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A 76-year-old man is admitted with a right hemiparesis. CT scan shows an ischaemic stroke and aspirin 300mg is
commenced. In terms of further management in the acute phase, which one of the following values should not be
corrected?ia
A.ABP 210/110ia
B.A Blood glucose 9.4 mmol/lia
C.A Oxygen saturation 94%ia
D.A Temp 38.3Cia
E.A Blood glucose 2.5 mmol/lia
Next question
Hypertension should not be treated in the initial period following a stroke
Elevated blood pressure should not be treated in the acute phase following a stroke unless complications develop.
Other physiological parameters should be kept within normal limits - an aggressive approach with respect to this has
been shown to improve outcome
Stroke: managementsqweqwesf erwrewfsdfs adasd dhe
The Royal College of Physicians published guidelines on the diagnosis and management of patients following a
stroke in 2004
he earaer aeraer asdsadas eerw dssdfsselleds
Selected points relating to the management of transient ischaemic attacks (TIA) include:
if a diagnosis of TIA is likely patients should be prescribed aspirin 300mg daily or an alternativeantiplatelet immediatelyhe
if there has been more than one TIA in a week then patients should be investigated in hospitalimmediatelyhe
he earaer aeraer asdsadas eerw dssdfsselleds
Selected points relating to the management of acute stroke include:
blood glucose, hydration, oxygen saturation and temperature should be maintained within normal limitshe blood pressure should not be lowered in the acute phase unless there are complications e.g. hypertensive
encephalopathyhe
aspirin 300mg orally or rectally should be given as soon as possible if a haemorrhagic stroke has beenexcludedhe
anticoagulation should not be started until an haemorrhagic stroke has been excluded and usually not until14 days have passed since the strokehe
if the cholesterol is > 3.5 mmol/l patients should be commence on a statinheA 29-year-old man presents to his GP complaining of visual disturbance. Examination reveals a right superior
homonymous quadrantanopia. Where is the lesion most likely to be?ia
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A.A Optic chiasmia
B.ALeft temporal lobeia
C.A Right temporal lobeia
D.A Left optic nerveia
E.A Left parietal lobeia
Next question
Visual field defects:
left homonymous hemianopia means visual field defect to the left, i.e. lesion of right optic tract homonymous quadrantanopias: PITS (Parietal-Inferior, Temporal-Superior) incongruous defects = optic tract lesion; congruous defects= optic radiation lesion or occipital cortex
Visual field defectssqweqwesf erwrewfsdfs adasd dhe
Greater detail is required in the MRCP when assessing visual field defects - quadrantanopias are described as are
incongruous and congruous defects
he earaer aeraer asdsadas eerw dssdfsselleds
The main points for the exam are:
left homonymous hemianopia means visual field defect to the left, i.e. lesion of right optic tracthe homonymous quadrantanopias: PITS (Parietal-Inferior, Temporal-Superior)he incongruous defects = optic tract lesion; congruous defects= optic radiation lesion or occipital cortexhe
he earaer aeraer asdsadas eerw dssdfsselleds
Homonymous hemianopia
incongruous defects: lesion of optic tracthe congruous defects: lesion of optic radiation or occipital cortexhe macula sparing: lesion of occipital cortexhe
he earaer aeraer asdsadas eerw dssdfsselleds
Homonymous quadrantanopias
superior: lesion of temporal lobehe inferior: lesion of parietal lobehe mnemonic = PITS (Parietal-Inferior, Temporal-Superior)he
he earaer aeraer asdsadas eerw dssdfsselleds
Bitemporal hemianopia
lesion of optic chiasmhe upper quadrant defect > lower quadrant defect = inferior chiasmal compression, commonly a pituitary
tumourhe
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lower quadrant defect > upper quadrant defect = superior chiasmal compression, commonly acraniopharyngiomahe
For patients with Parkinson's disease, which one of the following drugs is most useful in the management of
tremor?ia
A.A Apomorphineia
B.A Cabergolineia
C.A Selegilineia
D.A Amantadineia
E.A Benzhexolia
Next question
Parkinson's disease: managementsqweqwesf erwrewfsdfs adasd dhe
Currently accepted practice in the management of patients is to delay treatment until the onset of disabling
symptoms and then to introduce a dopamine receptor agonist. If patient is elderly, levodopa is sometimes used as an
initial treatment
he earaer aeraer asdsadas eerw dssdfsselleds
Dopamine receptor agonists
bromocriptine, apomorphinehe newer agents: ropinirole, cabergoline, pergolidehe
he earaer aeraer asdsadas eerw dssdfsselleds
Levodopa
usually combined with a decarboxylase inhibitor (e.g. carbidopa or benserazide) to prevent peripheralmetabolism of levodopa to dopaminehe
reduced effectiveness with time (usually by 2 years)he unwanted effects: dyskinesia, 'on-off' effect he no use in neuroleptic induced parkinsonismhe
he earaer aeraer asdsadas eerw dssdfsselleds
Selegiline
MAO-B inhibitorhe
reduces dopamine metabolismhe
he earaer aeraer asdsadas eerw dssdfsselleds
Antimuscarinics
useful for tremorhe reduces inhibition of excitatory cholingeric neuronshe e.g. procyclidine, benzotropine, benzhexolhe
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he earaer aeraer asdsadas eerw dssdfsselleds
Amantadine
prevents reuptake of dopamineheA 27-year-old man presents to A&E with 2 day history of severe headache and pyrexia (38.9C). A CT scan shows
petechial haemorrhages in the temporal and inferior frontal lobes. What is the most likely diagnosis?ia
A.A Brain abscessia
B.A Meningococcal meningitisia
C.A Cerebral malariaia
D.AHerpes simplex encephalitisia
E.A New variant CJDia
Next question
CT head showing temporal lobe changes - think herpes simplex encephalitis
Herpes simplex encephalitissqweqwesf erwrewfsdfs adasd dhe
Herpes simplex (HSV) encephalitis is a common topic in the MRCP. The virus characteristically affects the
temporal lobes - questions may give the result of imaging or describe temporal lobe signs e.g. aphasia
he earaer aeraer asdsadas eerw dssdfsselleds
Features
fever, headache, psychiatric symptoms, seizures, vomitinghe focal features e.g. aphasiahe peripheral lesions (e.g. cold sores) have no relation to presence of HSV encephalitishe
he earaer aeraer asdsadas eerw dssdfsselleds
Pathophysiology
HSV-1 responsible for 95% of cases in adultshe typically affects temporal and inferior frontal lobeshe
he earaer aeraer asdsadas eerw dssdfsselleds
Investigation
CSF: lymphocytosis, elevated proteinhe PCR for HSVhe CT: medial temporal and inferior frontal changes (e.g. petechial haemorrhages) - normal in one-third of
patientshe
MRI is betterhe EEG pattern: lateralised periodic discharges at 2 Hzhe
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he earaer aeraer asdsadas eerw dssdfsselleds
Treatment
aciclovirhehe earaer aeraer asdsadas eerw dssdfsselleds
Prognosis
treated 25%he untreated 80%he A 27-year-old woman presents to A&E with a one-day history of headache and feeling generally unwell.
She is pyrexial at 38.7C and there is no rash.
he earaer aeraer asdsadas eerw dssdfsselleds
Serum glucose 5.1 mmol/l
he earaer aeraer asdsadas eerw dssdfsselledsLumbar puncture reveals:
he earaer aeraer asdsadas eerw dssdfsselleds
Appearance Cloudy
Glucose 1.9 mmol/l
Protein 1.7 g/l
White cells 250 / mm (85% polymorphs)
he earaer aeraer asdsadas eerw dssdfsselledsWhat is the most likely diagnosis?ia
A.A Guillain-Barre syndromeia
B.A Viral meningitisia
C.ABacterial meningitisia
D.A Cerebral malariaia
E.A Tuberculous meningitisia
Next question
Meningitis: CSF analysissqweqwesf erwrewfsdfs adasd dhe
The table below summarises the characteristic CSF findings in meningitis:
he earaer aeraer asdsadas eerw dssdfsselleds
Bacterial Viral Tuberculous
Appearance Cloudy Clear/cloudy Fibrin web
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Glucose Low (< 1/2 plasma) Normal Low (< 1/2 plasma)
Protein High (> 1 g/l) Normal/raised* High (> 1 g/l)
White cells 10 - 5,000
polymorphs/mm
15 - 1,000
lymphocytes/mm
10 - 1,000
lymphocytes/mm
he earaer aeraer asdsadas eerw dssdfsselledsThe Ziehl-Neelsen stain is only 20% sensitive in the detection of tuberculous meningitis and therefore PCR
is sometimes used (sensitivity = 75%)
he earaer aeraer asdsadas eerw dssdfsselleds
*mumps is unusual in being associated with a low glucose level in a proportion of cases
A 33-year-old man presents to his GP complaining of visual disturbance. Examination reveals a bitemporal
hemianopia with predominately the upper quadrants being affected. What is the most likely lesion?ia
A.A Craniopharyngiomaia
B.A Brainstem lesionia
C.APituitary macroadenomaia
D.A Frontal lobe lesionia
E.A Right occipital lesionia
Next question
Bitemporal hemianopia
lesion of optic chiasm upper quadrant defect > lower quadrant defect = inferior chiasmal compression, commonly a pituitary
tumour
lower quadrant defect > upper quadrant defect = superior chiasmal compression, commonly acraniopharyngioma
An upper quadrant defect implies inferior chiasmal compression making a pituitary macroadenoma the most likely
diagnosis
Visual field defectssqweqwesf erwrewfsdfs adasd dhe
Greater detail is required in the MRCP when assessing visual field defects - quadrantanopias are described as are
incongruous and congruous defects
he earaer aeraer asdsadas eerw dssdfsselleds
The main points for the exam are:
left homonymous hemianopia means visual field defect to the left, i.e. lesion of right optic tracthe
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homonymous quadrantanopias: PITS (Parietal-Inferior, Temporal-Superior)he incongruous defects = optic tract lesion; congruous defects= optic radiation lesion or occipital cortexhe
he earaer aeraer asdsadas eerw dssdfsselleds
Homonymous hemianopia
incongruous defects: lesion of optic tracthe congruous defects: lesion of optic radiation or occipital cortexhe macula sparing: lesion of occipital cortexhe
he earaer aeraer asdsadas eerw dssdfsselleds
Homonymous quadrantanopias
superior: lesion of temporal lobehe inferior: lesion of parietal lobehe mnemonic = PITS (Parietal-Inferior, Temporal-Superior)he
he earaer aeraer asdsadas eerw dssdfsselleds
Bitemporal hemianopia
lesion of optic chiasmhe upper quadrant defect > lower quadrant defect = inferior chiasmal compression, commonly a pituitary
tumourhe
lower quadrant defect > upper quadrant defect = superior chiasmal compression, commonly acraniopharyngiomahe
What is the most common type of multiple sclerosis?ia
A.ARelapsing-remitting diseaseia
B.A Amyotrophic lateral sclerosisia
C.A Secondary progressive diseaseia
D.A Progressive-relapsing diseaseia
E.A Primary progressive diseaseia
Next question
Multiple sclerosis
sqweqwesf erwrewfsdfs adasd dhe
Multiple sclerosis is chronic disorder characterised by demyelination in the central nervous system.he earaer aeraer asdsadas eerw dssdfsselleds
Genetics
monozygotic twin concordance = 30%he dizygotic twin concordance = 2%he
he earaer aeraer asdsadas eerw dssdfsselleds
A variety of subtypes have been identified:
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he earaer aeraer asdsadas eerw dssdfsselleds
Relapsing-remitting disease
most common form, 70-80% of patients initiallyhe acute attacks (e.g. last 1-2 months) followed by periods of remissionhe
he earaer aeraer asdsadas eerw dssdfsselledsSecondary progressive disease
describes relapsing-remitting patients who have deteriorated and have developed neurological signs andsymptoms between relapseshe
he earaer aeraer asdsadas eerw dssdfsselleds
Primary progressive disease
accounts for 10% of patientshe progressive deterioration from onsethe more common in older peoplehe
he earaer aeraer asdsadas eerw dssdfsselleds
Progressive-relapsing disease
primary progressive patients with superimposed relapseheA 21-year-old female is seen in the first seizure clinic in the outpatient department. A decision is made not to start
her on anti-epileptic medication. What restrictions on driving should she be informed about?ia
A.ANo restrictions but inform DVLAia
B.A No restrictions, no need to inform DVLA if not on medicationia
C.A Cannot drive for 1 month from date of seizureia
D.A Cannot drive for 6 months from date of seizureia
E.A Cannot drive for 1 year from date of seizureia
Next question
Patients cannot drive for 1 year following a seizure
DVLA: neurological disorderssqweqwesf erwrewfsdfs adasd dhe
The guidelines below relate to car/motorcycle use unless specifically stated. For obvious reasons, the rules relating
to drivers of heavy goods vehicles tend to be much stricter
he earaer aeraer asdsadas eerw dssdfsselleds
Specific rules
first seizure - 1 year off drivinghe
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stroke - 1 month off drivinghe multiple TIAs over short period of times - 3 months off drivinghe craniotomy - 1 year off driving* he narcolepsy/cataplexy: cease driving on diagnosis, can restart once 'satisfactory control of symptoms'he
he earaer aeraer asdsadas eerw dssdfsselleds
*if the tumour is a benign meningioma and there is no seizure history, licence can be reconsidered 6 months aftersurgery if remains seizure free
A 65-year-old man is referred to the neurology outpatient clinic due to a resting tremor of his right hand. A
diagnosis of Parkinson's disease is made. He is otherwise well and is not currently disabled by his symptoms. What
is the most appropriate treatment?ia
A.A Selegilineia
B.ANo treatmentia
C.A New generation dopamine receptor agonist e.g. ropiniroleia
D.A Conventional dopamine receptor agonist e.g. bromocriptineia
E.A Antimuscarinicsia
Next question
Parkinson's disease: managementsqweqwesf erwrewfsdfs adasd dhe
Currently accepted practice in the management of patients is to delay treatment until the onset of disabling
symptoms and then to introduce a dopamine receptor agonist. If patient is elderly, levodopa is sometimes used as an
initial treatmenthe earaer aeraer asdsadas eerw dssdfsselleds
Dopamine receptor agonists
bromocriptine, apomorphinehe newer agents: ropinirole, cabergoline, pergolidehe
he earaer aeraer asdsadas eerw dssdfsselleds
Levodopa
usually combined with a decarboxylase inhibitor (e.g. carbidopa or benserazide) to prevent peripheralmetabolism of levodopa to dopaminehe
reduced effectiveness with time (usually by 2 years)he unwanted effects: dyskinesia, 'on-off' effect he no use in neuroleptic induced parkinsonismhe
he earaer aeraer asdsadas eerw dssdfsselleds
Selegiline
MAO-B inhibitorhe reduces dopamine metabolismhe
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he earaer aeraer asdsadas eerw dssdfsselleds
Antimuscarinics
useful for tremorhe reduces inhibition of excitatory cholingeric neuronshe e.g. procyclidine, benzotropine, benzhexolhe
he earaer aeraer asdsadas eerw dssdfsselleds
Amantadine
prevents reuptake of dopamineheEach one of the following is associated with normal pressure hydrocephalus, except:ia
A.APapilloedemaia
B.A Dementiaia
C.AUrinary incontinenceia
D.A Gait abnormalityia
E.A Enlarged fourth ventricleia
Next question
Urinary incontinence + gait abnormality + dementia = normal pressure hydrocephalus
Normal pressure hydrocephalussqweqwesf erwrewfsdfs adasd dhe
Normal pressure hydrocephalus is a reversible cause of dementia seen in elderly patients. It is thought to be
secondary to reduced CSF absorption at the arachnoid villi. These changes may be secondary to head injury,
subarachnoid haemorrhage or meningitis
he earaer aeraer asdsadas eerw dssdfsselleds
A classical triad of features is seen
urinary incontinencehe dementiahe gait abnormality (may be similar to Parkinson's disease)he
he earaer aeraer asdsadas eerw dssdfsselleds
Imaging
hydrocephalus with an enlarged fourth ventriclehehe earaer aeraer asdsadas eerw dssdfsselleds
Management
ventriculoperitoneal shuntinghe
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A 47-year-old man with a known history of schizophrenia is admitted to A&E due to confusion. A bottle of
procyclidine tablets are found in his pocket. On examination the temperature is 38.1C with a blood pressure of
155/100 mmHg. Neurological examination reveals a GCS of 13/15 but assessment of his peripheral nervous system
is difficult due to generalised increased muscle tone. What is the most likely diagnosis?ia
A.ANeuroleptic malignant syndromeia
B.A Procyclidine overdoseia
C.A Catatonic schizophreniaia
D.A Clozapine induced agranulocytosisia
E.A Quetiapine induced rhabdomyolysisia
Next question
Neuroleptic malignant syndromesqweqwesf erwrewfsdfs adasd dhe
Neuroleptic malignant syndrome is a rare but dangerous condition seen in patients taking antipsychotic medication.
It carries a mortality of up to 10% and can also occur with atypical antipsychotics
he earaer aeraer asdsadas eerw dssdfsselleds
Features
more common in young male patientshe onset usually in first 10 days of treatment or after increasing dosehe pyrexiahe rigidityhe tachycardiahe
he earaer aeraer asdsadas eerw dssdfsselledsA raised creatine kinase is present in most cases. A leukocytosis may also be seen
he earaer aeraer asdsadas eerw dssdfsselleds
Management
stop antipsychotiche IV fluids to prevent renal failurehe dantrolene may be useful in selected caseshe bromocriptine, dopamine agonist, may also be usedhe
In the treatment of migraine, sumatriptan is an example of a: ia
A.A Beta-blockeria
B.A Alpha-blocker and a partial 5-HT2 agonistia
C.ASpecific 5-HT1 agonistia
D.A 5-HT2 antagonistia
E.A Tricyclic antidepressantia
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Next question
Migraine
acute: 5-HT1 agonist prophylaxis: 5-HT2 antagonist
Migraine: drugssqweqwesf erwrewfsdfs adasd dhe
It should be noted that 5-HT receptor agonists are used in the acute treatment of migraine whilst 5-HT receptor
antagonists are used in prophylaxis
he earaer aeraer asdsadas eerw dssdfsselleds
Acute treatmenthe earaer aeraer asdsadas eerw dssdfsselleds
Standard analgesia
may be poorly absorbedhe often combined with anti-emetic e.g. metoclopramide to relieve associated nauseahe
he earaer aeraer asdsadas eerw dssdfsselleds
Sumatriptan
specific 5-HT1 agonist - opposes vasodilationhe very effectivehe
he earaer aeraer asdsadas eerw dssdfsselleds
Ergotamine
alpha-blocker and a partial 5-HT1 agonisthe often induces nausea and vomitinghe
he earaer aeraer asdsadas eerw dssdfsselleds
he earaer aeraer asdsadas eerw dssdfsselleds
Prophylaxishe earaer aeraer asdsadas eerw dssdfsselleds
Prophylaxis should be given if patients are experiencing two or more attacks per month. Modern treatment is effect
about 60% of patients
he earaer aeraer asdsadas eerw dssdfsselleds
5-HT2 antagonists
e.g. pizotifen, methysergidehehe earaer aeraer asdsadas eerw dssdfsselleds
Beta-blockers
e.g. propranololhehe earaer aeraer asdsadas eerw dssdfsselleds
Tricyclic antidepressants
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e.g. amitriptylineheIn patients with Guillain-Barre syndrome, respiratory function should be monitored with:ia
A.A Oxygen saturationsia
B.A PEFRia
C.AFlow volume loopia
D.A Arterial blood gasesia
E.A FVCia
Next question
FVC is used to monitor respiratory function in Guillain-Barre syndrome
Guillain-Barre syndrome: managementsqweqwesf erwrewfsdfs adasd dhe
Guillain-Barre syndrome describes an immune mediated demyelination of the peripheral nervous system often
triggered by an infection (classically Campylobacter jejuni)
he earaer aeraer asdsadas eerw dssdfsselleds
Management
plasma exchangehe IV immunoglobulinshe steroids and immunosuppressants have not been shown to be beneficialhe
FVC regularly to monitor respiratory functionhe
he earaer aeraer asdsadas eerw dssdfsselleds
Prognosis
20% suffer permanent disability, 5% dieheWhich one of the following is most characteristically associated with a very high protein level in the cerebrospinal
fluid?ia
A.A Myasthenia gravisia
B.A Multiple sclerosisia
C.A New variant CJDia
D.A Motor neuron diseaseia
E.A Guillain-Barre syndromeia
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Next question
Cerebrospinal fluid: raised proteinsqweqwesf erwrewfsdfs adasd dhe
Normal values of cerebrospinal fluid (CSF) are as follows:
pressure = 60-150 mm (patient recumbent)he protein = 0.2-0.4 g/lhe glucose = > 2/3 blood glucosehe cells: red cells = 0, white cells < 5/mmhe
he earaer aeraer asdsadas eerw dssdfsselleds
The following conditions are associated with raised protein levels
Guillain-Barre syndromehe TB/fungal/bacterial meningitishe spinal block (Froin's syndrome)he viral encephalitishe
What is the first line medication in the treatment of adults with generalised seizures?ia
A.A Gabapentinia
B.A Lamotrigineia
C.ASodium valproateia
D.A Carbamazepineia
E.A Phenytoinia
Next question
Epilepsy medication: first-line
generalised seizure: sodium valproate partial seizure: carbamazepine
Epilepsy: treatment
sqweqwesf erwrewfsdfs adasd dheMost neurologists now start antiepileptics following a second epileptic seizure. NICE guidelines suggest starting
antiepileptics after the first seizure if any of the following are present:
the patient has a neurological deficithe brain imaging shows a structural abnormalityhe the EEG shows unequivocal epileptic activity he the patient or their family or carers consider the risk of having a further seizure unacceptable he
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he earaer aeraer asdsadas eerw dssdfsselleds
Sodium valproate is considered the first line treatment for patients with generalised seizures with carbmazepine used
for partial seizures
he earaer aeraer asdsadas eerw dssdfsselleds
Tonic-clonic seizures
sodium valproatehe second line: lamotrigine, carbamazepinehe
he earaer aeraer asdsadas eerw dssdfsselleds
Absence seizures (Petit mal)
sodium valproate or ethosuximidehe sodium valproate particularly effective if co-existent tonic-clonic seizures in primary generalised
epilepsyhe
he earaer aeraer asdsadas eerw dssdfsselleds
Myoclonic seizures
sodium valproatehe second line: clonazepam, lamotriginehe
he earaer aeraer asdsadas eerw dssdfsselleds
Partial seizures
carbamazepinehe second line: sodium valproate, lamotriginehe
Which one of the following features is most associated with frontal lobe lesions?ia
A.A Wernicke's aphasiaia
B.A Gerstmann's syndromeia
C.APerserverationia
D.A Cortical blindnessia
E.A Superior homonymous quadrantanopiaia
Next question
Brain anatomysqweqwesf erwrewfsdfs adasd dhe
The following neurological disorders/features may allow localisation of a brain lesion:
he earaer aeraer asdsadas eerw dssdfsselleds
Parietal lobe lesions
sensory inattentionhe apraxiashe astereognosis (tactile agnosia) he
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inferior homonymous quadrantanopiahe Gerstmann's syndrome (lesion of dominant parietal): alexia, acalculia, finger agnosia and right-left
disorientationhe
he earaer aeraer asdsadas eerw dssdfsselleds
Occipital lobe lesions
homonymous hemianopiahe cortical blindnesshe visual agnosiahe
he earaer aeraer asdsadas eerw dssdfsselleds
Temporal lobe lesion
Wernicke's aphasiahe superior homonymous quadrantanopiahe auditory agnosiahe
he earaer aeraer asdsadas eerw dssdfsselledsFrontal lobes lesions
expressive (Broca's) aphasiahe disinhibitionhe perserverationhe anosmiahe
Which of the following features is least likely to be found in a patient with tuberose sclerosis?ia
A.A Adenoma sebaceumia
B.A Caf?au-lait spotsia
C.A Retinal hamartomasia
D.A'Ash-leaf' spotsia
E.A Lisch nodulesia
Next question
Lisch nodules are seen in neurofibromatosis
Tuberous sclerosissqweqwesf erwrewfsdfs adasd dhe
Tuberous sclerosis (TS) is a genetic condition of autosomal dominant inheritance. As is neurofibromatosis, the
majority of features seen are neuro-cutaneous
he earaer aeraer asdsadas eerw dssdfsselleds
Cutaneous features
depigmented 'ash-leaf' spots which fluoresce under UV lighthe roughened patches of skin over lumbar spine (Shagreen patches)he
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adenoma sebaceum: butterfly distribution over nosehe fibromata beneath nails (subungual fibromata)he caf?au-lait spots* may be seenhe
he earaer aeraer asdsadas eerw dssdfsselleds
Neurological features
developmental delayhe epilepsy (infantile spasms or partial)he intellectual impairmenthe
he earaer aeraer asdsadas eerw dssdfsselleds
Also
retinal hamartomas: dense white areas on retina (phakomata)he rhabdomyomas of the hearthe gliomatous changes can occur in the brain lesionshe polycystic kidneys, renal angiomyolipomatahe
he earaer aeraer asdsadas eerw dssdfsselleds
*these of course are more commonly associated with neurofibromatosis. However a 1998 study of 106 children with
TS found caf?au-lait spots in 28% of patients
An obese 24-year-old female presents with headache and blurred vision to her GP. Examination reveals bilateral
blurring of the optic discs but is otherwise unremarkable with no other neurological signs. Blood pressure is 130/74
and she is apyrexial. What is the most likely underlying diagnosis?ia
A.A Multiple sclerosisia
B.A Meningococcal meningitisia
C.A Brain abscessia
D.ANormal pressure hydrocephalusia
E.A Idiopathic intracranial hypertensionia
Next question
Obese, young female with headaches / blurred vision think idiopathic intracranial hypertension
The combination of a young, obese female with papilloedema but otherwise normal neurology makes idiopathic
intracranial hypertension the most likely diagnosis
Idiopathic intracranial hypertensionsqweqwesf erwrewfsdfs adasd dhe
Idiopathic intracranial hypertension (also known as pseudotumour cerebri and formerly benign intracranial
hypertension) is a condition classically seen in young, overweight females.
he earaer aeraer asdsadas eerw dssdfsselleds
Features
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headachehe blurred visionhe papilloedema (usually present)he enlarged blind spothe sixth nerve palsy may be presenthe
he earaer aeraer asdsadas eerw dssdfsselledsRisk factors
obesityhe female sexhe pregnancyhe drugs: oral contraceptive pill, steroids, tetracycline, vitamin A he
he earaer aeraer asdsadas eerw dssdfsselleds
Management
weight losshe diuretics e.g. acetazolamidehe repeated lumbar puncturehe
A 45-year-old man is noted to have a peripheral motor neuropathy on examination. He has a long history of
recurrent abdominal pain. What is the most likely diagnosis?ia
A.AAcute intermittent porphyriaia
B.A Myelomaia
C.A Huntingdon's diseaseia
D.A Lawrence-Moon-Biedl syndromeia
E.A Friedreich's ataxiaia
Next question
In the MRCP, neurological signs combined with abdominal pain is acute intermittent porphyria or lead poisoning
until proven otherwise
Acute intermittent porphyriasqweqwesf erwrewfsdfs adasd dhe
Acute intermittent porphyria (AIP) is a rare autosomal dominant condition caused by a defect in porphobilinogen
deaminase, an enzyme involved in the biosynthesis of haem. The results in the toxic accumulation of delta
aminolaevulinic acid and porphobilinogen. It characteristically presents with abdominal and neuropsychiatric
symptoms in 20-40 year olds. AIP is more common in females (5:1)
he earaer aeraer asdsadas eerw dssdfsselleds
Features
abdominal: abdominal pain, vomitinghe neurological: motor neuropathyhe
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psychiatric: e.g. depressionhe hypertension and tachycardia commonhe
he earaer aeraer asdsadas eerw dssdfsselleds
Diagnosis
classically urine turns deep red on standinghe raised urinary porphobilinogen (elevated between attacks and to a greater extent during acute attacks)he assay of red cells for porphobilinogen deaminasehe raised serum levels of delta aminolaevulinic acid and porphobilinogenhe
Which one of the following infections is most strongly associated with the development of Guillain-Barre
syndromeia
A.A Shigellaia
B.A Salmonellaia
C.A E. coli H7:0157ia
D.A Herpes simplexia
E.A Campylobacter jejuniia
Next question
Campylobacter jejuni is strongly associated with the development of Guillain-Barre syndrome
Guillain-Barre syndromesqweqwesf erwrewfsdfs adasd dhe
Guillain-Barre syndrome describes an immune mediated demyelination of the peripheral nervous system often
triggered by an infection (classically Campylobacter jejuni)
he earaer aeraer asdsadas eerw dssdfsselleds
Pathogenesis
cross reaction of antibodies with gangliosides in the peripheral nervous systemhe correlation between anti-ganglioside antibody (e.g. anti-GM1) and clinical features has been
demonstratedhe
anti-GM1 antibodies in 25% of patientshehe earaer aeraer asdsadas eerw dssdfsselleds
Miller-Fisher syndrome
variant of Guillain-Barre syndromehe associated with areflexia, ataxia, ophthalmoplegiahe anti-GQ1b antibodies are present in 90% of caseshe
A patient is referred by her GP due to a third nerve palsy associated with a headache. On examination meningism is
present. Which one of the following diagnoses needs to be urgently excluded?ia
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A.A Weber's syndromeia
B.A Internal carotid artery aneurysmia
C.A Multiple sclerosisia
D.APosterior communicating artery aneurysmia
E.A Anterior communicating artery aneurysmia
Next question
Painful third nerve palsy = posterior communicating artery aneurysm
Given the combination of a headache and third nerve palsy it is important to exclude a posterior communicating
artery aneurysm
Third nerve palsysqweqwesf erwrewfsdfs adasd dhe
Features
eye is deviated 'down and out'he ptosishe pupil may be dilated (sometimes called a 'surgical' third nerve palsy)he
he earaer aeraer asdsadas eerw dssdfsselleds
Causes
diabetes mellitushe vasculitis e.g. temporal arteritis, SLEhe false localizing sign due to uncal herniation through tentorium if raised ICPhe posterior communicating artery aneurysm (pupil dilated)he cavernous sinus thrombosishe Weber's syndrome: ipsilateral third nerve palsy with contralateral hemiplegia -caused by midbrain
strokeshe
other possible causes: amyloid, multiple sclerosisheA 34-year-old female presents with collapse and vomiting preceded by an occipital headache of acute onset. On
examination she was conscious and alert with photophobia but no neck stiffness. CT brain is reported as normal.
Which one of the following investigations would yield the diagnosis?ia
A.A CT brain with contrastia
B.A Repeat CT brain in 24hia
C.ACSF examinationia
D.A Cerebral angiographyia
E.A MRI brainia
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Next question
Subarachnoid haemorrhagesqweqwesf erwrewfsdfs adasd dhe
Causes
85% are due to rupture of berry aneurysms (conditions associated with berry aneurysms include adultpolycystic kidney disease, Ehlers-Danlos syndrome and coarctation of the aorta)he AV malformationshe traumahe tumourshe
he earaer aeraer asdsadas eerw dssdfsselleds
Investigations
CT: negative in 5%he LP: done after 12 hrs (allowing time for xanthochromia to develop)he
he earaer aeraer asdsadas eerw dssdfsselledsComplications
rebleeding (in 30%)he obstructive hydrocephalus (due to blood in ventricles)he vasospasm leading to cerebral ischaemiahe
he earaer aeraer asdsadas eerw dssdfsselleds
Management
neurosurgical opinion: no clear evidence over early surgical intervention against delayed interventionhe nimodipine (e.g. 60mg / 4 hrly, if BP allows) has been shown to reduce the severity of neurological deficits
but doesn't reduce rebleeding*he
he earaer aeraer asdsadas eerw dssdfsselleds
*the way nimodipine works in subarachnoid haemorrhage is not fully understood. It has been previously postulated
that it reduces cerebral vasopasm (hence maintaining cerebral perfusion) but this has not been demonstrated in
studies
A 45-year-old man presents to A&E following the sudden onset of pain in his right eye whilst hammering a nail into
the wall. The pain is described as severe with occasional exacerbations. On examination he has a mild right ptosis
and small right pupil. What is the most likely diagnosis?ia
A.A Trigeminal neuralgiaia
B.A Glaucomaia
C.ACarotid artery dissectionia
D.A Cluster headacheia
E.A Migraineia
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Next question
This patient has Horner's syndrome caused by a carotid artery dissection. This may be caused by relatively benign
trauma to the neck such as hyperextension whilst doing DIY
Horner's syndrome
sqweqwesf erwrewfsdfs adasd dheFeatures
miosis (small pupil)he ptosishe enophthalmos (sunken eye) he anhydrosis (loss of sweating one side)he
he earaer aeraer asdsadas eerw dssdfsselleds
Distinguishing between causes
heterochromia (difference in iris colour) is seen in congenital Horner'she
anhydrosis: see belowhe
he earaer aeraer asdsadas eerw dssdfsselleds
Anhydrosis
if affects head, arm and trunk suggests central lesionhe if affects just face suggests pre-ganglionic lesionhe if absent suggests post-ganglionic lesionhe
he earaer aeraer asdsadas eerw dssdfsselleds
Central causes (from origin of sympathetic supply)
strokehe syringomyeliahe multiple sclerosishe tumourhe encephalitishe
he earaer aeraer asdsadas eerw dssdfsselleds
Pre-ganglionic causes
Pancoast's tumourhe cervical ribhe thyroidectomyhe traumahe
he earaer aeraer asdsadas eerw dssdfsselleds
Post-ganglionic causes
carotid artery dissectionhe internal carotid aneurysmhe cavernous sinus thrombosishe
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Each of the following are causes of peripheral neuropathy. Which one is associated with predominately motor
loss?ia
A.A Vitamin B12 deficiencyia
B.AGuillain-Barre syndromeia
C.A Uraemiaia
D.A Diabetesia
E.A Leprosyia
Next question
Peripheral neuropathysqweqwesf erwrewfsdfs adasd dhe
Peripheral neuropathy may be divided into conditions which predominately cause a motor or sensory loss
he earaer aeraer asdsadas eerw dssdfsselleds
Predominately motor loss
Guillain-Barre syndromehe porphyriahe lead poisoninghe hereditary sensorimotor neuropathies (HSMN) - Charcot-Marie-Tooth he chronic inflammatory demyelinating polyneuropathy (CIDP)he diphtheriahe
he earaer aeraer asdsadas eerw dssdfsselleds
Predominately sensory loss
diabeteshe uraemiahe leprosyhe alcoholismhe vitamin B12 deficiencyhe amyloidosishe
he earaer aeraer asdsadas eerw dssdfsselleds
Alcoholic neuropathy
secondary to both direct toxic effects and reduced absorption of B vitaminshe sensory symptoms typically present prior to motor symptomshe
he earaer aeraer asdsadas eerw dssdfsselleds
Vitamin B12 deficiency
subacute combined degeneration of spinal cordhe dorsal column usually affected first (joint position, vibration) prior to distal paraesthesiahe
Which part of the brain does herpes simplex encephalitis characteristically affect?ia
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A.ATemporal lobeia
B.A Parietal lobeia
C.A Occipital lobeia
D.A Cerebellumia
E.A Medullaia
Next question
CT head showing temporal lobe changes - think herpes simplex encephalitis
The inferior frontal lobe may also be affected
Herpes simplex encephalitissqweqwesf erwrewfsdfs adasd dhe
Herpes simplex (HSV) encephalitis is a common topic in the MRCP. The virus characteristically affects the
temporal lobes - questions may give the result of imaging or describe temporal lobe signs e.g. aphasia
he earaer aeraer asdsadas eerw dssdfsselleds
Features
fever, headache, psychiatric symptoms, seizures, vomitinghe focal features e.g. aphasiahe peripheral lesions (e.g. cold sores) have no relation to presence of HSV encephalitishe
he earaer aeraer asdsadas eerw dssdfsselleds
Pathophysiology
HSV-1 responsible for 95% of cases in adultshe typically affects temporal and inferior frontal lobeshe
he earaer aeraer asdsadas eerw dssdfsselleds
Investigation
CSF: lymphocytosis, elevated proteinhe PCR for HSVhe CT: medial temporal and inferior frontal changes (e.g. petechial haemorrhages) - normal in one-third of
patientshe
MRI is betterhe EEG pattern: lateralised periodic discharges at 2 Hzhe
he earaer aeraer asdsadas eerw dssdfsselleds
Treatment
aciclovirhe
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he earaer aeraer asdsadas eerw dssdfsselleds
Prognosis
treated 25%he untreated 80%he
Which one of the following drugs is used in the management of multiple sclerosis?ia
A.ABeta-interferonia
B.A Gamma-interferonia
C.A Infliximabia
D.A Rituximabia
E.A Alpha-interferonia
Next question
Multiple sclerosis: managementsqweqwesf erwrewfsdfs adasd dhe
Treatment in multiple sclerosis is focused at reducing the frequency and duration of relapses. There is no cure. High
dose steroids (e.g. IV methylprednisolone) may be given for 3-5 days to shorten the length of an acute relapse.
Baclofen is helpful in controlling spasticity. Hallucinations are occasionally seen on the withdrawal of baclofen
he earaer aeraer asdsadas eerw dssdfsselleds
Beta-interferon has been shown to reduce the relapse rate by up to 30%. Certain criteria have to be met before it is
used:
relapsing-remitting disease + 2 relapses in past 2 years + able to walk 100m unaidedhe secondary progressive disease + 2 relapses in past 2 years + able to walk 10m (aided or unaided)he reduces number of relapses and MRI changes, however doesn't reduce overall disabilityhe
A 52-year-old man is prescribed apomorphine for Parkinson's disease. What is the mechanism of action?ia
A.ADopamine receptor agonistia
B.A Dopamine receptor antagonistia
C.AMAO-B inhibitoria
D.A Decarboxylase inhibitoria
E.A Antimuscarinicia
Next question
Apomorphine is one of the older dopamine receptor agonists. Newer agents such as ropinirole and cabergoline have
since been developed
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Parkinson's disease: managementsqweqwesf erwrewfsdfs adasd dhe
Currently accepted practice in the management of patients is to delay treatment until the onset of disabling
symptoms and then to introduce a dopamine receptor agonist. If patient is elderly, levodopa is sometimes used as an
initial treatment
he earaer aeraer asdsadas eerw dssdfsselleds
Dopamine receptor agonists
bromocriptine, apomorphinehe newer agents: ropinirole, cabergoline, pergolidehe
he earaer aeraer asdsadas eerw dssdfsselleds
Levodopa
usually combined with a decarboxylase inhibitor (e.g. carbidopa or benserazide) to prevent peripheralmetabolism of levodopa to dopaminehe
reduced effectiveness with time (usually by 2 years)he unwanted effects: dyskinesia, 'on-off' effect he no use in neuroleptic induced parkinsonismhe
he earaer aeraer asdsadas eerw dssdfsselleds
Selegiline
MAO-B inhibitorhe reduces dopamine metabolismhe
he earaer aeraer asdsadas eerw dssdfsselleds
Antimuscarinics
useful for tremorhe reduces inhibition of excitatory cholingeric neuronshe e.g. procyclidine, benzotropine, benzhexolhe
he earaer aeraer asdsadas eerw dssdfsselleds
Amantadine
prevents reuptake of dopamineheA 25-year-old female with a history of bilateral vitreous haemorrhage is referred due to progressive ataxia. What is
the likely diagnosis?ia
A.ANeurofibromatosis type Iia
B.A Neurofibromatosis type IIia
C.A Tuberose sclerosisia
D.AVon Hippel-Lindau syndromeia
E.A Sarcoidosisia
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Next question
Retinal and cerebellar haemangiomas are key features of Von Hippel-Lindau syndrome. Retinal haemangiomas are
bilateral in 25% of patients and may lead to vitreous haemorrhage
Von Hippel-Lindau syndrome
sqweqwesf erwrewfsdfs adasd dheVon Hippel-Lindau (VHL) syndrome is an autosomal dominant condition predisposing to neoplasia. It is due to an
abnormality in the VHL gene located on short arm of chromosome 3
he earaer aeraer asdsadas eerw dssdfsselleds
Features
cerebellar haemangiomas: he retinal haemangiomas: vitreous haemorrhagehe renal cysts (premalignant)he phaeochromocytomahe
Each one of the following is associated with the development of chorea, except:ia
A.AHaemochromatosisia
B.A Ataxic telangiectasiaia
C.ACarbon monoxide poisoningia
D.A SLEia
E.A Huntingdon's diseaseia
Next question
Choreasqweqwesf erwrewfsdfs adasd dhe
Chorea describes rapid, jerky movements which often move from one part of the body to another. Slower, sinuous
movement of the limbs is termed athetosis. Chorea is caused by damage to the basal ganglia, especially the caudate
nucleus
he earaer aeraer asdsadas eerw dssdfsselleds
Causes of chorea
Huntingdon's disease, Wilson's disease, ataxic telangiectasiahe SLE, anti-phospholipid syndromehe rheumatic fever: Sydenham's choreahe drugs: oral contraceptive pill, L-dopa, antipsychoticshe neuroacanthocytosishe chorea gravidarumhe thyrotoxicosishe polycythaemia rubra verahe carbon monoxide poisoninghe
Which one of the following features is not associated with an oculomotor nerve palsy?ia
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A.AMiosisia
B.A Ptosisia
C.A Eye is deviated 'down and out'ia
D.APain if due to a posterior communicating artery aneurysmia
E.A Diplopiaia
Next question
Ptosis + dilated pupil = third nerve palsy; ptosis + constricted pupil = Horner's
Oculomotor nerve palsy is typically associated with a dilated pupil
Third nerve palsysqweqwesf erwrewfsdfs adasd dhe
Features
eye is deviated 'down and out'he ptosishe pupil may be dilated (sometimes called a 'surgical' third nerve palsy)he
he earaer aeraer asdsadas eerw dssdfsselleds
Causes
diabetes mellitushe vasculitis e.g. temporal arteritis, SLEhe false localizing sign due to uncal herniation through tentorium if raised ICPhe posterior communicating artery aneurysm (pupil dilated)he cavernous sinus thrombosishe Weber's syndrome: ipsilateral third nerve palsy with contralateral hemiplegia -caused by midbrain
strokeshe
other possible causes: amyloid, multiple sclerosisheNeurofibromatosis type 1 is associated with a gene defect on which chromosome?ia
A.A Chromosome 4ia
B.A Chromosome 11ia
C.AChromosome 16ia
D.AChromosome 17ia
E.A Chromosome 22ia
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Next question
One of our registered users sent the following mnemonic to us:
NF1: chromosome 17 - as neurofibromatosis has 17 charactershe NF2: chromosome 22 - all the 2'she
Neurofibromatosissqweqwesf erwrewfsdfs adasd dhe
Overview
two types, NF1 and NF2he both autosomal dominanthe
he earaer aeraer asdsadas eerw dssdfsselleds
NF1
also known as von Recklinghausen's syndromehe caused by gene mutation on chromosome 17 which codes for neurofibrominhe affects 1 in 4,000he
he earaer aeraer asdsadas eerw dssdfsselleds
NF2
caused by gene mutation on chromosome 22he affects 1 in 100,000he
he earaer aeraer asdsadas eerw dssdfsselleds
NF1 features
caf-au-lait spots (>= 6)he
axillary/groin freckleshe peripheral neurofibromashe iris: Lisch nodules in > 90%he
he earaer aeraer asdsadas eerw dssdfsselleds
NF2 features
bilateral acoustic neuromasheWhich one of the following is least likely to produce a lymphocytosis in the cerebrospinal fluid?ia
A.A Systemic lupus erythematousia
B.AGuillain-Barre syndromeia
C.A Viral encephalitisia
D.APartially treated bacterial meningitisia
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E.A Behcet's syndromeia
Next question
Cerebrospinal fluid: raised lymphocytes
sqweqwesf erwrewfsdfs adasd dheNormal values of cerebrospinal fluid (CSF) are as follows:
pressure = 60-150 mm (patient recumbent)he protein = 0.2-0.4 g/lhe glucose = > 2/3 blood glucosehe cells: red cells = 0, white cells < 5/mmhe
he earaer aeraer asdsadas eerw dssdfsselleds
The following conditions are associated with raised lymphocytes
viral meningitis/encephalitishe
TB meningitishe partially treated bacterial meningitishe Lyme diseasehe Behcet's, SLEhe lymphoma, leukaemiahe
Which one of the following features is most associated with temporal lobe lesions?ia
A.A Astereognosisia
B.AAuditory agnosiaia
C.AVisual agnosiaia
D.A Disinhibitionia
E.A Expressive (Broca's) aphasiaia
Next question
Brain anatomysqweqwesf erwrewfsdfs adasd dhe
The following neurological disorders/features may allow localisation of a brain lesion:
he earaer aeraer asdsadas eerw dssdfsselleds
Parietal lobe lesions
sensory inattentionhe apraxiashe astereognosis (tactile agnosia) he inferior homonymous quadrantanopiahe Gerstmann's syndrome (lesion of dominant parietal): alexia, acalculia, finger agnosia and right-left
disorientationhe
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he earaer aeraer asdsadas eerw dssdfsselleds
Occipital lobe lesions
homonymous hemianopiahe cortical blindnesshe visual agnosiahe
he earaer aeraer asdsadas eerw dssdfsselleds
Temporal lobe lesion
Wernicke's aphasiahe superior homonymous quadrantanopiahe auditory agnosiahe
he earaer aeraer asdsadas eerw dssdfsselleds
Frontal lobes lesions
expressive (Broca's) aphasiahe disinhibitionhe perserverationhe anosmiahe
Each of the following features are seen in myotonic dystrophy, except:ia
A.A Mild mental impairmentia
B.ARound faceia
C.A Frontal baldingia
D.A Myotoniaia
E.A Cataractsia
Next question
Myotonic dystrophysqweqwesf erwrewfsdfs adasd dhe
Inherited myopathy with features developing at around 20-30 years old. Affects skeletal, cardiac and smooth muscle
he earaer aeraer asdsadas eerw dssdfsselleds
Genetics
autosomal dominanthe a trinucleotide repeat disorderhe CTG repeat at the end of the DPMK gene on chromosome 19he
he earaer aeraer asdsadas eerw dssdfsselleds
Facial features
myotonic facies (long, 'haggard' appearance)he frontal baldinghe
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bilateral ptosishe cataractshe dysarthriahe
he earaer aeraer asdsadas eerw dssdfsselleds
Other features
myotonia (tonic spasm of muscle)he weakness of arms and legs (distal initially)he mild mental impairmenthe diabetes mellitushe testicular atrophyhe cardiomyopathyhe dysphagiahe
A 34-year-old man is reviewed in the neurology clinic. He has been established on sodium valproate for primary
generalised epilepsy. Despite now taking a therapeutic dose he continues to have seizures and is troubled by weight
gain since starting sodium valproate. He asks to stop the his current medication and try a different drug. Which one
of the following drugs would be the most appropriate second-line treatment?ia
A.ALamotrigineia
B.A Ethosuximideia
C.A Pregabalinia
D.A Gabapentinia
E.A Tiagabineia
Next question
Monotherapy with another drug should be attempted before combination therapy is started. Caution should be
exercised when combining sodium valproate and lamotrigine as serious skin rashes such as Steven-Johnson's
syndrome may be provoked
Epilepsy: treatmentsqweqwesf erwrewfsdfs adasd dhe
Most neurologists now start antiepileptics following a second epileptic seizure. NICE guidelines suggest starting
antiepileptics after the first seizure if any of the following are present:
the patient has a neurological deficithe
brain imaging shows a structural abnormalityhe the EEG shows unequivocal epileptic activity he the patient or their family or carers consider the risk of having a further seizure unacceptable he
he earaer aeraer asdsadas eerw dssdfsselleds
Sodium valproate is considered the first line treatment for patients with generalised seizures with carbmazepine used
for partial seizures
he earaer aeraer asdsadas eerw dssdfsselleds
Tonic-clonic seizures
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sodium valproatehe second line: lamotrigine, carbamazepinehe
he earaer aeraer asdsadas eerw dssdfsselleds
Absence seizures (Petit mal)
sodium valproate or ethosuximidehe sodium valproate particularly effective if co-existent tonic-clonic seizures in primary generalised
epilepsyhe
he earaer aeraer asdsadas eerw dssdfsselleds
Myoclonic seizures
sodium valproatehe second line: clonazepam, lamotriginehe
he earaer aeraer asdsadas eerw dssdfsselleds
Partial seizures
carbamazepinehe second line: sodium valproate, lamotriginehe
As part of a routine cranial nerve examine the following results are obtained:
he earaer aeraer asdsadas eerw dssdfsselleds
Rinne's test: Air conduction > bone conduction in both ears
Weber's test: Localises to the right side
he earaer aeraer asdsadas eerw dssdfsselledsWhat do these tests imply?ia
A.A Left conductive deafnessia
B.A Normal hearingia
C.A Right conductive deafnessia
D.A Right sensorineural deafnessia
E.A Left sensorineural deafnessia
Next question
Rinne's and Weber's testsqweqwesf erwrewfsdfs adasd dhe
Performing both Rinne's and Weber's test allows differentiation of conductive and sensorineural deafness
he earaer aeraer asdsadas eerw dssdfsselleds
Rinne's test
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tuning fork is placed over mastoid process, followed by repositioning just over external acoustic meatushe air conduction (AC) is normally better than bone conduction (BC)he if BC > AC then conductive deafnesshe
he earaer aeraer asdsadas eerw dssdfsselleds
Weber's test
tuning fork is placed over middle of forehead, patient is asked which side is loudesthe in unilateral sensorineural deafness, sound is localised to the 'good' sidehe in unilateral conductive deafness, sound is localised to the 'bad' sidehe
Which one of the following is least characteristic of Wernicke's encephalopathy?ia
A.A Ataxiaia
B.A Confusionia
C.A Ophthalmoplegiaia
D.AConfabulationia
E.A Nystagmusia
Next question
An inability to acquire new memories and confabulation suggests the development of Korsakoff's syndrome
Wernicke's encephalopathysqweqwesf erwrewfsdfs adasd dhe
Wernicke's encephalopathy is a neuropsychiatric disorder caused by thiamine deficiency which is most commonly
seen in alcoholics. Rarer causes include: persistent vomiting, stomach cancer, dietary deficiency. A classic triad of
nystagmus, ophthalmoplegia and ataxia may occur. In Wernicke's encephalopathy petechial haemorrhages occur in a
variety of structures in the brain including the mamillary bodies and ventricle walls
he earaer aeraer asdsadas eerw dssdfsselleds
Features
nystagmushe ophthalmoplegiahe ataxiahe confusion, altered GCShe peripheral sensory neuropathyhe
he earaer aeraer asdsadas eerw dssdfsselledsInvestigations
decreased red cell transketolasehe MRIhe
he earaer aeraer asdsadas eerw dssdfsselleds
Treatment is with urgent replacement of thiamine
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