Neurological disease

21 Neurological disease

Questions

Please what is (are) the likely cause(s) of sudden sharp but brief pain (resembling pin prick) in the right lower abdomen?

Question 2

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

Question 3

What is the correct definition for dysaesthesia?

Question 4

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?

Question 5

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

Question 6

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

Question 7

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

Question 8

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

Question 9

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)?

Question 10

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

Question 11

How would you treat optic neuritis?

Question 12

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?

Question 13

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

Question 14

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.

Question 15

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

Question 16

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?

Question 17

Is gabapentin effective in the treatment of trigeminal neuralgia?

Question 18

What medication is best used for the treatment of carbamazepine-resistant trigeminal neuralgia?

Question 19

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

Question 20

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?

Question 21

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?

Question 22

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

Question 23

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?

Question 24

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

Question 25

Are steroids appropriate in the treatment for vestibular neuronitis?

Question 26

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?

Question 27

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?

Question 28

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?

Question 29

Is ankle clonus diagnostic of pyramidal tract lesion?

Question 30

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

Question 31

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

Question 32

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?

Question 33

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

Question 34

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

Question 35

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?

Question 36

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

Question 37

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

Question 38

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?

Question 39

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

Question 40

What is the difference between kinetic and intention tremors?

Question 41

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

Question 42

What is meant by ‘inversion of reflexes’? I have found this term in a few membership exams.

Question 43

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?

Question 44

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

Question 45

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

Question 46

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

Question 47

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?

Question 48

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?

Question 49

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

Question 50

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?

Question 51

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

Question 52

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?

Question 53

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

Question 54

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

Question 55

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

Question 56

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

Question 57

By what mechanism is vertebrobasilar insufficiency associated with circumoral numbness?

Question 58

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

Question 59

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

Question 60

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?

Question 61

I want to ask something about cerebrovascular accident (CVA). Can you please tell me how we can rapidly pinpoint the exact anatomical site of the neurological deficit using physical findings in the emergency room?

Question 62

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.

Question 63

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.

Question 64

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

Question 65

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?

Question 66

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

Question 67

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’?

Question 68

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?

Question 69

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

Question 70

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?

Question 72

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?

Question 73

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?

Question 74

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?

Question 75

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

Question 76

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

Question 77

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?

Question 78

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

Question 79

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?

Question 80

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

Question 81

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

Question 82

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

Question 83

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?

Question 84

What are uncinate fits?

Question 85

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

Question 86

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?

Question 87

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

Question 88

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

Question 89

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

Question 90

What is the difference between pseudoseizures and pseudo-pseudoseizures?

Question 91

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?

Question 92

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

Question 93

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?

Question 94

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

Question 95

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

Question 96

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?

Question 97

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?

Question 98

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

Question 99

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?

Question 100

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

Question 101

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.

Question 102

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

Question 103

Does a patient with refractory epilepsy benefit from acetazolamide?

Question 104

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?

Question 105

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

Question 106

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

Question 107

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?

Question 109

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)?

Question 110

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?

Question 111

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

Question 112

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?

Question 113

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?

Question 114

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

Question 115

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

Question 116

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

Question 117

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

Question 118

Why is the incidence of parkinsonism less common in smokers?

Question 119

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?

Question 120

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

Question 121

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?

Question 122

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

Question 123

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

Question 124

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?

Question 125

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

Question 126

Can multiple sclerosis (MS) be associated with lack of vitamin D, lack of sunlight or low fish/cod-liver oil in the diet? By looking at the epidemiology (none at the equator; more outside 40° latitude, both north and south; less on top of Swiss mountains than in the Swiss valleys; more in fishing coastal towns and in Eskimos) this seems to be very important.

Vitamin D modulates the immune system and active vitamin D given to rats with experimental MS (acute encephalomyelitis) lowers the monocyte count in cerebrospinal fluid (CSF) by 90% in 72 hours with return of power to their limbs. Japanese MS patients who ate plenty of fish were found to have vitamin-D-receptor pleomorphism. The staple grains and cereals (wheat, barley, oats) eaten in Scandinavian and northern European countries contain phytic acid, which blocks vitamin D absorption, and rice is the only cereal free of phytic acid.

Are there any studies where low vitamin D levels in blood are associated with MS relapse?

Question 127

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

Question 128

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?

Question 129

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

Question 130

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?

Question 131

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?

Question 132

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

Question 133

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

Question 134

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

Question 135

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

Question 136

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.

Question 137

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?

Question 138

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

Question 139

What is Hib meningitis?

Question 140

How often is tuberculosis a cause of chronic meningitis in comparison to other causes?

Question 141

Is cavernous sinus thrombosis a complication of meningitis?

Question 142

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

Question 143

Is lumbar puncture contraindicated in meningococcal meningitis?

Question 144

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

Question 145

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?

Question 146

‘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?

Question 147

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

Question 148

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

Question 149

How effective are steroids in the treatment of radiculomyelitis?

Question 150

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?

Question 151

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

Question 152

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

Question 153

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

Question 154

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

Question 155

What are the pathological diagnostic features of glioblastoma multiforme?

Question 156

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

Question 157

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

Question 158

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?

Question 159

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

Question 160

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

Question 161

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

Question 162

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

Question 163

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

Question 164

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?

Question 165

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

Question 166

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

Question 167

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?

Question 168

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

Tags: 1000 Questions and Answers from Kumar Clarks Clinical Medicine

Dec 3, 2016 | Posted by admin in GENERAL & FAMILY MEDICINE | Comments Off

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