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Y6 > Neurology > Flashcards

Neurology Flashcards

1
Q

What is conduction dysphasia?

A

Speech fluent, but repetition poor. Comprehension is relatively intact

Caused by lesions involving the supramarginal gyrus, which is located in the parietal lobe and receives blood supply from the middle cerebral artery.

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2
Q

What is Wernicke’s dysphasia?

A

Difficulty understanding written and spoken language despite intact speech fluency.

Caused by lesions involving the superior temporal gyrus.

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3
Q

What is Broca’s (expressive) dysphasia?

A

Typically presents with partial or complete loss of language production (spoken or written) despite retention of language comprehension.

Caused by lesions involving the inferior frontal gyrus.

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4
Q

What is global dysphasia?

A

Typically only able to produce and comprehend a very small number of words. The capacity to write and speak is significantly impaired and comprehension of language is similarly heavily affected.

Caused by lesions involving both the superior temporal gyrus and inferior frontal gyrus.

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5
Q

What is dysarthria?

A

Cerebellar lesions can cause dysarthria, which is a motor speech disorder distinct from aphasia. Patients with dysarthria find it difficult to form and pronounce words/phrases. However, the capacity to form meaningful spoken and written language, and understand language remains intact.

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6
Q

What is the medical treatment for seizures?

A

1st line - PR diazepam or buccal midazolam (prehospital); or IV lorazepam (hospital)

2nd line - IV phenytoin, levetiracetam or sodium valproate

3rd line (if 45 mins without success) - general anaesthesia or phenobarbital

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7
Q

What causes normal pressure hydrocephalus and what is the triad of symptoms?

A

Characterised by ventriculomegaly, usually with normal cerebrospinal fluid (CSF) pressures

Triad: dementia, urinary incontinence and gait abnormality

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8
Q

What is the presentation of a 4th nerve (trochlear) palsy?

A

Issues with the ability to look downward –> vertical diplopia. This would make activities such as reading and walking downstairs particularly difficult.

On examination, you would notice upward deviation that increases in adduction, slight limitation of abduction, and outward rotation of the affected eye.

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9
Q

What imaging should all TIA patients undergo?

A

Urgent carotid doppler

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10
Q

What is the preferred brain imaging modality for TIA patients?

A

MRI brain with diffusion-weighted imaging

*This is more sensitive to areas of ischaemia than contrast-enhanced MRI

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11
Q

Where is the lesion in a bitemporal hemianopia?

A

Lesion of optic chiasm

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12
Q

In bitemporal hemianopia, give an example of a lesion causing:

*Upper quadrant defect > lower quadrant defect
*Lower quadrant defect > upper quadrant defect

A

Upper quadrant defect > lower quadrant defect = inferior chiasmal compression, commonly a pituitary tumour

Lower quadrant defect > upper quadrant defect = superior chiasmal compression, commonly a craniopharyngioma

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13
Q

What are common signs in subacute combined degeneration of the spinal cord?

A
  • Damage to the posterior columns - loss of proprioception, light touch and vibration sense (sensory ataxia and a positive Romberg’s test).
  • Damage to lateral columns - spastic weakness and upgoing plantars (UMN signs).
  • Damage to peripheral nerves - absent ankle and knee jerks (LMN signs).
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14
Q

Which do you replace first, B12 or folate?

A

B12

*Think BeFOre

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15
Q

A patient presenting to the emergency department undergoes a CT head scan. The report describes a hypodense collection around the convexity of the brain that is not limited to suture lines.

What is the most likely radiological diagnosis?

  • Subarachnoid haemorrhage
  • Extradural haematoma
  • Acute subdural haematoma
  • Chronic subdural haematoma
  • Intracerebral haematoma
A

Chronic subdural haematoma

On CT imaging, acute haematomas appear bright (hyperdense) whereas chronic haematomas appear dark (hypodense). Extradural haematomas are limited by suture lines whereas subdural haematomas are not. Intraparenchymal haematomas arise within the brain substance. Subarachnoid haemorrhage are typically seen as hyperdensity within the basal cisterns and sulci of the subarachnoid space.

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16
Q

What needs to be monitored when giving phenytoin?

A

Cardiac monitoring due to pro-arrhythmogenic effects

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17
Q

What should you do if a patient on warfarin/a DOAC/ or has a bleeding disorder and they are suspected of having a TIA?

A

They should be admitted for a CT scan to rule out haemorrhage

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18
Q

What is the most common cause of cavernous sinus syndrome and what are the symptoms?

A

Most commonly caused by cavernous sinus tumours

Diagnosis is based on signs of pain, opthalmoplegia, proptosis, trigeminal nerve lesion (opthalmic branch) and Horner’s syndrome.

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19
Q

What is the first-line management for trigeminal neuralgia?

A

Carbamazepine

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20
Q

What is the management of Bell’s Palsy?

A

Oral prednisolone if within 72 hours of presentation

Eye drops to prevent exposure keratopathy

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21
Q

What drugs can cause idiopathic intracranial hypertension?

A
  • COCP
  • Steroids
  • Tetracyclines
  • Retinoids (isotretinoin, tretinoin) / vitamin A
  • Lithium
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22
Q

A 72-year-old man who is being treated for Parkinson’s disease is reviewed. Which one of the following features should prompt you to consider an alternative diagnosis?

  • Micrographia
  • Impaired olfaction
  • REM sleep behaviour disorder
  • Diplopia
  • Psychosis
A

Diplopia

Diplopia is not common in Parkinson’s disease and may suggest an alternative cause of parkinsonism such as progressive supranuclear palsy

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23
Q

What is pituitary apoplexy and what causes it?

A

Sudden enlargement of a pituitary tumour (usually non-functioning macroadenoma) secondary to haemorrhage or infarction.

Precipitating factors:
* hypertension
* pregnancy
* trauma
* anticoagulation

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24
Q

What is the management of pituitary apoplexy?

A
  • urgent steroid replacement due to loss of ACTH
  • careful fluid balance
  • surgery
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25
Q

What is the usual cause of a painful 3rd nerve palsy?

A

Posterior communicating artery aneurysm

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26
Q

What are two important causes of seizure that you should rule out first?

A

Hypoxia and hypolgycaemia

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27
Q

How does a common peroneal nerve palsy present?

A

Weakness of foot dorsiflexion and foot eversion (foot drop) + sensory loss over the lateral aspect of the lower leg

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28
Q

What are common oculomotor dysfunction signs seen in Wernicke’s encephalopathy?

A

Nystagmus
Ophthalmoplegia - lateral rectus palsy, conjugate gaze palsy

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29
Q

What are features of a temporal lobe seizure?

A

An aura occurs in most patients:
* typically a rising epigastric sensation
* also psychic or experiential phenomena, such as déjà vu, jamais vu
* less commonly hallucinations (auditory/gustatory/olfactory)

Automatisms (e.g. lip smacking/grabbing/plucking)
Post-ictal dysphasia

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30
Q

What is the first line treatment of focal seizures?

A
  • first line: lamotrigine or levetiracetam
  • second line: carbamazepine, oxcarbazepine or zonisamide
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31
Q

What is the first line treatment of long-term generalised tonic-clonic seizures?

A

males: sodium valproate
females: lamotrigine or levetiracetam

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32
Q

What type of food diet is useful in hard-to-treat epilepsy such as in Lennox-Gastaut syndrome?

A

Ketogenic diet

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33
Q

What is Miller Fisher syndrome?

A
  • variant of Guillain-Barre syndrome
  • associated with ophthalmoplegia, areflexia and ataxia. The eye muscles are typically affected first
  • usually presents as a descending paralysis rather than ascending as seen in other forms of Guillain-Barre syndrome
  • anti-GQ1b antibodies are present in 90% of cases
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34
Q

What is thoracic outlet syndrome?

A

Thoracic outlet syndrome (TOS) is a disorder involving compression of brachial plexus, subclavian artery or vein at the site of the thoracic outlet. TOS can be neurogenic or vascular; the former accounts for 90% of the cases.

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35
Q

What is the clinical presentation of neurogenic vs vascular thoracic outlet syndrome (TOS)?

A

Neurogenic TOS
* painless muscle wasting of hand muscles, with patients complaining of hand weakness e.g. grasping
* sensory symptoms such as numbness and tingling may be present
* if autonomic nerves are involved, the patient may experience cold hands, blanching or swelling

Vascular TOS:
* subclavian vein compression leads to painful diffuse arm swelling with distended veins
* subclavian artery compression leads to painful arm claudication and in severe cases, ulceration and gangrene

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36
Q

What is the classic history of vestibular schwannoma (acoustic neuroma)?

A

Vertigo
Unilateral hearing loss
Unilateral tinnitus
Absent corneal reflex

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37
Q

What is the role of IV mannitol in raised ICP?

A

Used in patients with raised ICP due to trauma

It is a hypertonic agent which increases systemic osmolality, causing an osmotic shift of water out of the brain parenchyma. This medication is used in patients with raised intracranial pressure (ICP) secondary to traumatic brain injury to reduce the pressure and increase diuresis.

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38
Q

What is the role of IV steroids in raised ICP?

A

Used in raised ICP secondary to vasogenic oedema from central nervous system infections or neoplasms.

It has no role in treating raised ICP in traumatic brain injury and hence would not be appropriate in this patient.

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39
Q

What is Steven Johnson syndrome?

A

Life-threatening skin and mucous membrane disorder, commly as a reaction to certain medication

  • Fever
  • A sore mouth and throat
  • Fatigue
  • Burning eyes
  • Unexplained widespread skin pain
  • A red or purple rash that spreads
  • Blisters on your skin and the mucous membranes of the mouth, nose, eyes and genitals
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40
Q

Which medications can cause Steven Johnson syndrome?

A
  • Anti-gout medications, such as allopurinol
  • Medications to treat seizures and mental illness (anticonvulsants and antipsychotics)
  • Antibacterial sulfonamides (including sulfasalazine)
  • Pain relievers, such as acetaminophen (Tylenol, others), ibuprofen (Advil, Motrin IB, others) and naproxen sodium (Aleve)
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41
Q

What is the management of Steven Johnson syndrome?

A

Stop all medication, obtain IV access and begin fluid hydration

You can also consider:
* creams and dressings to moisturise and protect the skin
* strong painkillers to help ease any pain
* medicines to control inflammation and prevent infection

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42
Q

What investigation is important in acute angle-closure glaucoma?

A

Tonometry

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43
Q

What would you see on LP in GBS?

A

Isolated raise in protein - rise in protein with a normal white blood cell count (albuminocytologic dissociation), found in 66% of patients

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44
Q

What is the first investigation you do in a multiple sclerosis patient with bladder dysfunction?

A

USS of kidneys, ureter and bladder to assess for bladder emptying

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45
Q

What is syringomelia?

A

Dilatation of a CSF space within the spinal cord. It occurs within the cervical and thoracic segments and causes compression of the spinothalamic tracts decussating in the anterior white commissure. This results in dissociative loss of sensation of pain, temperature and non-discriminative touch. There is classically a ‘cape-like’ distribution of this sensory loss.

*Associated with Chiari formations which is herniation of cerebellar tonsils through foramen magnum

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46
Q

What is autonomic dysreflexia?

A

It is a medical emergency that usually occurs above the T6 level when there is a spinal cord injury. There is abnormal and excessive response of the autonomic nervous system where the parasymaphetic nervous system is prevented by the cord lesion. These are usually trigerred by faecal impaction and urinary retention

This results in an unbalanced physiological response, characterised by extreme hypertension, flushing and sweating above the level of the cord lesion, agitation, and in untreated cases severe consequences of extreme hypertension have been reported, e.g. haemorrhagic stroke.

Treatment: removal/control of the stimulus and treatment of any life-threatening hypertension and/or bradycardia.

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47
Q

What are the differences in the antibodies of Myasthenia Gravis and Lambert Eaton syndrome?

A

Myasthenia Gravis - antibody against Ach Receptor

Lambert Eaton syndrome - antibody against voltage gated calcium channels

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48
Q

How do features of Lambert Eaton syndrome differ compared to Myasthenia Gravis?

A

Autonomic symptoms - dry mouth, impotence, difficulty micturating
Weakness improves with exercise
No ophthalmoplegia and ptosis unlike in MG

49
Q

How do EMGs of Myasthenia Gravis and Lambert Eaton syndrome differ?

A

Myasthenia Gravis - on repeated nerve stimulation, there is decremental response

Lambert Eaton syndrome - on repeated nerve stimulation, there is incremental response

50
Q

How does acute blood look like on a CT?

A

White hyperdense collection

51
Q

Which lobe does herpes simplex encephalitis usually affect?

A

Temporal lobe (hypodensities on CT, or hyperintensities on MRI)

Presentation: aphasia, hemiparesis, memory loss

52
Q

What are features of an essential tremor and what is the management?

A

Autosomal dominant condition usually affecting both upper limbs:
* postural tremor: worse if arms outstretched
* improved by alcohol and rest
* most common cause of titubation (head tremor)

Management:
* propranolol is first-line
* primidone is sometimes used

53
Q

What is the acute and prophylactic management of cluster headache?

A

Acute:
* 100% oxygen (80% response rate within 15 minutes)
* subcutaneous triptan (75% response rate within 15 minutes)

Prophylaxis:
* verapamil is the drug of choice

54
Q

What is paroxysmal hemicrania?

A

Attacks of severe, unilateral headache, usually in the orbital, supraorbital or temporal region. These attacks are often associated with autonomic features, usually last less than 30 minutes and can occur multiple times a day.

Treatment = indomethacin

*Shares may similarities with cluster headaches

55
Q

What is Hoffman’s sign?

A

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.

It is associated with upper motor neurone disease such as multiple sclerosis or degenerative cervical myelopathy

56
Q

What is amyotrophic lateral sclerosis?

A

ALS is a form of MND characterised by LMN signs in the arms and UMN signs in the legs. Asymmetric limb weakness is the most common presentation of ALS.

57
Q

What is primary lateral sclerosis?

A

Although this is also a form of MND, it presents with UMN signs only, therefore only brisk reflexes and increased tone would be present. Since there are no LMN signs, there would not be any absent or weak reflexes, fasciculations, or atrophy.

58
Q

Which cranial nerves are affected in a vestibular schwannoma?

A

CN V: absent corneal reflex
CN VII: facial palsy
CN VIII: vertigo, unilateral sensorineural hearing loss, unilateral tinnitus

*Vestibular schwannomas (saka acoustic neuromas) account for approximately 5% of intracranial tumours and 90% of cerebellopontine angle tumours.

59
Q

What condition is associated with bilateral vestibular schwannomas?

A

Neurofibromatosis type 2

60
Q

What hand muscles does the median nerve supply?

A

LOAF:
* Lateral 2 lumbricals
* Opponens pollicis
* Abductor pollicis brevis
* Flexor pollicis brevis

*median nerve may be injured in a Colle’s fracture

61
Q

When do you refer Bell’s palsy to ENT?

A

If the paralysis shows no sign of improvement after 3 weeks

62
Q

What is used as prophylaxis for cluster headaches?

A

Verapamil

63
Q

What can be given in an acute cluster headache attack?

A
  • 100% oxygen (80% response rate within 15 minutes)
  • Subcutaneous triptan (75% response rate within 15 minutes)
64
Q

How does a pontine haemorrhage present?

A
  • Reduced GCS
  • Paralysis
  • Bilateral pin point pupils
65
Q

What is the management of a myasthenic crisis?

A

Intravenous immunoglobulin & plasma electrophoresis

66
Q

What is the management of long-term myasthenia gravis?

A
  • Long-acting acetylcholinesterase inhibitors (pyridostigmine)
  • Immunosuppresion (prednisolone, azathioprine, cyclosporine)
  • Thymectomy
67
Q

What are causes of syringomelia?

A
  • A Chiari malformation: strong association
  • Trauma
  • Tumours
  • Idiopathic
68
Q

What are features of syringomelia?

A
  • Loss of sensation to temperature but the preservation of light touch, proprioception and vibration - classic examples are of patients who accidentally burn their hands without realising - due to the crossing spinothalamic tracts in the anterior commissure of the spinal cord being the first tracts to be affected
  • Spastic weakness (predominantly of the lower limbs)
  • Neuropathic pain
  • Upgoing plantars
  • Autonomic features: Horner’s syndrome due to compression of the sympathetic chain & bowel and bladder dysfunction
  • Scoliosis will occur over a matter of years if the syrinx is not treated
69
Q

What is an ataxic gait?

A

Wide-based gait and unable to coordinate his lower limbs to walk in a heel-to-toe fashion

*This is usually seen in cerebellar disease

70
Q

What is an antalgic gait?

A

Limping caused by pain that is worse when weight-bearing on the affected limb

71
Q

What is a high stepping gait?

A

Seen in patients that have foot drop (due to a common peroneal nerve injury).

This presents with the patient lifting the affected leg up higher to prevent their foot from dragging across the floor as they walk.

72
Q

What is a trendelenburg gait?

A

The pelvis drops to the contralateral side causing the trunk to shift while walking and is often due to congenital hip problems, hip fractures, and gluteus medius muscle weakness.

73
Q

What is a waddling gait?

A

This is due to weakness in the pelvic girdle and thigh muscles and is characterised by the patient circumducting their leg when walking to compensate for the weakness. It is often due to pregnancy, muscular dystrophies and congenital hip problems.

74
Q

What is the management of a brain abscess?

A
  • Surgery: a craniotomy is performed and the abscess cavity debrided
  • IV antibiotics: IV 3rd-generation cephalosporin + metronidazole
  • Intracranial pressure management: e.g. dexamethasone
75
Q

In acute stroke, when should you start anticoagulation?

A

2 weeks after event to prevent haemorrhagic transformation.

In the meantime, provide dual antiplatelet therapy

76
Q

What scale is used to measure the disability or dependence in activities of daily living in stroke patients?

A

Barthel index

77
Q

What can be given in neuropathic pain in peripheral neuropathy caused by diabetes?

A

Amitriptyline
Duloxetine
Gabapentin
Pregabalin

78
Q

How does controlled hyperventilation help reduce raised ICP?

A

Reduce pCO2 → vasoconstriction of the cerebral arteries → reduced ICP
leads to rapid, temporary lowering of ICP.

However, caution needed as may reduce blood flow to already ischaemic parts of the brain

79
Q

How does a basilar artery infarct present?

A

“locked-in syndrome”

  • An acute decreased GCS and advanced motor symptoms.
  • Insidious, gradual deterioration in GCS and motor symptoms with a subsequent sudden advanced decrease in GCS and motor symptoms.
  • A ‘herald hemiparesis’ with associated headache and vision changes prior to the onset of permanent symptoms of motor loss.
80
Q

What is a common trigger of cluster headaches?

A

Alcohol

81
Q

What can be seen on head CT or MRI in Alzheimer’s disease?

A

Cerebral atrophy mainly in the regions of the cortex and hippocampus

82
Q

In which condition do you see atrophy of the frontal and temporal lobes?

A

Frontotemporal dementia

83
Q

In which condition do you see hyper-attenuating area in the basilar cistern (Circle of Willis)?

A

Subarachnoid haemorrhage

Hyper-attenuating (bright areas) areas are seen in the basilar cistern and spread out via the Sylvian fissures forming the classic ‘star sign’ as blood fills the subarachnoid space.

84
Q

What does several, small, hypo-attenuating areas spread out in the cerebral cortex suggest on a CT scan?

A

Many transient ischaemic attacks (TIAs) or previous strokes

85
Q

What are psychogenic non-epileptic seizures?

A

aka pseudoseizures

Factors favouring pseudoseizures:
* pelvic thrusting
* family member with epilepsy
* much more common in females
* crying after seizure
* don’t occur when alone
* gradual onset

Factors favouring true epileptic seizures:
* tongue biting
* raised serum prolactin

86
Q

What are the different subtypes of multiple sclerosis?

A

Relapsing-remitting disease
Secondary progressive disease
Primary progressive disease
Progressive-relapsing disease

87
Q

What investigations are done in multiple sclerosis?

A

MRI
* high signal T2 lesions
* periventricular plaques
* Dawson fingers: often seen on FLAIR images - hyperintense lesions penpendicular to the corpus callosum

CSF
* oligoclonal bands (and not in serum)
* increased intrathecal synthesis of IgG

Visual evoked potentials
* delayed, but well preserved waveform

88
Q

What treatments are commonly given in relapsing-remitting MS?

A

Corticosteroids
Cyclophosphamide
IV immunoglobulins
Plasmapheresis

89
Q

What is the first-line management of idiopathic intracranial hypertension

A

Weight loss

90
Q

What is the management of post-lumbar puncture headache?

A

This is a low pressure headache which can be managed with:
* supportive initially (analgesia, rest)
* blood patch, epidural saline and intravenous caffeine

91
Q

How does lewy body dementia present?

A

Fluctuating confusion
Hallucinations
Features of Parkinsonism tend to manifest at the same time or after the onset of dementia

*Whilst in parkison’s dementia usually presents after 1 year of parkinsonian symptoms

92
Q

Name causes of bilateral facial nerve palsy

A
  • sarcoidosis
  • Guillain-Barre syndrome
  • Lyme disease
  • bilateral acoustic neuromas (as in neurofibromatosis type 2)
  • Bell’s palsy (1% are bilateral)
93
Q

How does a upper vs lower motor neurone lesion in a facial nerve palsy present?

A

upper motor neuron lesion ‘spares’ upper face i.e. forehead
lower motor neuron lesion affects all facial muscles

94
Q

What are signs of a cerebellar disease?

A

DANISH

Dysdiadokinesia / dysmetria
Ataxia
Nystagmus
Intention tremor
Speech - slurred or scanning
Hypotonia

95
Q

What are the three different types of syncope?

A

Reflex - most common
Orthostatic
Cardiac

96
Q

What are some causes of reflex syncope?

A
  • Vasovagal: triggered by emotion, pain or stress. Often referred to as ‘fainting’
  • Situational: cough, micturition, gastrointestinal
  • Carotid sinus syncope
97
Q

What are some causes of orthostatic syncope?

A
  • Primary autonomic failure: Parkinson’s disease, Lewy body dementia
  • Secondary autonomic failure: e.g. Diabetic neuropathy, amyloidosis, uraemia
  • Drug-induced: diuretics, alcohol, vasodilators
  • Volume depletion: haemorrhage, diarrhoea
98
Q

What are some causes of cardiac syncope?

A

Arrhythmias: bradycardias (sinus node dysfunction, AV conduction disorders) or tachycardias (supraventricular, ventricular)
Structural: valvular, myocardial infarction, hypertrophic obstructive cardiomyopathy
Others: pulmonary embolism

99
Q

What is the mnemonic to spot an acute stroke presentation?

A

BEFAST:
* Balance loss
* Eyesight changes
* Facial droop
* Arm weakness
* Speech difficulties
* Time to call 999

100
Q

What are features of idiopathic intracranial hypertension?

A
  • headache
  • blurred vision
  • papilloedema (usually present)
  • enlarged blind spot ± transient visual disturbances
  • pulsatile tinnitus
  • sixth nerve palsy may be present
101
Q

What drugs are commonly used in idiopathic intracranial hypertension?

A

1st line: acetazolamide (carbonic anhydrase inhibitor)
2nd line: topimarate

102
Q

What is the rule behind driving in epilepsy and seizures?

A

If first unprovoked/isolated seizure: 6 months seizure-free before driving again. If this is not met, then it is increased to 12 months

If established epilepsy diagnosis or multiple unprovoked seizures: seizure-free for 12 months.

If withdrawing from epilepsy medication: should not drive whilst anti-epilepsy medication is being withdrawn and for 6 months after the last dose

103
Q

What is Uhthoff’s phenomenon?

A

Seen in MS, where there is worsening of vision following rise in body temperature

104
Q

What is Lhermitte’s syndrome?

A

Seen in MS, where there is paraesthesiae in limbs on neck flexion

105
Q

What is the reason for performing carotid endarterectomy?

A

Carotid endarterectomy is considered in a patient who has had a TIA with carotid artery stenosis exceeding 70% on the side contralateral to the symptoms (of stroke or TIA). This is according to the ECST criteria

106
Q

What is a beta-2-transferrin test?

A

β-2-transferrin is a carbohydrate-free (desialated) form of transferrin, almost exclusively found in the CSF - this test is to detect the presence of CSF in bodily fluids

107
Q

What scoring system is used for pressure ulcers?

A

Waterlow score

108
Q

What is seen on imaging of normal pressure hydrocephalus?

A

Hydrocephalus with ventriculomegaly and no sulcal enlargement

109
Q

What are the differences in presentation of a posterior inferior cerebellar artery stroke vs anterior inferior cerebellar artery stroke?

A

Posterior inferior cerebellar artery stroke (lateral medullary syndrome, Wallenberg syndrome):
* Ipsilateral: facial pain and temperature loss
* Contralateral: limb/torso pain and temperature loss
* Ataxia, nystagmus

Anterior inferior cerebellar artery (lateral pontine syndrome):
* Symptoms are similar to Wallenberg’s (see above), but
* Ipsilateral: facial paralysis and deafness

110
Q

What is the management of medication overuse headaches?

A

Simple analgesia + triptans: stop abruptly
Opioid analgesia: withdraw gradually

111
Q

What is Hoffman’s sign?

A

Reflex test to assess for degenerative cervical myelopathy.

It is performed by gently flicking one finger on a patient’s hand. A positive test results in reflex twitching of the other fingers on the same hand in response to the flick.

112
Q

What common autonomic dysfuction is seen in Parkinson’s?

A

Postural hypotension

113
Q

What should you do if SAH is suspected but CT head done within 6 hours is normal?

A

Consider alternative diagnosis

New guidelines suggest that CT is very highly sensitive for SAH if it is done within 6 hours of onset. Therefore if CT is normal within 6 hours, it rules out a SAH and so no need to do an LP.

114
Q

What causes neurogenic shock?

A

Most often following a spinal cord transection, usually at a high level –> resultant interruption of the autonomic nervous system –> decreased sympathetic tone or increased parasympathetic tone –> decrease in peripheral vascular resistance mediated by marked vasodilation

115
Q

What test can be done to distinguish between an organic and non-organic cause of leg weakness?

A

Hoover’s sign

Hoover’s sign of functional leg weakness is a clinical examination maneuver used to assess for non-organic or functional weakness of the lower extremities. It is often employed in neurological examinations to distinguish between true weakness caused by a neurological disorder and functional or psychogenic weakness.

Here’s how Hoover’s sign is performed:

Patient Position:
The patient lies supine on an examination table.
Examiner’s Hand Placement:
The examiner places one hand under the heel of the patient’s affected leg, with the palm of the hand cupping the patient’s heel.
Instructions to the Patient:
The examiner instructs the patient to lift the affected leg straight up off the table while keeping the opposite leg relaxed on the table.
Observation:
While the patient attempts to lift the affected leg, the examiner assesses for any involuntary downward pressure or resistance on the hand under the heel.
Interpretation:
In a positive Hoover’s sign, if the patient is truly making an effort to lift the affected leg, there should be downward pressure on the examiner’s hand as a natural consequence of the action. If the examiner does not feel this downward pressure, it may suggest non-organic or functional weakness.

116
Q

What is the mechanism of action of alteplase?

A

Alteplase, also known as tissue plasminogen activator (tPA), is a thrombolytic agent used in the management of acute myocardial infarction. Its mechanism of action involves binding to fibrin in a thrombus (blood clot) and converting the entrapped plasminogen to plasmin. Plasmin then degrades fibrin, leading to clot dissolution and restoration of blood flow.

117
Q

What abx are given in cranial abscess?

A

IV 3rd-generation cephalosporin (e.g. ceftriaxone) + metronidazole

118
Q

How do the following nerve palsies present?

Oculomotor (III)
Trochlear (IV)
Abducens (VI)

A

Oculomotor (III):
* Ptosis
* ‘down and out’ eye
* Dilated, fixed pupil

Trochlear (IV):
* Affects superior oblique (eye cannot move down and out)
* Defective downward gaze → vertical diplopia

Abducens (VI):
* Affects lateral rectus
* Defective abduction → horizontal diplopia

119
Q

What is the treatment of normal pressure hydrocephalus?

A

Ventriculoperitoneal shunting

If no suitable for surgery: control of CVD riskfactors ± repeated LPs for removal of CSF

Y6 (24 decks)

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