered in someone with neuromyelitis optica?

A

Aquaporin antibodies

127
Q

What is the treatment for someone with neuromyelitis optica?

A

IV Methylprednisolone, IV antibodies, immunosuppression

128
Q

What is acute disseminated encephalomyelitis and who is it most common in?

A

Severe and sudden onset demyelinating syndrome

More common in children (after immunisation)

129
Q

How might acute disseminated encephalomyelitis present?

A

Seizures, meningism, features of myelitis

130
Q

What would a brain and spinal MRI show in someone with acute disseminated encephalomyelitis?

A

Demyelination lesions would be present in both the brain and spinal MRI.

131
Q

Would you see oligoclonal bands in someone with acute disseminated encephalomyelitis?

A

Oligoclonal bands are present in a third of patients with acute disseminated encephalomyelitis

132
Q

What is the treatment for acute disseminated encephalomyelitis?

A

IV methylprednisolone +/- IV Abs

133
Q

What is the most common cause of acute flaccid paralysis?

A

GBS

134
Q

Describe the paralysis patients with GBS would get

A

Rapidly progressive ascending paralysis

Tetraparesis more marked distally

135
Q

What happens to reflexes in GBS?

A

Reflexes are absent

136
Q

Name 2 neurology features commonly associated with GBS

A

LMN lesion of 7th nerve and bulbar involvement

137
Q

What may precede GBS?

A

URTI or diarrhoea

138
Q

What type of neuropathy is GBS? Consequently, what might you find in the CSF of a patient with GBS?

A

Demyelinating - High protein in CSF

139
Q

What is the main treatment for GBS?

What prophylactic medicine must you also give?

A

IV immunoglobulins

Low dose subcutaneous heparin to prevent a DVT

140
Q

Name 3 things you must monitor in a patient with GBS and why?

A
  • FVC (as patient is at risk of respiratory failure)

- BP and heart rhythm as patient is at risk of autonomic neuropathy

141
Q

What are the autoantibodies in myasthenia gravis against?

A

They are acetylcholine receptor antibodies - block the post-synaptic receptors

142
Q

Which muscles tend to be affected in MG?

A

Mainly proximal muscles

Facial and neck weakness

143
Q

Other than limb and facial weakness, how does MG present?

A

Double vision, ptosis, speech and swallowing difficulties, respiratory muscles may get affected (–> breathing difficulties)

144
Q

What would show up on an electromyograph of someone with MG?

A

Decrement on repetitive stimulation

145
Q

What was the ice pack used for? What did it show?

A

Used to be used to diagnose MG

The cold improves neuromuscular transmission, so would see an improvement in symptoms

146
Q

What was the Edrophonium (Tensilon) test used for and how did it work?

A

Used to be used to diagnose MG

Inject acetylcholinesterase inhibitor IV –> would see a big improvement in patient’s weakness for 3-5 minutes

147
Q

Once the diagnosis of MG is confirmed, what extra imaging should then be undertaken?

A

CT/MRI of thorax to check for thymic hyperplasia or thymoma

148
Q

What is the main treatment for MG? How does it work?

A

Pyridostigmine - it is a acetylcholinesterase inhibitor that increase Ach availability at the neuromuscular junction.

149
Q

What is a side effect of Pyridostigmine and how can you treat this?

A

Abdo cramps and diarrhoea - can treat this by giving antimuscarinic drugs e.g. propantheline

150
Q

Other than pyridostigmine, what other treatment options are available for MG? What must you warn patients about one of the available treatments?

A
  • Immune TX to suppress production of the abnormal antibodies e.g. prednisolone (warn patients that their condition may deteriorate initially - ‘Steroid dip’)
  • Azathioprine can be used as a steroid-sparing treatment
  • If severe, treat with IV immunoglobulins or plasmapheresis
151
Q

How does amyotrophic lateral sclerosis present?

A

Weakness (mainly in hands) with UMN signs (brisk reflexes) and LMN signs (wasted muscles and fasciculations)

152
Q

How does progressive bulbar palsy present?

A

Progressive dysarthrtia, then swallowing difficulties. Wasted muscles and fasciculations.

153
Q

How does progressive muscular atrophy present?

A

LMN type weakness

154
Q

How is the bladder involved in motor neurone disease?

A

NO bladder involvement

155
Q

What investigation would you do to confirm the diagnosis of motor neurone disease?

A

NCS/EMG would show denervation and fasciculation in both wasted and normal muscles

156
Q

Name the medication used as disease modifying treatment in motor neurone disease? How does it work?

A

Riluzole (glutamate antagonist) - may increase survival by a few months

157
Q

What do patients with motor neurone disease die off?

A

Respiratory failure

158
Q

Name 3 organisms that most commonly cause acute bacterial meningitis?

A
  • Streptococcus pneumoniae
  • Neisseria meningitidis
  • Haemophilus influenzae
159
Q

Name a common cause of viral meningitis

A

Enteroviruses

160
Q

How would viral meningitis present?

A

Headache and fever with no impairment of consciousness

161
Q

What is Kernig’s sign?

A

Thigh is flexed at hip and knee at 90 degree angles - subsequent extension of the knee is painful

162
Q

What is Brudzinski’s sign?

A

Forced flexion of neck elicits a reflex flexion of hips

163
Q

What would show on a brain CT of someone with meningitis?

A

Normal!

164
Q

How would a cerebral abscess appear on CT? What investigation would you do if you noticed one?

A

On CT, a cerebral abscess will be a ring-enhancing lesion with surrounding oedema.
Can do PCR of CSF to identify organism

165
Q

A CSF sample is taken. There is a high WCC, with mainly polymorphs - diagnosis?

A

Bacterial meningitis

166
Q

CSF sample results:

  • Slightly raised protein
  • High WCC (up to 500/mm3)
  • Normal glucose level

Diagnosis?

A

Herpes simplex encephalitis

167
Q

A CSF sample is taken - there is low glucose (<50% of blood glucose!) - Diagnosis?

A

Tuberculosis meningitis

168
Q 
CSF sample results:
- Slightly raised protein levels 
- High WCC (<200/mm3) Mainly lymphocytes
- Normal glucose levels 
Diagnosis?
A

Viral meningitis

169
Q

What is the specific treatment for viral meningitis?

A

No specific treatment as it is self-limiting

170
Q

What is the management of bacterial meningitis?

A

Broad-spectrum IV Abx: 3rd generation cephalosporin e.g. ceftriaxone ASAP
IV dexamethasone for 4 days

171
Q

What is the treatment for cryptocccal meningitis?

A

Antifungal treatment e.g. fluconazole or amphotericin B ASAP

172
Q

What does a grade IV glioma mean?

A

It is very malignant

173
Q

What is an acoustic neuroma?

A

A benign tumour from 8th CN @ cerebellopontine angle

174
Q

Name a medication used to treat prolactinomas

A

Cabergoline (a dopamine agonist)

175
Q

What is the pathophysiology of Huntington’s disease?

A

CAG repeats on chromosome 4

176
Q

How does Huntington’s disease present?

A

Chorea, dementia, psych problems

177
Q

Is myotonic dystrophy recessive or dominant?

A

Dominant

178
Q

How does myotonic dystrophy present?

A

Frontal baldness, ptosis, wasting of masseter and temporalis muscles, bilateral facial weakness

Other symptoms: cataract, cardiac conduction defects. diabetes, testicular atrophy, impairment of intellectual function

179
Q

What are 2 simple tests you can do with someone suffering from myotonia?

A

1) Get the patient to make a fist and release it - there is a delay in relaxing the hand
2) Percussion myotonia: Strike thenar eminence with a tendon hammer - will take a long time for dimple to return to normal

180
Q

What is the treatment for myotonic dystrophy? What monitoring needs to be done?

A

No specific treatment.
Do cardiac monitoring with regular ECG (increased risk of cardiac conduction defects) and regularly check blood sugar (at an increased risk of diabetes)

181
Q

What is the cause of subacute combined degeneration of cord?

A

Vitamin B12 deficiency

182
Q

Which neural pathways get disturbed in subacute combined degeneration of cord?

A
  • Dorsal column dysfunction: impairment of vibration and position sense
  • Corticospinal tract dysfunction: motor weakness
183
Q

What would you find on examination of someone with subacute combined degeneration of cord?

A

Sensory ataxia
Spastic legs
W/ absent ankle reflexes
Upgoing plantars

184
Q

What is the most common form of muscle disease in those over 50 years old? Which parts of the body get involved early?

A

Inclusion body myositis

Early involvement of finger flexors, foot extensors and quadriceps

185
Q

Is Charcot-Marie Tooth Disease dominant or recessive?

A

Dominant

186
Q

How does Charcot-Marie Tooth Disease present?

A

Bilateral distal weakness
Bilateral foot drop
Pes Cavus (high arch)
Absent ankle and knee jerks

187
Q

What type of neuropathy is Charcot-Marie Tooth Disease?

A

Both - demyelinating and axonal!

188
Q

What is the pathophysiology behind syringomyelias?

What is it linked to/what causes it?

A

Abnormal fluid collection (syrinx) within several segments of SC
Linked to Chiari’s malformation (medulla and lower cerebellum descending below foramen magnum)
Can be caused by tumour/ trauma

189
Q

How does syringomyelias present?

A

Loss of pain and temperature –> burn marks in upper limbs

Wasting, weakness and loss of reflexes in upper limbs. Spastic limbs

190
Q

Name 2 drugs used to treat narcolepsy?

A

Modafinil and dexamphetamine (CNS stimulants)

191
Q

Consciousness depends on which part of the brainstem being intact?

A

Reticular activating system

192
Q

Describe the scoring system for GCS

A

Eye opening ( /4)
Verbal ( /5)
Motor ( /6)

193
Q

How do you diagnose syringomyelia?

A

Do MRI of the spine

194
Q

What happens to a patient’s consciousness level when they are having a subdural haemorrhage?

A

Conscious level fluctuates, “evolving stroke”

195
Q

Name 3 risk factors for subdural haemorrhages?

A

Anticoagulants, old age, falls

196
Q

What is the pathophysiology of subdural haemorrhages?

A

Bleeding from bridging veins between cortex and venous sinuses - this leads to a haematoma between the dura and arachnoid which increases ICP and shifts midline structures

197
Q

What may happen if subdural haemorrhages are not treated?

A

Tentorial herniation and coning

198
Q

What fruit does a subdural haemorrhage look like lol?

A

Banana

199
Q

How long may the lucid interval in a patient with an extradural haemorrhage last?

A

Lucid interval may last hours-days before GCS drops due to increased ICP

200
Q

How do extradural haemorrhages present?

A

Increasingly severe headache, vomiting, confusion and seizures +/- hemiparesis with brisk reflexes and upgoing planters

201
Q

What are some of the late signs of extradural haemorrhages?

A

If bleeding continues –> ipsilateral pupil dilates, coma deepens, bilateral limb weakness, breathing deep and irregular (brainstem compression)

202
Q

What fruit does an extradural haemorrhage look like on imaging?

A

A lemon

203
Q

How does a subarachnoid haemorrhage present?

A

With an acute headache

204
Q

What does anosognosia and agnosia mean? When might a patient present with these symptoms?

A

Anosognisia = Lack of insight
Agnosia = Cannot recognise self
May be seen in patients with AD

205
Q

What is the pathophysiology behind Lambert Eaton Myasthenic Syndrome?

A

Antibodies against voltage-gated Ca 2+ channels on pre-synaptic membrane

206
Q

How does Lambert Eaton Myasthenic Syndrome present?

A

Gait difficulty, autonomic involvement (dry mouth, constipation and impotence), hyporeflexia and weakness

207
Q

When would the weakness associated with Lambert Eaton Myasthenic Syndrome improve?

A

After exercise

208
Q

What are the treatment options for Lambert Eaton Myasthenic Syndrome?

A
  • Pyridostigmine (is a acetylcholinesterase inhibitor)
  • 3,4- diaminopyridine
  • IV Igs
209
Q

Which malignancy is Lambert Eaton Myasthenic Syndrome linked to?

A

Small-cell lung cancer

210
Q

What regular imaging must you do for a patient with Lambert Eaton Myasthenic Syndrome, and why?

A

Regular CXR/HRCT as symptoms may precede cancer

211
Q

What would happen if you give Edrophonium to someone in cholinergic crisis?

A

It will worsen their muscle weakness by inducing depolarizing block.

212
Q

What sort of respiratory failure would neuromuscular disease cause?

A

Type 2 respiratory failure

Medicine (15 decks)

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