Special senses + neurology

Question 1

Does central vertigo decrease with time?

Answer 1

Most patients with vertigo improve within days but continuous true
vertigo with nystagmus suggests a central lesion. Physiotherapy helps
the ‘compensation’ process by the brain.

Question 2

Are vestibular sedatives such as betahistine indicated in the treatment of
benign paroxysmal positional vertigo?

Answer 2

No; the best treatment is the Epley manoeuvre, which consists of gentle
but specific manipulation and rotation of the patient’s head to shift the
loose otoliths from the semicircular canals.

Question 3

Does the absence of nystagmus in Hallpike’s manoeuvre exclude benign
paroxysmal positional vertigo (BPPV), even in the presence of a typical
clinical picture and an absence of other possibilities? Does wearing
Frenzel’s goggles increase sensitivity?

Answer 3

The absence of nystagmus would bring the diagnosis into doubt,
although the sensitivity of the Hallpike manoeuvre is variable (50–80%).
Frenzel’s goggles are used to prevent visual fixation, which suppresses
nystagmus due to a peripheral lesions such as BPPV; they might help.

Question 4

With Ménière’s disease, what steps should be taken:

1. In acute attacks?
2. Before an attack starts?

Answer 4

1. In an acute attack, give cinnarizine

2. Low-salt diet, avoid caffeine, try betahistine

Question 5

proven medicine for tinnitus in UK

Answer 5

The treatment is that of the underlying cause, e.g. removal of earwax,
treatment of otitis media. Drugs (e.g. betahistine dihydrochloride) are
often used; their benefit is variable. Carbamazepine and phenytoin are
used in persistent cases. Intolerable tinnitus can sometimes be masked by
a hearing aid.

Question 6

Why do patients with Goldenhar’s syndrome experience speech delay,
despite the fact that they might be able to use their unaffected ear to
listen with?

Answer 6

Many have middle ear defects with impairment of hearing in addition to
the change in the ear itself

Question 7

In sinusitis, it is not the nasal cavity that is congested by excessive mucus
but the openings between the paranasal sinuses and nasal cavity. Why,
therefore, does sinusitis cause difficulty breathing?

Answer 7

two reasons: first, the sinusitis is usually secondary to an upper
respiratory tract infection (often viral); second, there is nasal obstruction.
Both of these will cause difficulty with breathing.

Question 8

What is the modern treatment and prognosis for glaucoma

Answer 8

Primary open-angle glaucoma is the common type and of course it does
lead to irreversible blindness (Box 20.1). The aim of treatment is to reduce
the intra-ocular pressure. This can be done either by reducing aqueous
production (with a topical beta-blocker, e.g. timolol) or increasing
aqueous drainage (uveoscleral outflow) with a prostaglandin analogue latanoprost. Sympathomimetics and carbonic anhydrase inhibitors are
also used. Reduction in the intraocular pressure reduces visual loss.
Apart from medical treatment, laser therapy and surgery are used but
without good evidence of their efficacy.

Question 9

What is the recommended treatment for slow age-related macular
degeneration of the eye?

Answer 9

A number of treatments have been introduced for neovascular (or
wet) age-related macular degeneration (ARMD) in the last few years.
Photodynamic therapy with verteporfin was the first to show a decrease
in visual loss. This has, however, been superseded by bevacizumab and
ranibizumab, both monoclonal antibodies that neutralize endothelial
growth factor A. They are very expensive.

Question 10

What does the term pseudo-papilloedema mean?

Answer 10

conditions that simulate disc oedema

Question 11

Could direct ophthalmoscopy falsely detect papilloedema due to error of
refraction?

Answer 11

Long-sighted refractive errors make the disc appear pink and ill-defined.
Opaque (myelinated) nerve fibres at the disc margin and hyaline bodies
can be mistaken for disc swelling

Question 12

What is the cause of bilateral macular oedema?

Answer 12

Diabetes mellitus is the most common cause. There is gradual onset
of blurring of vision. Fundoscopy often shows no other evidence of
retinopathy. Annual visual acuity should be checked

Question 13

How can one differentiate between papilloedema and a tilted disc on
fundus examination?

Answer 13

Venous congestion is present in true papilloedema. Fluorescent retinal
angiography is occasionally necessary to show true papilloedema.

Question 14

On fundus examination, does the preservation of the disc cup (no
obliteration) despite nasal blurring of the edges of the cup mean an
absence of papilloedema?

Answer 14

Preservation of disc cup – no papilloedema.

Question 15

What findings should be looked for during routine fundus examination
in patients on long-term chloroquine or other anti-malarial therapy for
treatment of systemic lupus erythematosus (SLE)?

Answer 15

The early changes are macular oedema, increased pigmentation and
granularity of the retina. The characteristic lesion is a central area of
depigmentation of the macula surrounded by an area of pigmentation – a
‘bull’s eye lesion’. This is usually accompanied by visual disturbances

Question 16

Which diseases are commonly associated with a macular star on
ophthalmoscopic examination?

Answer 16

A macular star is a ring of exudates between the disc and the macula.
It occurs with oedema of the disc, for example in hypertensive
encephalopathy, and in some infections, for example cat scratch fever

Question 17

Can a cataract in one eye produce an afferent pupillary defect in that eye?

Answer 17

yes

Question 18

What is meant by copper and silver wiring of retinal vessels on
ophthalmoscopy, what do they look like and which of them signifies
atherosclerosis?

Answer 18

Copper and silver wiring imply arteriolar thickening and both indicate
mild hypertensive retinopathy

Question 19

What is the mechanism of papilloedema? Is it that the intracranial
pressure exceeds the pressure of the central retinal vein?

Answer 19

Papilloedema means bilateral optic disc swelling. It is due to raised
intracranial pressure damaging the optic nerve sheath, giving rise to
optic disc swelling

Question 20

Painless loss of vision

Answer 20

● Cataract
● Open-angle glaucoma
● Retinal detachment
● Central retinal vein occlusion
● Central retinal artery occlusion
● Diabetic retinopathy (see K&C 7e, p. 1051)
● Vitreous haemorrhage
● Posterior uveitis
● Age-related macular degeneration
● Optic nerve compression
● Cerebral vascular disease

Question 21

Painful loss of vision

Answer 21

● Acute angle-closure glaucoma
● Giant cell arteritis (see K&C 7e, p. 1138)
● Optic neuritis (see K&C 7e, p. 1101)
● Uveitis
● Scleritis
● Keratitis
● Shingles
● Orbital cellulitis
● Trauma

Question 22

What are the causes of foot drop, and what is the likely treatment?

Answer 22

Foot drop with loss of eversion and dorsiflexion of the foot occurs when
the common peroneal nerve is injured at the head of the fibula (e.g.
from fracture or from compression by a leg plaster). The nerve is very
superficial at this point. Prolonged crossing of the legs, particularly in an
emaciated person, is a further cause. It can also occur in diseases affecting
the peripheral nerves and motor neurones in the spinal cord.

Question 23

What is the correct definition for dysaesthesia?

Answer 23

Abnormal sensations, often tingling or painful, occurring with minimal
stimulation.

Question 24

What is the difference between ‘light touch’ and ‘fine touch’ sensations
passed in the posterior column, and which one of these is tested with a
wisp of cotton?

Answer 24

There is no difference; most use the term ‘light touch’, which is used to
test sensation via the posterior columns

Question 25

What is apraxia of gait and what is Brun’s apraxia?

Answer 25

Apraxia means loss of ability to perform a function despite no sensory or motor abnormalities; in this case loss of ability to walk. It is due to bilateral frontal lesions. Brun’s syndrome is due to an intermittent blockage of the aqueduct of Sylvius, usually due to a brain tumour. Apraxia is one of the signs of this syndrome.

Question 26

Why is it that, when eliciting the plantar reflex, we are supposed to stop just before the ball of the great toe?

Answer 26

When eliciting the plantar reflex the stick should run along the outer edge of the sole of the foot from the heel towards the little toe. Babinski did not use a medial movement across the sole of the foot.

Question 27

Is there any rationale for giving dopamine agonists to aphasic patients?

Answer 27

Dopamine agonists are not of value in aphasic patients.

Question 28

Have either carbamazepine or dopamine agonists a role in the treatment of aphasia? If yes, what type of aphasia?

Answer 28

They have no confirmed role.

Question 29

Is bilateral VIth cranial nerve palsy always a false-localizing sign (i.e. does it indicate an increased intracranial pressure and not pathology of the nerves or their nuclei)?

Answer 29

The VIth nerve nucleus sends axons directly into the VIth nerve to supply the lateral rectus, and also into the contralateral medial longitudinal fasciculus and up into the IIIrd nerve nucleus where they synapse with neurones from the medial rectus. Damage to the VIth nerve nucleus prevents both eyes moving ipsilaterally. A bilateral VIth nerve palsy is always a false localizing sign.

Question 30

Can an optic tract lesion, which is mononuclear field loss (i.e. loss of vision in one eye) also be called ‘incongruous homonymous hemianopia’?

Answer 30

‘incongruous homonymous hemianopia’ is used for lesions in the optic tracts or chiasm. The word homonymous can only be used when the same half of both fields of vision is lost.

Question 31

How would you treat optic neuritis?

Answer 31

Optic neuritis is usually due to a demyelinating process, most commonly multiple sclerosis. Methylprednisolone iv is given with severe visual loss or two or more lesions on brain MRI. Interferon beta is also used to delay onset of clinical multiple sclerosis (MS).

Question 32

After two episodes of optic neuritis, one affecting each eye and 2 months apart, confirmed to be demyelinating in nature by visual evoked potentials, could a diagnosis of multiple sclerosis be reached in the absence of periventricular lesions on the MRI?

Answer 32

This is likely to be MS and MRI shows lesions in 85% of patients with clinical MS.

Question 33

While assessing the pupillary reflexes, the consensual light reflex is really difficult to see in the other eye. Are there any tips for that?

Answer 33

You might find that reducing the background illumination will help, with patient fixating a distant object.

Question 34

Is it clinically significant to examine the consensual light reflex? If there is a lesion of the IIIrd cranial nerve of the unilluminated eye to impair the consensual response, this will be clear by the other symptoms and signs of the IIIrd cranial nerve palsy on that eye. If there is a lesion of the optic nerve of the unilluminated eye, the patient will not have a direct light reflex of that eye when examining its own direct reflex. I am not sure how the IIIrd cranial nerve can lose only its parasympathetic fibres. It is difficult to see the unilluminated pupil when light is not directly shining on it.

Answer 34

Interruption of the oculomotor nerve abolishes the light reflex on the side of the lesion; the reflex (consensual) stays in the other eye. Damage to the retina or optic nerve causes absent light reflex in both eyes when light is shone into the eye on the side of the lesion.

Question 35

Should every patient with trigeminal neuralgia be given an MRI of the brain?

Answer 35

Yes, trigeminal neuralgia can occur in, for example multiple sclerosis and tumours of the 5th nerve.

Question 36

Is carbamazepine more effective than phenytoin in the treatment of trigeminal neuralgia? Would this patient need a higher dose of carbamazepine, and what is the upper limit?

Answer 36

Usually, yes. The maximum dose is 1.6 g daily.

Question 37

Is gabapentin effective in the treatment of trigeminal neuralgia?

Answer 37

Yes, although there are no good controlled trials.

Question 38

What medication is best used for the treatment of carbamazepineresistant trigeminal neuralgia?

Answer 38

Combination therapy, e.g. carbamazepine with phenytoin, baclofen or gabapentin.

Question 39

What are the common causes of recurrent lower motor facial nerve palsy?

Answer 39

Recurrent facial palsy is rare; it is usually idiopathic. It is called Melkersson’s syndrome

Question 40

In a case of facial nerve palsy, what is the value of preserved taste sensation? Does its preservation exclude upper motor affection and/or nuclear lesion or is it localized between the facial canal and the cerebellopontine angle?

Answer 40

Taste is not affected in supranuclear lesions (i.e. upper motor neurone lesions). Involvement of the facial nerve proximal to the origin of the chorda tympani will cause loss of taste. Lesions beyond the stylomastoid foramen will not affect taste

Question 41

Can Synacthen be used instead of steroids in the treatment of idiopathic Bell’s palsy and how long should the treatment last? What is the recommended dose?

Answer 41

No. Synacthen (tetracosactide) is an analogue of corticotrophin (adrenocorticotrophin hormone; ACTH). It is only used in stimulation tests to assess adrenocortical function

Question 42

Is aciclovir a helpful treatment for idiopathic Bell’s palsy?

Answer 42

Trials have shown benefit. Aciclovir with steroids (prednisolone 60 mg daily initially) is usually given for severe facial palsy and should be started in the first three days of the illness.

Question 43

In a child aged 5 years, can the presence of horizontal, fine, bilateral nystagmus with the fast component towards the point of fixation, with no other neurological or system abnormality, be considered a normal variant?

Answer 43

yes

Question 44

Are inner ear sedatives, and betahistine in particular, effective in the treatment of vertigo due to lateral medullary syndrome or any central lesion?

Answer 44

No these drugs are not very effective in this type of vertigo

Question 45

Are steroids appropriate in the treatment for vestibular neuronitis?

Answer 45

Yes; methylprednisolone alone is as effective as is the combination of methylprednisolone and valaciclovir, and better than valaciclovir alone. More trials are needed, but it is reasonable to use steroids.

Question 46

Why is there no gag reflex during the act of deglutition as I have seen that when we touch any thing to the posterior third of the tongue there is always gag reflex?

Answer 46

Fortunately we can overcome any gag reflex that is present when we swallow.

Question 47

Can cerebellar lesions cause head nodding? Is this involuntary movement diagnostic for a cerebellar lesion in a patient who does not display Parkinsonian features or essential tremor?

Answer 47

Head nodding is due to a basal ganglia lesion not a cerebellar lesion. It does occur without features of parkinsonism.

Question 48

1. What is the treatment of choice in symptomatic myoclonus resulting from a lesion of the cerebral cortex or spinal cord? 2. Does piracetam have a role in treatment of symptomatic myoclonus resulting from lesion of the cerebral cortex or spinal cord?

Answer 48

1. Valproate is sometimes used, particularly when the myoclonus is related to epilepsy. 2. Yes.

Question 49

Is ankle clonus diagnostic of pyramidal tract lesion?

Answer 49

Yes, if sustained. Unsustained ankle clonus can occur normally

Question 50

Is pronator drift pathognomonic of a pyramidal tract lesion or does it occur with any lesion of the motor system?

Answer 50

Providing there is no marked weakness of the outstretched limbs, pronator drift is pathognomonic of a pyramidal lesion.

Question 51

Can proximal muscle weakness be more than that of the distal muscles in cases of upper motor neurone lesions?

Answer 51

The weakness often starts distally, e.g. the hands, but then spreads to involve forearms, the biceps and triceps followed by shoulder muscles

Question 52

In the absence of either myopathy or radiculopathy, could a pyramidal tract lesion be diagnosed despite a distribution of weakness that is proximal more than distal?

Answer 52

Proximal weakness can occur with a pyramidal tract lesion.

Question 53

Are brisk deep tendon reflexes, rather than hyperreflexia, pathognomonic of pyramidal tract lesion?

Answer 53

This is a question of terminology. Brisk reflexes, to most clinicians, mean slightly exaggerated reflexes as seen in an anxious person. Hyperreflexia usually implies a pathological increase, i.e. an upper motor neurone (UMN) lesion

Question 54

What is Wartenberg’s reflex (sign), and is it diagnostic of a pyramidal tract lesion?

Answer 54

Pyramidal lesions sometimes produce only minor degrees of weakness accompanied by loss of skilful movements. In Wartenberg’s reflex the patient is asked to flex the terminal phalanges of the fingers of one hand against the flexed fingers of the examiner. On striking the back of the examiner’s fingers with a patellar hammer, the thumb remains extended and abducted in normals. Following a pyramidal lesion (corticospinal tract) the thumb adducts and flexes. This sign would only be very suggestive but not diagnostic of a pyramidal lesion; it is not often used

Question 55

Must an extensor plantar response be present in order to diagnose a pyramidal tract lesion even in the presence of weakness of pyramidal distribution and other pathological reflexes?

Answer 55

An extensor plantar response is a valuable sign in diagnosing a pyramidal tract lesion. However, it can sometimes be difficult to elicit, and in the presence of typical weakness and pathological reflexes a pyramidal lesion can still be diagnosed

Question 56

Is it common to find Babinski’s sign positive in Todd’s paralysis?

Answer 56

No; it is not common and investigation (cerebral CT or MRI) is required. Incidentally, it is better to use the term extensor plantar response rather than Babinski (which was described in babies).

Question 57

In a case of paraplegia owing to an upper motor neuron lesion, does the ability of the patient to sit indicate intact thoracic segments?

Answer 57

This is not a reliable observation. Remember the cord ends at L1, so a paraplegia by definition must occur with a lesion above this and below the cervical region.

Question 58

Can the Brown–Séquard syndrome be diagnosed with pyramidal weakness of one lower limb and hypoaesthesia of the other lower limb but with no dissociative sensory loss of the hypoaesthetic limb?

Answer 58

Brown–Séquard syndrome – hemisection of the cord – gives ipsilateral diminished proprioception and vibration sense and weakness, with contralateral decrease in pain and temperature sensation (because of crossing of the fibres of the spinothalamic tract). A small lesion in, for example, MS may give ipsilateral weakness and diminished sensation only. It is not strictly the Brown–Séquard syndrome.

Question 59

Is there more than one method of demonstrating dysdiadochokinesia in upper limbs?

Answer 59

Method 1 With the patient’s arm flexed to a right angle, the patient is then asked to pronate and supinate the forearm as rapidly as possible. Normal is rapid with no jerking; with dysdiadochokinesis, movements are slow and irregular. Method 2 The patient is asked to tap the examiner’s palm with the fingertips alternating in supination and pronation as fast as possible. This is irregular and slow in dysdiadochokinesis. If the tapping is done onto a hard surface, the sound will also be irregular.

Question 60

What is the difference between kinetic and intention tremors?

Answer 60

Kinetic and intention tremors are the same.

Question 61

What is the best treatment for rubral tremors besides treating the aetiology?

Answer 61

Treatment is unsatisfactory. Try propranolol, primidone or piracetam.

Question 62

What is meant by ‘inversion of reflexes’?

Answer 62

When the biceps and supinator reflexes are brisk this might be accompanied by finger flexion. Sometimes, however, finger flexion still occurs with depression of the direct reflex and this is called inversion. It is due to a lesion at C5–C6, which interrupts the reflex arc but if it compresses the corticospinal tract as well it will give exaggerated reflexes in lower segments (i.e. C7–C8 – finger flexion). An inverted knee jerk occurs with a lesion at L2–L4.

Question 63

Is it possible for patients with posterior column lesions to be suffering from allodynia, with pain on pressure to different musculoskeletal points? Or is this more likely to be caused by fibromyalgia?

Answer 63

Allodynia is an abnormal sensory experience (usually painful) to a normal stimulus. Patients with posterior column lesions do not suffer with allodynia.

Question 64

How do the clinical success rates of gabapentin and carbamazepine compare?

Answer 64

In patients with neuropathic pain, carbamazepine is still first-line therapy. Gabapentin is effective in painful diabetic neuropathy and postherpetic neuralgia

Question 65

What clinical tests can be done to determine dissociative sensory loss?

Answer 65

Dissociative means dissociation between posterior column sensation (light touch, vibration) and spinothalamic tracts (pain and temperature). These can be tested, e.g. with cotton wool and a sterile pin.

Question 66

What is the recommended dose of urograffin before performing contrastenhanced computed tomography? How far in advance should this be administered before imaging when an intracerebral abscess or glial tumour is suspected?

Answer 66

Any non-ionic monomeric contrast agent can be used. The dose is equivalent of 15 g iodine.

Question 67

How many urografin ampoules (76% concentration) should be administered before a CT brain scan with contrast searching for a mass lesion, and how many minutes before imaging should these be injected?

Answer 67

Use 300 mg iodine/mL dosage. Give 50 mL 10 minutes before the procedure.

Question 68

1. What is the difference between fluid-attenuated inversion recovery (FLAIR) and T2-weighted MRI scans? 2. What is the advantage of magnetization transfer pulse over a FLAIR MRI scan?

Answer 68

1. On T2-weighted images, tissue with short T2 decay times (fat) appears dark, while tissues with long T2 decay times (water) appear bright. FLAIR is used, for example, to suppress the high cerebrospinal fluid signal in T2 so that lesions can be seen more clearly. 2. Magnetization transfer coherence is a technique to increase the contrast-to-noise ratio between normal and pathological tissues

Question 69

Does lumbosacral MRI refer to lumbosacral spines or to lumbosacral cord segments?

Answer 69

It refers to lumbosacral spines.

Question 70

What type of painful stimuli can be applied in calculating the Glasgow Coma Scale for both motor and eye-opening responses, and how should these be applied?

Answer 70

Squeezing the Achilles tendon and rubbing the front of the chest hard are two common stimuli. Try to be consistent for comparison

Question 71

How can the Glasgow Coma Scale be assessed in a patient with receptive or expressive aphasia?

Answer 71

With difficulty! Do your best.

Question 72

How common is it for someone suffering a transient ischaemic attack (TIA) to totally lose consciousness? Also, what is the mechanism for losing consciousness with a TIA?

Answer 72

Loss of consciousness occurs but is rare. It usually occurs in TIAs affecting the posterior circulation. TIA is now defined as a transient episode of focal dysfunction caused by ischaemia without infarction. The time of <24 hours has been removed.

Question 73

What should the management be for a stenosis in the carotid artery causing transient ischaemic attack (TIA), and when is surgery recommended?

Answer 73

Surgery is recommended in TIA and stroke patients when stenosis narrows the carotid lumen by more than 70%; but not in patients with a total stenosis.

Question 74

In a patient with central retinal artery branch occlusion with carotid artery stenosis, what is the best management: warfarin, aspirin or carotid endarterectomy?

Answer 74

Stenosis of the carotid artery by greater than 70% should be managed surgically or by placing a stent.

Question 75

If a young patient who has suffered a stroke has a normal mental state, would this exclude a cerebral venous occlusion as an aetiology?

Answer 75

No.

Question 76

Does persistent hiccough following cerebrovascular ischaemic stroke localize to the medulla or to any other site?

Answer 76

Medulla and brainstem, but the anatomy is not clear.

Question 77

By what mechanism is vertebrobasilar insufficiency associated with circumoral numbness?

Answer 77

The symptoms of vertebrobasilar insufficiency can be vague, e.g. dizziness, which might be associated with hyperventilation, which can lead to circumoral numbness

Question 78

Why does lateral medullary syndrome result in ipsilateral diplopia due to cranial nerve VI?

Answer 78

Wallenberg, in his original description of the lateral medullary infarction syndrome, did not include diplopia. Diplopia does occur; remember that the VIth nerve is very near to the Vth nerve nucleus

Question 79

I have seen many established ischaemic stroke patients with CTdocumented capsular infarction and hemi-hypotonia despite exaggerated reflexes. How would you explain the hypotonia? Could it be due to a corticorubral fibre lesion?

Answer 79

Hypotonia is a feature of an acute upper motor neurone lesion, which may last for several days. This is replaced by hypertonia due to loss of the inhibiting effects of the corticospinal pathways.

Question 80

Thrombolytic therapy is used in patients with a cerebral infarct within the first 3 hours, whereas stroke by definition lasts 24 hours. So how do we define that it is infarct and not a transient ischaemic attack (TIA) on a CT scan within the first 3 hours in order to start tissue plasminogen activator (tPA) treatment?

Answer 80

Most patients with TIAs do not lose consciousness and also are not seen in hospital. Because the episodes are transient it is something that you get from the history. However, a CT/MRI scan is mandatory to rule out haemorrhage so that thrombolytic therapy can be started. Remember, an infarction will only be detected later on CT.

Question 81

Why do you treat dissection of the carotid artery with an anticoagulant in the acute management of stroke secondary to dissection? To me this seems paradoxical as it would increase the severity of dissection

Answer 81

Patients with a carotid artery dissection are often treated with anticoagulants despite the underlying bleeding into the vessel wall. As the blood enters the wall of the artery the lumen becomes progressively narrowed and thrombosed. It is to try to prevent further thrombosis and emboli occurring that anticoagulants are given.

Question 82

Last week, in a neurology viva, I was asked about the indications for heparinization in patients with a stroke. I want to know when I can stop heparin and what test I should use for assessing its therapeutic range

Answer 82

Heparin can be used in patients not suitable (because of lapse in time or risks) for thrombolysis but the data on benefit are scant. Aspirin is of benefit. On the whole heparin is not recommended. Active thromboplastin time (APTT) is used for monitoring heparin therapy

Question 83

Has heparin a role in the management of acute ischaemic stroke not accompanied by atrial fibrillation?

Answer 83

In general no, but occasionally heparin has been used in patients with recurrent transient ischaemic attacks on antiplatelet therapy

Question 84

1. In the treatment of a stroke, does low-molecular-weight heparin (LMWH) have an advantage over heparin? 2. In an ischaemic stroke in evolution, for how long should heparin be administered?

Answer 84

1. No; heparin is not used in most stroke cases. Studies with LMWH have shown similar results to unfractionated heparin. 2. In one trial, 7 days. At 3 months there was no benefit

Question 85

Can streptokinase be used in acute cerebral infarction and, if so, what is the dose?

Answer 85

No, streptokinase is not now used as altepase is preferred. Dose is 0.9 mg/kg (maximum 90 mg).

Question 86

There seems now to be a consensus about starting aspirin therapy in acute ischaemic strokes as early as possible. Why has this changed from past recommendations to avoid aspirin early (during the first 48 hours) during the ischaemic stroke on the pretext that it could convert an ischaemic infarct into a haemorrhagic one, thus increasing the dangers of complications like cerebral oedema and raised intracranial pressure? If both opinions are based on clinical trials, what is the significance of the much hyped ‘evidence-based medicine’?

Answer 86

The CAST study, which involved over 21 000 patients, showed a clear benefit of aspirin for acute ischaemic strokes. Because of this, it is now recommended that aspirin be given to all patients who are not eligible for thrombolytic (altepase) therapy. Accurate CT or MRI can rule out haemorrhage quickly so that aspirin can be used.

Question 87

I understand that a loading dose of clopidogrel 600–900 mg can be given to ischaemic stroke in evolution and can stop the evolving deficit. Would you agree?

Answer 87

The evidence is inconclusive. CT/MRI must always be performed to rule out haemorrhage. Aspirin is probably just as good; the combination better, but with a higher risk of haemorrhage.

Question 88

Is there any rationale for giving patients with recurrent strokes a combination of aspirin and anticoagulant?

Answer 88

There is little rationale for this treatment although it is sometimes advocated for recurrent strokes, particularly transient ischaemic attacks.

Question 89

1. Does a dipyridamol–aspirin combination have any superiority over aspirin alone in the secondary prevention of a stroke? 2. Is an aspirin plus anticoagulant combination superior to a dipyridamol— aspirin combination in the treatment of recurrent ischaemic stroke not controlled by aspirin alone?

Answer 89

1. There may be some value in the dipyridamol–aspirin combination but there is no very good evidence of efficacy and this adds to the expense of therapy 2. No, there is no evidence that aspirin plus anticoagulant combination is superior to antiplatelet therapy.

Question 90

1. Is it safe to give piracetam to patients with primary intracerebral haemorrhage? Does it have a neuroprotective effect? 2. Is it safe to give a patient with excessively high blood pressure (as a sequela to recent primary intracerebral haemorrhage) angiotensin-converting enzyme inhibitors to lower the blood pressure? 3. Is it indicated to give piracetam or vincamine to a patient with middle cerebral artery territorial infarction? Do these have any neuroprotective effect?

Answer 90

1. Yes it is safe. There is no good evidence of neuroprotective effect. 2. Yes it is safe but it is probably wiser to use atenolol or amlodipine, which have been more widely used. 3. Neither are of real help.

Question 91

What is the mechanism by which subarachnoid haemorrhage is associated with subhyaloid haemorrhages on fundus examination, and how can cerebrospinal fluid (CSF) gain access to the subhyaloid space inside the eye?

Answer 91

Tracking of blood beneath the retinal hyaloid membrane. CSF does not gain access to the subhyaloid space

Question 92

What is the recommended dosage for nimodipine given intravenously in cases of subarachnoid haemorrhage, and when should the treatment start? For how long should the dose be continued?

Answer 92

● Prevention: nimodipine 60 mg orally (or by nasogastric tube). This should be given every 4 hours starting within 4 days of haemorrhage. Give for 21 days. ● Treatment: intravenous infusion into central veins, initially 1 mg/hour increasing to 2 mg/hour if no fall in blood pressure. Continue for 5–10 days and at least 5 days after surgery.

Question 93

I read recently that hyperuricaemia has something to do with stroke? Is it recommended to give allopurinol to stroke patients irrespective of their serum uric acid?

Answer 93

No, allopurinol should not be given to stroke patients.

Question 94

Is there a link between hyperuricaemia (although asymptomatic) and atherosclerosis and cerebral ischaemic stroke?

Answer 94

There is, of course, a causal link between atherosclerosis and ischaemic stroke. Hyperuricaemia is often seen in obese, diabetic, hypertensive patients, particularly if they drink excess alcohol. It is not causal.

Question 95

Are phenytoin and carbamazepine indicated in myoclonus, occasionally seen in ischemic strokes?

Answer 95

No. They are not helpful

Question 96

What is the treatment of chorea or action myoclonus resulting from embolic stroke to the area of basal ganglia? Does the L-dopa that is given by some neurologists improve the condition? Does valproate have a role if the case is action myoclonus?

Answer 96

Valproate is only useful if the myoclonus is part of the epileptic syndrome. L-dopa is not usually of benefit.

Question 97

How should a patient with a haemorrhagic cerebrovascular accident be managed while also having an extensive inferior wall myocardial infarction?

Answer 97

This is very difficult as thrombolytic therapy is completely out of the question. Angioplasty with stenting might be an option but this usually requires antiplatelet therapy, which would be contraindicated. All in all, a patient such as you describe would not be a good-risk candidate.

Question 98

What is the best way to manage cortical vein thrombosis? If heparin is to be used, what is the recommended dosage and how long should this treatment last?

Answer 98

There are a few well-constructed randomized controlled trials (RCTs) in this condition. Heparin is given in standard doses but the evidence for its value is small. It is followed by warfarin and heparin is stopped when the international normalized ratio is in the target range of 2.5.

Question 99

In the case of cortical vein thrombosis, for how long should | anticoagulation be continued?

Answer 99

Possibly for 1 year.

Question 100

How long should antiepileptic treatment be continued for a stroke patient who has the first seizure within the first 24 hours of the stroke?

Answer 100

Seizures occur in 3% of hospitalized acute-stroke patients, usually those with a large cortical infarct or haemorrhage. Recurrence rates after first seizures are higher in groups with vascular disease than within idiopathic epilepsy.

Question 101

For how long should antiepileptic drugs be given to patients having their first seizure within the first week of their cerebrovascular stroke?

Answer 101

Epilepsy in the first week after a cerebrovascular accident does not usually lead to persistence. Drugs could be withdrawn after about 6 months

Question 102

What are the causes of epilepsy with a normal electroencephalogram (EEG), other than metabolic causes? Could epilepsy due to CNS causes be associated with a normal EEG? Could epilepsy due to the gradual withdrawal of an antiepileptic drug occur as much as 1 year later?

Answer 102

During a seizure, the EEG is almost invariably abnormal because spikes reach the brain surface. Many people with epilepsy have a normal EEG between fits and thus a normal EEG between attacks is of no help in diagnosis. Similarly, mild EEG abnormalities are not uncommon in the general population and should not in themselves be used to diagnose epilepsy. Metabolic brain disorders, e.g. hepatic encephalopathy, give specific EEG abnormalities but again are not helpful in the diagnosis of epilepsy. Whenever antiepileptic drugs are withdrawn there is a risk that the patient will have another epileptic attack; this is not due to the drugs.

Question 103

What are uncinate fits?

Answer 103

Uncinate fits are characterized by an olfactory or gustatory aura often with motor movement, e.g. licking lips.

Question 104

Are epileptic fits occurring strictly during sleep pathognomonic for frontal or temporal lobe epilepsy or any other epileptic syndrome?

Answer 104

Epilepsy during sleep is not pathognomonic for any particular epileptic syndrome.

Question 105

Despite childhood somnambulism often disappearing later in life, could its first presentation after puberty on a nearly daily basis, raise the possibility of frontal lobe epilepsy or other organic pathology? Would an electroencephalogram (EEG) or polysomnography confirm this?

Answer 105

An organic pathology is possible. It must be distinguished from postictal automatism following sleep seizures and from complex partial seizures. An abnormal EEG would help in the diagnosis.

Question 106

Could masticatory automatisms follow a generalized tonic–clonic fit? If so, would these or would these not be considered part of the same fit?

Answer 106

These are not usual in tonic–clonic fits. They occur more often in a complex partial seizure in the period of behavioural arrest before the ictal phase

Question 107

Is it common for epileptic patients to have postictal vomiting? If so, how often does this occur?

Answer 107

It is very uncommon.

Question 108

In temporal lobe epilepsy, what is meant by ‘cephalic aura’ and how does this manifest itself?

Answer 108

In partial seizures arising from the temporal lobe, auras are common. They can be visual (flashing lights) or olfactory (smell), for example.

Question 109

What is the difference between pseudoseizures and pseudopseudoseizures?

Answer 109

‘Pseudoseizures’ is the term used for seizures that appear to be epileptic but are not. ‘Pseudo-pseudoseizures’ is a term occasionally used to suggest a psychogenic cause

Question 110

Does a delay in controlling seizures result in more frequent seizures and a more resistant epileptic disorder? And, if so, does this apply to all seizure types?

Answer 110

No, delay does not result in more frequent seizures

Question 111

What genetic tests are recommended for epilepsy and Huntington’s disease?

Answer 111

Genetic disorder accounts for less than 1% of patients with epilepsy and tests are not recommended. Mutation analysis is available for suspected Huntington’s disease but should only be performed by designated centres.

Question 112

Is it useful to take an electroencephalograph (EEG) after a patient’s first-ever seizure and, if so, when is the best time to do so? Would you recommend taking an EEG after every seizure and before diagnosis?

Answer 112

Despite its limitations, an EEG is still worthwhile doing after a first fit. It might be useful to show an abnormality, which helps to confirm the diagnosis. A normal EEG, however, does not exclude epilepsy (see K&C 7e, p. 1141). Once a diagnosis is established, further EEGs are not required

Question 113

How often can drop attacks with loss of consciousness be due to atonic fits in the absence of any other type of fit?

Answer 113

‘Drop attacks’, by definition, result in the patient falling to the ground, but there is no loss of consciousness.

Question 114

How often are atonic fits the cause of falls with loss of consciousness in a patient not suffering from any other type of seizure?

Answer 114

They do not cause falls very often.

Question 115

Can mild anaemia (haemoglobin 10.8 g/dL) in a young female cause syncopal attacks that are preceded by a sense of falling, followed by a loss of consciousness and drowsiness for up to 1 hour? Do these data favour complex partial seizures rather than syncope?

Answer 115

The data favour complex partial seizures. Most patients with a haemoglobin of 10.8 g/dL are asymptomatic

Question 116

I am confused between simple and complex partial seizures. Does the loss of consciousness define complex partial seizures in an otherwise what seems to be ‘simple partial’ clinically?

Answer 116

Yes, loss of consciousness does differentiate between the two seizures. Loss of consciousness occurs in complex partial seizures, but not in simple

Question 117

What is the definition of accepted rather than complete control of seizures in both partial and generalized tonic clonic seizures?

Answer 117

Twenty per cent of patients with epilepsy still have seizures despite good therapy. In these patients, this is the best that can be done so is ‘accepted’. Complete control means no seizures or seizures very rarely

Question 118

In an otherwise normal adolescent patient with no history of drug or alcohol intake, is it recommended that anti-epileptic drugs be started after the first generalized tonic–clonic fit?

Answer 118

Patients who have a low risk of recurrence are those with a normal electroencephalogram, no history of head injury, normal brain imaging and no family history. These patients can be left untreated after the first seizure if they are carefully counselled and know exactly what to expect. However, there is a 40% risk of a further seizure. They must not drive for 1 year in the European Union

Question 119

Do antiepileptic drugs decrease libido in the long term? If they do, what treatment is recommended?

Answer 119

Not usually, although it has been reported with carbamazepine. Ethosuximide increases libido. Treatment is with phosphodiesterase type-5 inhibitors, e.g. sildenafil.

Question 120

I’d like to know the possibility of giving these drugs in epileptics: vincamine (Oxicebral), cinnarizine, piribedil (Trivastal) and pentoxyphylline (Trental). I’d like to know if they are contraindicated

Answer 120

Vincamine (a natural substance derived from the Vinca minor plant; a vasodilator) and piribedil (a dopamine agonist) are not available as drugs in the UK. Cinnarizine is not contraindicated but pentoxyfylline should not be given.

Question 121

If an epileptic patient, treated with oxcarbazepine, develops a rash, should this drug be withdrawn or the dosage decreased and then increased gradually again?

Answer 121

The drug should be withdrawn as the rash is probably a hypersensitive reaction. It is better to change to another drug

Question 122

Does a patient with refractory epilepsy benefit from acetazolamide?

Answer 122

Acetazolamide has been used with carbamazepine in refractory cases

Question 123

What anti-epileptic drug is recommended for a child with epilepsy and co-morbid attention deficit hyperactivity disorder (ADHD)? Can Ritalin safely be used for treatment?

Answer 123

There is no one drug in this situation. It partly depends on the type of epilepsy. Any drug must be used carefully. Either valproate or ethosuximide is a reasonable choice but both are associated with hyperactivity. Do not use Ritalin.

Question 124

What is the difference in efficacy and pharmacokinetics between sodium valproate and valproic acid?

Answer 124

None: pharmacokinetic studies show absorption, distribution and protein binding to be similar

Question 125

Is it safe to give valproic acid to infants below 12 months of age?

Answer 125

Hepatotoxicity is more common in children under 2 years. Close supervision is required, particularly if multiple drugs are being used

Question 126

How many times must the liver transaminases (SGOT and SGPT) rise to justify a discontinuation of valproic acid therapy in children? Which of these enzymes is more sensitive and reliable in this situation?

Answer 126

SGOT (serum glutamic oxaloacetic transaminase) (or AST (aspartate transferase)) and SGPT (serum glutamic pyruvic transaminase) (or ALT (Alanine transferase)) are often transiently raised, usually in the first 6 months of therapy. Prothrombin time (a measure of liver function) is a useful guide to therapy, and valproate should be stopped if prothrombin time is prolonged.

Question 127

1. Does valproic acid block the photosensitivity phenomenon in reflex epilepsy? 2. Can a patient with this photosensitivity be safely exposed to computer games or other photic stimuli when receiving valproic acid treatment? 3. Does the photosensitivity phenomenon occur in partial seizures?

Answer 127

1. Valproic acid is used in reflex epilepsy. 2. Yes; providing the fits have been controlled and are not induced by the photic stimuli. 3. Yes

Question 128

1. Can an epileptic fit be induced in idiopathic and symptomatic focal epilepsy syndromes by flickering lights? 2. Is valproate effective against the photosensitive phenomenon (seizure induction by flickering light)?

Answer 128

1. Yes. 2. Valproate is effective, but less so than when used for generalized seizures. Carbamazepine is probably first choice.

Question 129

How much time should one give before a loading dose of phenytoin is judged to be ineffective in controlling seizures and an alternative should be instituted?

Answer 129

Phenytoin has a narrow therapeutic index. The time to peak concentration after an oral dose of phenytoin is 4–12 hours with a half-life of 9–140 hours. This implies a long time with measurements of the blood level of phenytoin to check whether they are in the therapeutic range.

Question 130

What is the maintenance dose of phenytoin in seizures arising as a complication of chronic renal failure?

Answer 130

Usually 150–300 mg with plasma phenytoin monitoring.

Question 131

I know that the loading dose of phenytoin in status epilepticus is 20 mg/kg with an upper limit of 1000 mg but if the same situation arose as a complication of chronic renal failure (on regular dialysis), should this dose remain the same or be reduced? If reduced, what should the dose be?

Answer 131

The dose is the same

Question 132

1. What is the most effective antiepileptic for a patient with simple partial motor status epilepticus who is not responding to a loading dose of phenytoin? 2. How long does phenytoin, given in a loading dose, take to work?

Answer 132

1. Carbamazepine is a good choice. | 2. Up to 30 minutes.

Question 133

Is valproate effective if given rectally in status epilepticus and, if so, what dose is recommended?

Answer 133

Valproate is not recommended for rectal use

Question 134

In simple partial motor status epilepticus, if the patient does not respond to diazepam and phenytoin, is it justifiable to proceed to anaesthetic medication?

Answer 134

The patient is conscious in simple partial motor status epilepticus. If initially refractory to diazepam and phenytoin, care in an ITU is required, with repeat of the initial therapy. Anaesthetic medication would be the last resort and only with good anaesthetic and monitoring facilities

Question 135

What is the recommended upper limit dose of lamotrigine when | combined with both carbamazepine and valproate?

Answer 135

Carbamazepine is an enzyme inducer and tends to reduce blood levels of lamotrigine; valproate increases the levels. Monotherapy is best if possible. Dose: lamotrigine 100–200 mg daily with valproate; 200–400 mg without valproate.

Question 136

Is a valproate–lamotrigine combination more effective than | carbamazepine on its own against partial seizures?

Answer 136

Carbamazepine is the drug of choice; valproate–lamotrigine is only second-line therapy. Remember, valproate increases the plasma lamotrigine concentration and therefore dose reduction might well be required with this combination.

Question 137

Why is the incidence of parkinsonism less common in smokers?

Answer 137

It is quite true that parkinsonism is much less common in smokers. There is no obvious reason for this.

Question 138

Is it recommended to start the treatment of parkinsonism with dopamine agonists alone in elderly (over 60 years old) patients, and to delay using L-dopa until the disease has progressed much further? Is there a rationale for this protocol in younger patients?

Answer 138

Because of the major distressing side-effects of L-dopa therapy over time, it is now thought that treatment with L-dopa should be delayed as long as possible in all age groups. It does not alter the natural progression of Parkinson’s disease.

Question 139

Does amantadine increase the endogenous release of dopamine, thus aiding early treatment of parkinsonism?

Answer 139

Yes, Amantadine stimulates the release of dopamine stored in nerve terminals. It also reduces re-uptake of released dopamine by the presynaptic neurone.

Question 140

A 25-year-old woman, pregnant in her second trimester, starts to experience chorea and bilateral ankle arthralgia but has no past history of rheumatic chorea. In the first hour, her erythrocyte sedimentation rate is 70. Could this be no more than chorea gravidarum?

Answer 140

You must exclude other causes, e.g. rheumatic fever, antiphospholipid syndrome, Wilson’s disease and ingestion of toxic substances. Chorea gravidarum does, however, occur in the second trimester.

Question 141

Is valproate as equally effective as haloperidol in the treatment of chorea, in particular rheumatic chorea?

Answer 141

Diazepam is usually used in Sydenham’s (rheumatic) chorea. Dopamine antagonists are next in line. Valproate has no proven effect.

Question 142

Does a lesion of Guillain–Mollaret’s triangle in the brain stem cause a type of myoclonus other than symptomatic palatal myoclonus?

Answer 142

Central tegmental olivary lesions occur which can be the result of vascular, neoplastic or traumatic injury. Symptomless palatal myoclonus is rare; no other type of myoclonus occurs with this lesion.

Question 143

1. In West’s syndrome, after the fits have been suppressed, for how long should treatment with adrenocorticotrophic hormone (ACTH) continue? 2. Does complete suppression of resistant infantile myoclonic jerks by ACTH characterize West’s syndrome?

Answer 143

‘Infantile spasms’ occur in West’s syndrome: 1. The length of time to give ACTH is uncertain but 2 weeks has been used in many studies. A further course is given for relapses. 2. No; response can be as low as 40%, although 80% is a more usual figure.

Question 144

Are anticholinergics the first line of treatment for primary torsion dystonia?

Answer 144

They should be called antimuscarinics and, yes, they are first-choice therapy.

Question 145

What are the diagnostic criteria of ‘definitive’ multiple sclerosis (MS) – as taught to a medical student? We have found different information from different sources.

Answer 145

The diagnostic criteria depend on the clinical demonstration of a lesion in the CNS that is disseminated in time and space. The first episode might be localized and only time will make the diagnosis clear when another lesion in another place occurs. MRI is fairly sensitive but not specific

Question 146

How reliable is a CT-brain scan with contrast in showing MS lesions as enhancing lesions in the presence of a contraindication to use MRI?

Answer 146

Not reliable; MRI is the gold standard.

Question 147

``` Is magnetic resonance (MR) spectroscopy of value in differentiating multiple sclerosis from cerebral autosomal dominant arteriopathy with subcortical infarctions (CADASIL)? ```

Answer 147

CADASIL is rare but characteristic findings are seen in the subcortical white matter. MR findings in multiple sclerosis are usually periventricular. However, this is not entirely specific on its own but usually with the clinical picture (dissemination of symptoms and signs in time and position) the diagnosis can be reached.

Question 148

Does hemiplegia due to multiple sclerosis present with hemiparesis rather than dense hemiplegia (which is more characteristic of a stroke)? Other than age, what are the clinical signs that would help differentiate between the two?

Answer 148

Hemiparesis, rather than a dense hemiplegia, would be more likely in MS but remember to be careful in making a diagnosis of MS if the signs are not disseminated in time and space. This is how you differentiate MS clinically from other conditions, plus an MRI for confirmation.

Question 149

If a female patient with multiple sclerosis wants to become pregnant, what are the risks, family planning advice and treatment, etc? What is the best advice to give to her?

Answer 149

There have been many studies, with an impression that the risk of a relapse of the disease is slightly increased in pregnancy, particularly in the puerperium. There is no evidence that pregnancy affects the longterm prognosis, and most clinicians no longer advise against pregnancy

Question 150

Is there a role for methotrexate and azathioprine in the treatment of remitting-relapsing multiple sclerosis?

Answer 150

Randomized controlled trials of methotrexate have shown no benefit. Meta-analysis of seven trials with azathioprine has shown a slight benefit but this is offset by the side-effects.

Question 151

Do steroids have a role in preventing or ameliorating the relapses in relapsing-remitting multiple sclerosis?

Answer 151

No, steroids have no role in the prevention of relapses but they are used when a relapse occurs.

Question 152

Has cyclophosphamide a role in decreasing the rate and number of relapses in relapsing-remitting multiple sclerosis?

Answer 152

It has been used in small trials but there is no overall effect.

Question 153

Is there evidence of the efficacy of cyclic pulse cyclophosphamide therapy in the treatment of relapsing-remitting multiple sclerosis?

Answer 153

Small clinical trials have been performed with no consistent evidence of efficacy.

Question 154

Glatiramer acetate and interferon-beta are recommended by some people for the treatment of multiple sclerosis. Which drug should I use for a patient with a 2-year history of relapsing-remitting MS.

Answer 154

Both drugs have been approved by the US Food and Drug Administration for relapsing-remitting MS. You can use either as first choice but they are expensive

Question 155

1. Most neurological books available to me say that high-dose IV dexamethasone can be used in acute relapses of multiple sclerosis (MS). What is the recommended dosage and regimen for this drug? 2. I understand that depot preparations of betamethasone (Depofos) can also be used in acute relapses of MS, as well as treatment for idiopathic Bell’s palsy. If so, can you tell me the recommended dosage and regimen for this drug?

Answer 155

1. The best studies use IV methylprednisolone 1 g per day for 3 days. 2. Bell’s palsy can be helped by steroids; use prednisolone combined with aciclovir.

Question 156

What are the most common causes of chronic meningitis and what investigations must be done?

Answer 156

The common causes are tuberculosis and fungal, e.g. cryptoococcal. Sarcoidosis, syphilis and Behçet’s syndrome can also cause chronic meningitis (see K&C 7e, p. 1155). Lumbar puncture is the most valuable investigation.

Question 157

What is Hib meningitis?

Answer 157

Meningitis caused by Haemophilus influenzae type b (Hib). This is now rare in countries where the Hib vaccine is available.

Question 158

Is cavernous sinus thrombosis a complication of meningitis?

Answer 158

No, cavernous sinus thrombosis is not a complication, although cortical vein thrombosis is. The CSF is usually abnormal in cavernous sinus thrombosis, which may be a cause of confusion

Question 159

What is the mechanism of paraparesis that comes as a late (i.e. postresolution) complication to meningitis?

Answer 159

This is rare; the mechanism is unclear

Question 160

Is lumbar puncture contraindicated in meningococcal meningitis?

Answer 160

In a case of meningococcal meningitis and a purpuric rash, lumbar puncture is not necessary and can be dangerous. If there is doubt about the diagnosis and no evidence of a mass lesion on CT/MRI, lumbar puncture should be performed

Question 161

What should the cerebrospinal fluid (CSF) picture be when the treatment of acute bacterial meningitis is complete, and after how many days of treatment?

Answer 161

It is not usual to repeat the lumbar puncture in acute bacterial meningitis but the findings should parallel the clinical condition. Antibiotics are usually given for 7–10 days and by then the CSF should be returning to normal.

Question 162

In the management of meningococcaemia, can chloramphenicol be used as an alternative? Are there any advantages practically? The book quotes benzylpenicillin or cefotaxime (alternative). Are they a standard regimen?

Answer 162

Chloramphenicol was used in meningococcaemia. It is often extremely effective but of course does have the disadvantage of, albeit rarely, causing aplastic anaemia. The treatment of choice is still penicillin with cefotaxime as an alternative. Chloramphenicol can be used in the severely beta-lactam-allergic patient.

Question 163

‘The immediate management of suspected meningococcal meningitis infection is benzylpenicillin 1200 mg either by slow IV injection or intramuscularly, prior to investigations.’ Is this always true? Should you not perform a lumbar puncture for culture first?

Answer 163

Primary care physicians should give penicillin as soon as possible in a suspected case of meningococcal meningitis. Minutes count in this disease. A lumbar puncture can be performed later.

Question 164

Should children with bacterial meningitis be treated with steroids to prevent complications?

Answer 164

Meta-analysis shows no reduction in mortality but a reduction of neurological or hearing deficits if dexamethasone is given early at the time of the first antibiotic dose. Dexamethasone should certainly be given to children with Hib meningitis.

Question 165

What is the role of anticonvulsants in a case of encephalitis and how long should one continue them?

Answer 165

Any seizures that occur in a patient with encephalitis will need treatment which should be continued for approximately 3 months although there is no firm evidence on the time frame.

Question 166

How effective are steroids in the treatment of radiculomyelitis?

Answer 166

Sometimes temporary relief is obtained but it depends on the cause of the radiculomyelitis.

Question 167

Should you treat a patient who has a brain cysticercosis lesion? The text seems to say ‘Yes’ but there is great uncertainty about it. Also, should one ‘worm’ the patient’s gut when you find brain lesions; if so, with what?

Answer 167

Answer 150 Yes, treat with albendazole although there is little evidence of benefit. Patients and the members of their households should be examined for tapeworms. If found, they should be treated with praziquantel 10–20 mg/kg single dose after a light breakfast.

Question 168

Is there any rationale for giving either propranolol, valproate or buspirone to patients with cerebellar ataxia?

Answer 168

no

Question 169

Is there a laboratory marker for cerebral dominant arteriopathy with subcortical infarcts and leucoencephalopathy (CADASIL)? Is serum lactic acid elevated?

Answer 169

MRI is characteristic with abnormalities in the subcortical white matter. Genetic analysis (a NOTCH3 mutation) or a skin biopsy showing granular osmiophilic material (GOM) within small vessels establish the diagnosis. Lactic acid levels are normal.

Question 170

Primary brain tumours rarely metastasize outside the brain but malignancies outside the brain frequently metastasize to the brain. Why?

Answer 170

This is an interesting point that many have dwelt on over the years. There is no complete understanding of the mechanism.

Question 171

In a case of brain tumour, can papilloedema occur without a headache?

Answer 171

Yes, although usually a headache is present.

Question 172

What are the pathological diagnostic features of glioblastoma multiforme?

Answer 172

The World Health Organization classifies glioblastoma multiforme as grade 4 astrocytomas with endothelial proliferation and necrosis. They also have high mitotic activity. New genetic abnormalities have been described with this tumour.

Question 173

Is acetazolamide effective in cases of normal pressure hydrocephalus? How effective is low-dose digoxin?

Answer 173

Neither acetazolamide nor digoxin are effective

Question 174

If dementia and incontinence are present, but gait apraxia is not, can normal pressure hydrocephalus be diagnosed?

Answer 174

The exact existence of normal pressure hydrocephalus, as a true separate entity from dementia, has been questioned. The classic clinical triad is as you have described. MR shows ventriculomegaly but this is also seen in dementia.

Question 175

Is a normal CT (plain and with contrast) in patients with headache, bilateral papilloedema and a clear conscious level sufficient to diagnose benign intracranial hypertension?

Answer 175

No, you also need to measure the cerebrospinal fluid (CSF) pressure. It is high and CSF can be removed to reduce the pressure.

Question 176

What is the value above which cerebrospinal fluid (CSF) pressure is said to be raised?

Answer 176

Normal CSF pressure is 60–150mm H2O. CSF pressure is only of diagnostic value in benign intracranial hypertension, in which the figure is greater than 250mmHg.

Question 177

Could benign intracranial hypertension be diagnosed without headache as a complaint?

Answer 177

Young children can present with irritability or behavioural disorders rather than headache. Some patients are picked up with papilloedema on examination with no headache.

Question 178

Can pyramidal tract lesions present as false localizing signs in benign intracranial hypertension?

Answer 178

No. Sixth nerve palsies can occur.

Question 179

How often can increased intracranial hypertension be present without papilloedema on examination?

Answer 179

Papilloedema is not always present. The frequency will depend on the cause, e.g. papilloedema is rare in raised intracranial pressure associated with hepatic encephalopathy.

Question 180

Which is the most effective method of reducing raised intracranial pressure: mannitol, steroids or ventilation?

Answer 180

Hyperventilation via intermittent positive-pressure ventilation reduces intracranial pressure by cerebral vasoconstriction within minutes. This is the quickest way to reduce intracranial pressure and is used particularly in unconscious patients who need to be ventilated for respiratory problems. Mannitol intravenously 1–2 g/kg as a 20% solution over 10–20 minutes reduces cerebral oedema by renal excretion of water. The peak effect is at 90 minutes. It is useful in hepatic failure. Dexamethasone 10 mg intravenously reduces oedema around a brain tumour or an abscess

Question 181

In the case of pseudotumour cerebri, if this is proved to be due to sagittal sinus thrombosis with no explanation for the thrombosis, should the patient receive lifelong anticoagulation treatment?

Answer 181

There is no definite recommendation on the use of anticoagulants. The consensus would probably be not life long.

Question 182

Does digitalis help reduce cerebrospinal fluid (CSF) formation, specifically in the treatment of resistant benign intracranial hypertension?

Answer 182

Digoxin has been used but there is little data for its use. Acetazolamide 250 mg 4 daily, increasing to 500 mg and then 1 g 4 daily (if tolerated) is the preferred choice

Question 183

``` Is it safe to combine hydrochlorothiazide, amiloride, acetazolamide and digitalis (125 μg per day) in a hypertensive patient with idiopathic intracranial hypertension (pseudotumour cerebri)? ```

Answer 183

Yes, with careful monitoring

Question 184

What is the best indicator for monitoring the efficacy of treatment or the progress of the disease in pseudotumor cerebri? Is it by the disappearance of papilloedema, the relief of headache or by frequent visual field examination or cerebrospinal fluid (CSF) pressure?

Answer 184

The relief of symptoms, particularly headache and resolution of visual loss.

Question 185

What is the definition of ‘bursting’ when describing a headache?

Answer 185

Sudden, acute headache usually associated with intracerebral | haemorrhage.

Question 186

1. What drugs, other than tricyclic antidepressants, can be used in prophylaxis for daily tension headache? 2. Is propranolol an effective treatment?

Answer 186

1. There is no effective treatment/prophylaxis for tension headache, apart from analgesics. 2. Propranolol is of no value.

Question 187

Are maprotiline and imipramine as effective as amitriptyline in the treatment of tension headache?

Answer 187

All these drugs are antidepressants. They are used in conditions such as tension headaches, particularly if depression is present. Amitriptyline is most often used, but maprotiline and imipramine are as good.

Question 188

How often does migraine headache present unilaterally?

Answer 188

In 60–70% of cases.

Question 189

Are ergotamine-containing preparations contraindicated in the treatment of resistant migraine in hypertensive patients? Can I give it, under close supervision of the blood pressure, in the emergency room?

Answer 189

No. In severe or inadequately controlled hypertension, ergotamine is contraindicated.

Question 190

Should ergotamine be given to abort a migrainous attack in a pregnant female? If not, what is the recommended alternative?

Answer 190

Ergot derivatives are not used often for migraine and they are contraindicated in pregnancy. Use paracetamol

Question 191

What is the frequency of migrainous attacks above which prophylactic therapy should be commenced? If commenced, for how long should the treatment be continued and what should be done if frequent attacks recur after discontinuation of the prophylactic treatment?

Answer 191

Two or more attacks a month that are disabling. Treatment will be for at least a year and long term if necessary.

Question 192

Is verapamil more effective in migraine prophylaxis than flunarizine?

Answer 192

Both are used; there are no good comparative studies.

Question 193

Are imipramine and fluoxetine effective as a prophylactic treatment against migraine? Are they as effective as amitriptyline?

Answer 193

There are no comparative data and selective serotonin re-uptake inhibitors (SSRIs) have been little used so far in migraine.

Question 194

1. Is sodium valproate more effective than valproic acid with regard to migraine prophylaxis and anti-epileptic activity? 2. Is carbamazepine effective as a prophylaxis against migraine?

Answer 194

1. Both are used. They have very similar effects. | 2. Carbamazepine is not used.

Question 195

Can flunarizine, diltiazem and nifedipine be used in the treatment of a cluster headache and do they have the same efficacy as verapamil?

Answer 195

Verapamil is the only calcium-channel blocker used widely in cluster headaches. In a controlled trial it was as effective as lithium with fewer side-effects.

Question 196

If cluster headache migraine is confidently diagnosed in general practice, is it worth trying lithium prophylaxis or should this commence at secondary care level? Which other treatment is recommended?

Answer 196

Yes, it is worth trying prophylaxis in general practice. Drugs shown to be useful are verapamil, topiramate or lithium. Use whichever drug you are familiar with.

Question 197

Is ergotamine effective in preventing an attack of cluster headache?

Answer 197

Ergotamine can be used for patients with short bouts of cluster headaches. However, sumatriptan by SC injection is the drug of choice for treatment. Oxygen sometimes aborts an attack

Question 198

In the case of anterior spinal artery occlusion is bladder function preserved or is there urine retention?

Answer 198

There is urinary retention.

Question 199

In the case of anterior spinal artery occlusion, can the patient have intact sensations in the lower limbs?

Answer 199

``` No. A dissociated sensory loss is characteristic with loss of temperature and pain sensation (spinothalamic) with sparing of proprioception and light touch (posterior column). ```

Question 200

In the case of anterior spinal artery occlusion, will the paraplegia be of a spastic or a flaccid type?

Answer 200

It will be initially flaccid at the time of spinal ‘shock’, then spastic as ‘shock’ wears off.

Question 201

Can fasciculations occur in radiculopathy or peripheral neuropathy or is it pathognomonic to anterior horn cell lesion?

Answer 201

Fasciculations occur with any lower motor neurone lesion, e.g. if a nerve is cut, the muscle it supplies will atrophy and fasciculations occur. Generalized fasciculations are characteristic of motor neurone disease.

Question 202

What are the principal causes of frontotemporal dementia and how can the cause be diagnosed

Answer 202

Frontotemporal dementia used to be known as Pick’s disease (see K&C 7e, p. 1168). It is often difficult to differentiate it from Alzheimer’s disease but characteristically there is much more personality change, disinhibition, and obsessive and compulsive behaviour.

Question 203

What are the associated features of meningomyelocele other than hydrocephalus, urinary incontinence and paraplegia? Do patients have congenital heart disease and congenital dislocation of hips?

Answer 203

They do have congenital dislocation of the hips and clubbed feet.

Question 204

Can a patient with neurofibromatosis type I have a neurofibroma arising from a nerve root or radicle causing cervical or compressive lumbar radiculopathy?

Answer 204

Yes. Although most are type 2, central neurofibromas can occur in type 1.

Question 205

Is there a way to retard the rate of development of cutaneous or other manifestations of neurofibromatosis type 1? Has a cure for this condition yet been found?

Answer 205

No; unfortunately, there is no effective treatment.

Question 206

How does neurofibromatosis type 2 (NF2) affect the heart?

Answer 206

It has no effect on the heart. NF1 has been associated with a cardiomyopathy.

Question 207

1. How often is leprosy a cause of mononeuritis multiplex? | 2. How often is diabetes mellitus a cause of mononeuritis multiplex?

Answer 207

a. In lepromatous leprosy the nerves are diffusely and progressively involved, so mononeuritis multiplex is common. b. 30% of diabetics have a neuropathy, the most common being a motor– sensory neuropathy.

Question 208

What is the expected response of straight leg-raising if the meningeal stretch test is positive? Is it back pain, pain in the sciatic distribution, or limitation in the range of leg-raising?

Answer 208

A positive response produces pain and spasm in the back of the thigh (the hamstrings).

Question 209

1. Does radiculopathy due to systemic disease produce positive meningeal stretch signs or are these limited to radiculopathy as a result of disc prolapse? 2. Where no cause is found for radiculopathy, is steroid treatment indicated?

Answer 209

1. Radiculopathy due to systemic disease can produce a positive stretch test. 2. There is no indication for steroid therapy.

Question 210

What are the most common causes of radiculopathy?

Answer 210

Disc protrusion, degenerative spinal disease, diabetes and metastatic deposits are some common causes.

Question 211

1. Does the absence of a positive straight leg-raising test exclude radiculopathy? 2. Can radiculopathy be diagnosed by meningeal stretch tests or is it diagnosed electrophysiologically?

Answer 211

a. It makes it unlikely. b. Straight leg raising producing pain and limitation is often due to a prolapsed disc with involvement of the sciatic nerve. MRI is the best way to make a diagnosis

Question 212

Why does ascending paralysis occur in the Guillain–Barré syndrome?

Answer 212

The paralysis is thought to be due to cross-reacting antibodies to GM1 ganglioside, which is present in high concentrations in the myelin sheath of peripheral nerves. The central spinal fluid usually contains only a few mononuclear cells but has a high protein concentration, sometimes 5 g/L, reflecting immunological rather than infective damage

Question 213

Is systemic steroid therapy indicated in cases of carpal tunnel syndrome not responsive to conservative measures?

Answer 213

Only local steroid injections are used.

Question 214

Is there a role for acetazolamide in the treatment of carpal tunnel syndrome? What is the dose? How can paraesthesia induced by the drug be overcome?

Answer 214

There is no evidence on the value of acetazolamide in the carpal tunnel syndrome.

Question 215

Can an MRI scan of the cervical spine detect cervical rib or does this merit an individual scan?

Answer 215

As in all scans, the radiologist must know what he or she is looking for

Question 216

Please explain the mechanism by which cervical spondylosis causes acroparaesthesia without proximal sensory affection. Does this happen by compromising the blood supply?

Answer 216

Acroparaesthesia does not occur with cervical spondylosis. Beware of false correlations; spondylosis on X-ray is common. The thoracic outlet syndrome produces both vascular and neurogenic symptoms.

Question 217

Can chronic inflammatory demyelinating polyradiculoneuropathy be associated with positive stretch tests such as Lasègue’s sign?

Answer 217

No.

Question 218

1. If a patient with a spastic paraplegia due to a spinal cord lesion is able to sit unaided, does this indicate intact dorsal segments (T7–T12)? 2. What mechanism underlies the inability of some patients with spastic paraplegia to sit in bed with their lower limbs straight on the bed, while able to sit on the edge of the bed with their lower limbs hanging?

Answer 218

1. No, this is not a reliable indication. Remember the cord ends at L1, so a paraplegia by definition must occur with a lesion above this and below the cervical region lest a quadriplegia occur. 2. The mechanism is unclear

Question 219

What is the scientific definition of asthenia and weakness?

Answer 219

There is no scientific definition of these two terms. ‘Asthenia’ is an old Greek word describing a lack of strength. ‘Weakness’ can imply lack of muscle power but is often used to imply tiredness

Question 220

Why do the following cause weakness that is more proximal than distal: ● Muscle disease. ● Radiculopathy. ● Anterior horn cell disease

Answer 220

It is not known why many muscle diseases involve proximal rather than distal muscles, causing weakness. In radiculopathies and anterior horn cell disease, the muscles involved depend on which cord level is affected. For example, a disc lesion pressing on L5–S1 produces a distal lesion, whereas involvement of anterior horn cells with polio will affect the muscles of the thigh.

Question 221

What is the difference between fibrillation, fasciculations and myokymia?

Answer 221

On electromyography (EMG), spontaneous rhythmic discharges of single muscle fibres are called fibrillations and are not seen clinically. A fasciculation represents a spontaneous discharge of a motor unit, which is seen as a large action potential on EMG and clinically as a muscle twitch. Persistent fasciculation with weakness is seen in motor neurone disease. Myokymia describes a rare continuous, fine, sinous or wave like movement of the lower face that is seen in brainstem lesions, e.g. multiple sclerosis

Question 222

What is the difference between ‘Isaac’s syndrome’ and ‘stiff person syndrome’?

Answer 222

Electromyographic studies show continuous motor activity in the paraspinal muscles in the stiff person syndrome and not in Isaac’s syndrome

Question 223

What is the most common cause for fibrosis of the quadriceps femoris muscle?

Answer 223

The most common cause is trauma.

Question 224

In a patient receiving long-term oral steroids and gradually developing proximal muscle weakness, how does one differentiate between steroid myopathy and myositis?

Answer 224

In steroid myopathy the serum creatine phosphokinase (CPK) is normal, as is electromyography. Biopsy (usually not necessary) shows type-2 muscle fibre atrophy in steroid-induced myopathy. The CPK is greatly raised in myositis.

Question 225

What is viral myositis?

Answer 225

Myositis is a non-suppurative skeletal muscle inflammation. It is often due to a viral cause, e.g. Coxsackie

Question 226

Does myositis affect the facial and neck muscles?

Answer 226

Yes it can, and can be confused with myasthenia, which commonly affects these muscles

Question 227

I am a neurologist and would like to know: ● What precautions I should take with regard to the cardiovascular system, before and after prescribing mexiletine for cases of myotonia. ● Whether there is a group of patients who should not receive this drug.

Answer 227

Patients with both chloride channelopathies (e.g. myotonia congenita) and sodium channelopathies (e.g. hyperkalaemic or hypokalaemic periodic paralysis) have been treated with mexilitene. You should not give the drug to patients with bradycardia or high-degree atrioventricular (AV) block (unless the patient has a pacemaker). The major cardiovascular effects are hypotension and arrhythmias, so that electrocardiograms and careful blood pressure monitoring are required. Nausea and vomiting often prevent the drugs being given by mouth.

Question 228

Can myasthenia gravis be unilateral and, if so, how often?

Answer 228

No; however, the muscles can be affected to a variable degree so that it can appear to be unilateral

Question 229

Can the creatine phosphokinase (CPK) level in the blood, or the presence of certain auto-antibodies, help to differentiate muscle dystrophies from myositis?

Answer 229

The CPK is raised in both myositis and muscle dystrophies. Clinical patterns and electromyography are often more helpful.

Question 230

Can percussion myotonia occur with motor neurone disease? If so, please explain the mechanism and cause–effect for this.

Answer 230

Percussion myotonia – a persistent dimpling after a sharp blow on a muscle, e.g. the thenar eminence or the tongue – is not seen in motor neurone disease. It is seen in myotonia congenita.

Question 231

Can benign intracranial hypertension be diagnosed on the basis of persistent headache and CT-brain scan findings of slit ventricles with no papilloedema and preserved spontaneous venous pulsations on ophthalmoscopy? And do you recommend cerebrospinal fluid (CSF) pressure measurement as a routine investigation in the diagnosis of this type of disorder?

Answer 231

You can’t make the diagnosis without papilloedema. CSF pressure measurement is usually performed but repeat lumbar puncture with removal of fluid is used as a treatment.

Question 232

In my experience in the treatment of stroke patients, the combination of atenolol 50 mg, hydrochlorothiazide 25 mg and amlodipine 10 mg is very effective in the treatment of resistant hypertension. Can you tell me whether this combination of antihypertensives is contraindicated in diabetic patients?

Answer 232

Yes; this combination is contraindicated because: ● beta-blockers and thiazide diuretics impair glucose metabolism ● angiotensin-converting enzyme (ACE) inhibitors or antagonists are renoprotective and are therefore first-line treatment in any diabetic.

Question 233

Can diabetic mononeuropathy of the third cranial nerve cause ipsilateral pain of the face and tenderness (but not redness) of the affected eye? Can these symptoms be explained by Tolosa–Hunt syndrome?

Answer 233

Tolosa–Hunt syndrome causes unilateral eye pain, irritation or damage to the IIIrd, IVth or VIth nerves. The pain is relieved by steroids. It is due to cavernous sinus inflammation. CT or MRI will usually show up inflammation.

Question 234

1. For how long should adrenocorticotrophic hormone (ACTH) be given to patients after stoppage of myoclonic seizures in West’s syndrome? 2. If seizures recur after stoppage, should ACTH be re-administered?

Answer 234

1. How long ACTH should be given is unclear; some series suggest months whereas in one big series 75% responded to 2 weeks’ therapy. 2. In one study re-administration of ACTH was successful in four out of five patients.

Question 235

In acute attacks of multiple sclerosis (MS), where methylprednisolone is not available, can pulse steroid therapy be given with a one-off dose of 200 mg dexamethasone?

Answer 235

Steroids are used only for acute attacks of MS. Most studies are with methylprednisolone but dexamethasone has been used with success. 200 mg is a very high dose: 20 mg is more appropriate

Question 236

Is there a role for aciclovir in idiopathic Bell’s palsy?

Answer 236

Yes; aciclovir and steroids should be given together. Trials have shown a benefit

Question 237

Does temporal arteritis headache or other pain respond to non-steroidal anti-inflammatory drugs?

Answer 237

You must use corticosteroids for temporal arteritis to prevent blindness. Start prednisolone immediately

Question 238

What is the recommended target of total and low-density lipoprotein (LDL) cholesterol in secondary prevention of ischaemic stroke?

Answer 238

LDL cholesterol: 100 mg/dL (2.6 mmol/L). Total: 4 mmol/L | 150 mg/dL

Question 239

Is intravenous sodium nitroprusside contraindicated in lowering resistant hypertension secondary to primary intracerebral haemorrhage?

Answer 239

Intravenous nitroprusside is rarely necessary even when hypertension is severe. Even with a brain haemorrhage, reduction over 24 hours with oral therapy does less harm than rapid reduction with nitroprusside

Question 240

After how long can a patient with primary intracerebral haemorrhage safely be prescribed aspirin for secondary prophylaxis of further ischemic strokes? Or should aspirin no longer be prescribed in this case?

Answer 240

Aspirin is contraindicated in someone who has had a previous primary intracerebral haemorrhage.

Question 241

Does occlusion of the recurrent Heubner’s artery result in weakness of the upper limb that is proximal more than distal?

Answer 241

Heubner’s artery is a medial lenticulostriate artery that arises from the proximal segment of the anterior communicating artery. It supplies the anterior medial part of the head of the caudate nucleus and the anterior inferior internal capsule. It is identified by surgeons when operating for intracranial aneurysms. There is a spectrum of clinical features of infarction in this area, which partly depends on whether the left or the right side is involved and there are descriptions of predominant weakness of the upper limbs with sparing of the lower limbs in patients with infarction in the territory of Heubner’s artery.

Question 242

I have recently been told by fellow cardiologists that statins have a role to play in the acute management of myocardial infarction: is this true? And does this extend to the acute management of ischemic stroke?

Answer 242

The view is that statins have a role in plaque stabilization and therefore they are usually given early as you indicate, in the management of myocardial infarction. There is no data on acute management of ischaemic stroke but statins are being used more and more frequently.

Question 243

What is captocormia?

Answer 243

Captocormia is sometimes called the ‘Bent spine syndrome’. It was originally described in a group of servicemen, in whom it was thought to be a psychological reaction to pain. However, this severe forward flexion of the upper spine can occur in several neuro–muscular diseases, e.g. motor neurone disease.

Question 244

Should mannitol be prescribed to patients with primary intracerebral haemorrhage with signs of impending herniation and is it contraindicated in patients with heart failure or liver cell failure?

Answer 244

Yes; mannitol should be used in the situation you describe. It is contraindicated in severe heart failure but as in all clinical situations you have to weigh up the benefits against the possible harm

Question 245

What is the clinical significance of a positive Babinski sign with no knee jerk?

Answer 245

A positive Babinski sign (it is better to use the term extensor plantar response because the Babinski sign is described in babies) indicates an upper motor neurone lesion. Absent knee jerks indicates a lower motor neurone lesion. The two occur together when both lesions are present. The classic example is in B12 deficiency where you get a peripheral neuropathy (absent knee jerks) with subacute combined degeneration of the cord which gives an upper motor lesion, i.e. extensor plantar response.

Question 246

Is a high serum level of triglycerides 200–400 mg a risk factor for ischaemic stroke?

Answer 246

Above 200 mg/dL is high and attempts should be made to reduce this level with lifestyle changes and dietary modifications. Elevated serum triglyceride levels are an independent risk factor for the development of atherosclerosis. The data on whether raised triglycerides are a risk factor for ischaemic stroke are, however, poor

Question 247

What is ‘Melkersson’s syndrome’? How can it be a source of recurrent Bell’s palsy as suggested in Neurology in Clinical Practice by Walter Bradley?

Answer 247

Melkersson’s syndrome is recurrent facial palsy, chronic oedema of the face and lips and fissuring of the tongue due to a granulomatous infiltration. It is this infiltration that causes the recurrent Bell’s palsy

Question 248

Are the pathological terms ‘neurinoma’ and ‘schwannoma’ interchangeable? Do these differ from neurofibroma as some neurology textbooks do not differentiate between these terms and seem to apply the terms neurinoma and neurofibroma interchangeably to spinal nerve tumours arising from neurilemmal sheaths?

Answer 248

The terms are used interchangeably; they are tumours arising from the neurilemmal sheath.

Question 249

Should a patient presenting three times with recurrent facial nerve palsy, generalized lymphadenopathy and skin nodules, suspected of having sarcoidosis, be maintained on steroids or given steroid courses only during attacks?

Answer 249

In this case, you may well need long-term steroids. You start with a high dose 20–30 mg of prednisolone daily, tapering the dose slowly when the symptoms are improved. Hopefully, you can get to a dose of <10 mg a day without a recurrence of symptoms. The dose is relatively safe in the long term, but keep a check on bone density with yearly DEXA.

Question 250

a. What is the clinical significance of raised cerebrospinal fluid (CSF) lactate dehydrogenase levels in focal brain lesions? b. Does this imply a primary central nervous system (CNS) lymphoma or lymphomatous deposits in the CNS?

Answer 250

Increased lactate dehydrogenase in the cerebrospinal fluid occurs with meningitis but also with focal brain lesions, e.g. lymphoma, metastatic brain lesions. It is not widely measured as it is not that helpful in diagnosis. It has been used as a marker of response to therapy in patients with malignant lesions.

Question 251

a. Is it safe to give antiplatelet medication as a secondary prophylaxis in stroke patients with hepatic impairment? b. Should aspirin be used in this instance?

Answer 251

a. Yes; secondary prophylaxis is indicated following an ischaemic stroke. b. Aspirin is used except in a patient with severe hepatic impairment. Dipyridamole should be given with aspirin, which is also safe except when the hepatic disease is severe.

Question 252

Should sciatic pain in the distribution of the sciatic nerve, with no back pain, be considered non-compressive mononeuropathy? If so, does this require the workup of mononeuropathy including searching for collagen disorder?

Answer 252

Sciatica can occur without back pain. As the commonest cause of sciatica is a lumbar disc lesion this would still be the most likely diagnosis and a more detailed workup would not normally be required.

Question 253

In what percentage of patients with viral meningitis and encephalitis does the CSF have an elevated number of inflammatory cells?

Answer 253

100%.