Neurology Flashcards
Describe the acute treatment, and prophylaxis, of migraines
Conservative: Trigger avoidance, medication review
Acute medical treatment: Basic analgesia (NSAIDs, paracetamol), oral triptan (usually Sumatriptan), and potentially an anti-emetic (e.g. Prochlorperazine)
If vomiting restricts oral medication, give an intranasal or subcut triptan.
NB: Triptans should be taken when the headache starts, NOT when the aura starts
Prophylaxis: Propranolol, Topiramate, or Amitryptiline
Follow-up in 2-8 weeks
Prophylaxis should be given where migraines are having severe impact on life, acute treatment is contraindicated or ineffective, or there is a risk of medication overuse headache from acute treatments (e.g. NSAIDs)
A 56 year old man attends A&E with sudden one-sided weakness and loss of the right visual field. His symptoms resolve spontaneously after 3 hours. How should this patient now be managed?
On presentation:
Give aspirin 300mg
Specialist review within 24 hours
Specialist to consider carotid imaging and/or MRI to assess damage
Long-term: Prevention with 75mg Clopidogrel Start high intensity statins Anti-hypertensives if needed Risk factor modification Anticoagulate if afib or flutter present
Management of TIA acutely and long-term:
https: //www.nice.org.uk/guidance/ng128/chapter/Recommendations#thrombectomy-for-people-with-acute-ischaemic-stroke
https: //cks.nice.org.uk/topics/stroke-tia/management/secondary-prevention-following-stroke-tia/
How should a patient presenting with symptoms of a stroke be managed?
A-E assessment
History (collateral if needed)
Use ROSIER tool to establish if stroke +/- quick neuro exam
Organise urgent CT head
If ischaemic - 300mg aspirin for 2 weeks, then 75mg clopidogrel lifelong
Perform ECG and take bloods including FBC, U&Es, VBG, clotting
Contact stroke team
Stroke team will then thrombolyse/ thrombect
A 64 year old woman is brought to hospital by ambulance having collapsed. She now has new-onset left-sided weakness, expressive dysphasia, and loss of the left visual field in both eyes.
What is the most likely diagnosis?
A. TACS (total anterior circulation stroke)
B. PACS (partial anterior circulation stroke)
C. POCS (posterior circulation stroke)
D. LACS (lacunar stroke)
E. Brainstem infarct
A. TACS (total anterior circulation stroke)
This is asking you to classify this stroke according to the Bamford stroke classification:
TACS: requires all 3 criteria:
Unilateral weakness and/or sensory deficit
Homonymous hemianopia
Higher cerebral deficit (e.g. dysphasia, visuospatial disorder)
PACS: requires 2 of 3 criteria:
Unilateral weakness and/or sensory deficit
Homonymous hemianopia
Higher cerebral deficit (e.g. dysphasia, visuospatial disorder)
LACS: requires one of 4 criteria: Pure motor deficit Pure sensory deficit Sensori-motor deficit Ataxic hemiparesis
POCS: requires one of 4 criteria:
Cranial nerve palsy + contralateral motor/sensory deficit
Bilateral motor/ sensory deficit
Conjugate eye movement disorder (e.g. gaze palsy)
Cerebellar dysfunction (e.g. ataxia, vertigo, nystagmus)
A 73 year old man presents with new onset left sided hemiparesis, but with preserved sensation. A cranial nerve exam is normal, as is speech.
What is the most likely diagnosis?
A. TACS (total anterior circulation stroke)
B. PACS (partial anterior circulation stroke)
C. POCS (posterior circulation stroke)
D. LACS (lacunar stroke)
E. Brainstem infarct
D. LACS (lacunar stroke)
This is asking you to classify this stroke according to the Bamford stroke classification:
TACS: requires all 3 criteria:
Unilateral weakness and/or sensory deficit
Homonymous hemianopia
Higher cerebral deficit (e.g. dysphasia, visuospatial disorder)
PACS: requires 2 of 3 criteria:
Unilateral weakness and/or sensory deficit
Homonymous hemianopia
Higher cerebral deficit (e.g. dysphasia, visuospatial disorder)
POCS: requires one of 4 criteria:
Cranial nerve palsy + contralateral motor/sensory deficit
Bilateral motor/ sensory deficit
Conjugate eye movement disorder (e.g. gaze palsy)
Cerebellar dysfunction (e.g. ataxia, vertigo, nystagmus)
LACS: requires one of 4 criteria: Pure motor deficit Pure sensory deficit Sensori-motor deficit Ataxic hemiparesis
An F1 clerks in a patient with a 2 hour history of sudden onset left-sided hemiparesis, dysphasia, and homonymous hemianopia. There is a family history of MIs and strokes, and the F1 strongly suspects a stroke. The patient has had an ECG and has had bloods taken for FBC, U&Es, LFTs, and clotting.
What should the first step in the F1’s management be?
A. Give warfarin and a LMWH
B. Give a 300mg loading dose of aspirin
C. Order an urgent non-contrast CT head
D. Give 300mg of aspirin and 300mg clopidogrel
E. Take the patient to a cathlab immediately for thrombolysis
C. Order an urgent non-contrast CT head
15% of strokes are haemorrhagic and thrombolysing a patient with a haemhorragic stroke will kill them quickly - hence it is important to check with an urgent CT head.
What are the signs of cerebellar dysfunction?
The acronym ‘DANISH’ is useful for remembering cerebellar signs:
Dysdiadochokinesia Ataxia Nystagmus Intention tremor Slurred or staccato speech Hypotonia/ Heel-shin test positivity
Match each of the following findings to the corresponding disease:
- Elevated CSF protein but normal WCC (albuminocytologic dissociation)
- Reduced CSF glucose
- Oligoclonal bands and IgG present in CSF
A. Bacterial meningitis
B. Gullain-Barré syndrome
C. Multiple sclerosis
- Elevated CSF protein but normal WCC (albuminocytologic dissociation) - B. Gullain-Barré syndrome
- Reduced CSF glucose - A. Bacterial meningitis
- Oligoclonal bands and IgG present in CSF - C. Multiple sclerosis
A 53 year old woman with a diagnosis of relapsing-remitting multiple sclerosis (MS) presents with 4 weeks of progressive clumisness and weakness of her hands. Her MS is controlled with Natalizumab and she is currently not experiencing her usual relapse symptoms. An MRI shows diffuse white matter lesions.
What complication has developed in this patient?
A. CNS lymphoma B. Periventricular leucomalacia C. HIV infection D. Progressive multifocal leucoencephalopathy E. Toxoplasmosis infection
D. Progressive multifocal leucoencephalopathy
PML is caused by the JC virus - a virus present in ~half of the normal population but is kept under control by the immune system. In immunocompromised individuals it may activate and cause progressive demyelination. It is particularly linked to Natalizumab.
A 62 year old man presents to the GP concerned that his voice has changed. He finds himself slurring his words and his wife comments his voice sounds more nasal. He also mentions episodes of laughing or crying in response to things his wife had said that didn’t warrant the reaction. On examination he has weakness of tongue protrusion with some wasting, and a brisk jaw jerk.
Given the likely diagnosis, what would be the most useful diagnostic test?
A. B12 and folate B. MRI brain and spinal cord C. Electromyography D. AChR and voltage-gated calcium channel antibodies E. HIV test
C. Electromyography
This is a history of amyotrophic lateral sclerosis (ALS) - a form of motor neurone disease. It is a progresisve neurodegenerative condition featuring both upper and lower motor neuron signs. It is a clinical diagnosis but a range of investigations should be undertaken both to rule out alternative diagnoses and to confirm ALS. Electromyography may both support a diagnosis of ALS and rule out other causes by demonstrating diffuse acute and chronic motor denervation. The other tests are important to rule out other causes, but will not directly support a diagnosis of ALS.
A 34 year old woman presents to her GP with weakness in her left hand. On examination there is wasting of the thenar and hypothenar eminences and weakness of finger abduction and adduction, and thumb abduction, but power grip is preserved. There is no sensory deficit in the hand, but there is some loss of sensation over the anteromedial forearm and arm.
What is the most likely causative lesion?
A. Ulnar nerve palsy B. Median nerve palsy C. Anterior interosseous nerve palsy D. C8 nerve palsy E. T1 nerve palsy
E. T1 nerve palsy
T1 supplies the intrinsic muscles of the hands (e.g. interossei, lumbricals, thenar and hypothenar muscle groups) which are responsible for fine motor movements. The muscles controlling power grip are in ther anterior compertment of the forearm and would most likely be preserved. The sensory deficit described corresponds to the T1 dermatome.
Which anti-emetic is used for Parkinson’s patients?
Domperidone
Domperidone is a dopamine antagonist but does not cross the BBB and so doesn’t worsen Parkinsonian symptoms. Metoclopramide and cyclizine can both worsen symptoms.
Why is carbidopa given with levodopa?
Carbidopa inhibits dopa decarboxylase and so prevents metabolism of levodopa to dopamine. Carbidopa cannot cross the blood-brain barrier and so is active only in the periphery. This increases delivery of levodopa to the CNS.
A 45 year old woman presents to A&E with a severe headache. Her cranial nerve examination is abnormal - her left eye struggles to move and is fixed in the down and out position. The pupil of her left eye is fixed and dilated, but the right eye is normal.
Which condition is suggested by this presentation?
A. Posterior communicating artery aneurysm B. Subarachnoid haemorrhage C. Epidural haemorrhage D. Meningitis E. A cerebral metastasis
A. Posterior communicating artery aneurysm
A painful 3rd nerve palsy is a flag for a posterior communicating artery aneurysm, as the aneurysm presses onto the Occulomotor nerve from above at the point shortly after it exits the midbrain causing pain and palsy.
Describe the motor innervation of the hand
The following muscles are innervated by the median nerve: The lateral 2 lumbricals Opponens policis Abductor pollicis brevis Flexor pollicis brevis
All other muscles of the hand are innervated by the ulnar nerve
A 42 year old man presents to his GP with altered sensation in his arm which he describes as “feeling like something wet’s on it”. This has been going on for the past 5 hours. His only past medical history is previous investigation for a self-resolving blurring of vision in his left eye 1 year ago which lasted for 3 days. The GP make a referral to see a specialist.
Which investigation will be most useful in confirming the likely diagnosis?
A. HLA B27 screening B. MRI brain and spinal cord C. Lumbar puncture D. B12 and folate E. Anti-AChR antibodies and TFTs
B. MRI brain and spinal cord
This is a presentation of multiple sclerosis: two neurological lesions distinct in time and place. The main investigation for MS is MRI to be carried out in a specialist setting. It is also important to carry out FBC, B12, folate, glucose, U&Es, and TFTs to rule out other causes. Lumbra puncture and other investigations may well also be carried out to lend weight to the diagnosis of MS and exclude other causes or concomitant illness.
A woman presents with a history of weakness in her left leg. On examination, left-sided hip flexion and knee extension is 3/5, but all other movement are 5/5. The neurologist who reviews the patient suspects a single nerve root compression.
Given the likely nerve root compressed, which of the following sensory deficits is most likely to be present?
A. Loss of sensation in the mid leg
B. Loss of sensation of the lateral thigh and leg
C. Loss of sensation of the medial thigh and leg
D. Loss of sensation in the mid thigh
E. Loss of sensation to the lateral border of the foot
D. Loss of sensation in the mid thigh
The loss of power in both hip flexion and knee extension implies compression of the L3 nerve root. The corresponding dermatome runs in a band from the lateral thigh near at the level of the crotch, diagonally down to the medial epicondyle of the femur, hence loss of sensation in the mid thigh is to be expected.
Hip extension - L4/L5 Hip flexion - L2/L3 Knee extension - L3/L4 Knee flexion - L5/S1 Ankle dorsiflexion - L4/L5 Ankle plantarflexion - S1/S2
NB: Anatomically speaking, the thigh is the upper leg, but the lower leg is just referred to as ‘the leg’
What percentage of strokes are haemorrhagic?
~15%
A 34 y/o male is involved in an RTC and sustains a C7 fracture which causes an acute cord compression. He is seen 1 hour after the collision in Resus.
Which of the following signs is most likely to be present?
A. Hyperreflexia B. Fasiculations C. Flaccid paralysis D. Clonus E. Wasting
C. Flaccid paralysis
This is an important point: it takes between a few days and a few weeks for spasticity to manifest after the injury in cord compression. In the early presentation there will be a flaccid paralysis. This is also true to a degree for strokes, some of which will present with spasticity, some will develop it after a few days/ weeks, and some will never develop it.
A 55 year old man visits his GP complaining of progressive clumsiness and unsteadiness when walking over the past couple of months. His neurology appointment is delayed, and by the time he sees the neurologist his symptoms have worsened. On examination he has increased tone in all 4 limbs, 5/5 power in all muscle groups, brisk reflexes, impaired proprioception, and paraesthesia and reduced sensation in his fingers and toes.
Which investigation is most appropriate in this case?
A. MRI of the whole spine B. EMG studies C. Fasting serum glucose D. CT spine E. A lumbar puncture
A. MRI of the whole spine
This is a history of gradual spinal cord compression, in which patients will commonly initially notice gait ataxia and a loss of fine motor control in the fingers. If allowed to progress, the patient will develop sensory deficits (including loss of proprioception) and signs of an upper motor neuron lesion.
