Neurology Flashcards

1
Q

What is a TACS, and what features must be present for diagnosis?

A

= a large cortical stroke affecting the areas of the brain suppled by both the middle & anterior cerebral artery territories.

  • All three of the following must be present for a TACS diagnosis:
    • Unilateral weakness (and/or sensory deficit) of the face, arm, and leg
    • Homonymous hemianopia
    • Higher cerebral dysfunction → dysphasia, visuospatial disorder.
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2
Q

What is a PACS & what must be present for a diagnosis?

A

= a less severe form of TACS, in which only part of the anterior circulation has been compromised.

  • Two of the following need to be present for a PACS diagnosis:
    • Unilateral weakness (and/or sensory deficit) of the face, arm, and leg
    • Homonymous hemianopia
    • Higher cerebral dysfunction → dysphasia, visuospatial disorder
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3
Q

What is a lacunar stroke (LACS) and what needs to be present for a diagnosis?

A

= a subcortical stroke that occurs secondary to small vessel disease. There is no loss of higher cerebral functions.

  • One of the following needs to be present for LACS diagnosis:
    • Pure sensory stroke
    • Pure motor stroke
    • Sensori-motor stroke
    • Ataxic hemiparesis
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4
Q

How does a stroke involving the Anterior Cerebral Artery present? What is the key feature?

A
  • Leg weakness is key !! Leg>arm/face weakness due to arrangement of the motor homunculus
  • Sensory weakness → less common
  • Motor aphasia → difficulty initiating speech, comprehension
  • Urinary incontinence
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5
Q

How does a stroke involving the Middle Cerebral Artery present? What is the key feature?

A
  • Face/upper limb weakness
    • Arm/Face > leg weakness
    • Expressive aphasia → if lesion is on the dominant hemisphere, typically the left, due to Broca’s area being on the dominant side.
    • Receptive aphasia → if lesion is on dominant hemisphere, due to Wernicke’s area being affected.
    • Contralateral hemineglect → if the lesion is on the non-dominant side
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6
Q

What antiplatelet therapy is giving to people following an ischaemic stroke? What preparation can these be given?

A

Aspirin 300mg for 2 weeks (or until discharge).
- Change to 75mg clopidogrel OD after 2 weeks or once discharged.
- Oral, rectal, via NG tube

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7
Q

When can a patient be thrombolysed in the event of a stroke?

A

Alteplase can be used within 4.5hrs of symptom onset & once a haemorrhagic stroke has been ruled out on CT.

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8
Q

What secondary prevention is given following an ischaemic stroke long term?

A
  • Clopidogrel 75mg OD
  • Atorvastatin 20-80mg (after 48hrs)
  • Blood pressure & diabetes control
  • Address modifiable risk factors → smoking, obesity, exercise
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9
Q

When is an endarterectomy done following an ischaemic stroke?

A

If there is >50% occlusion on the affected side, and it can be done within a week

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10
Q

How does an extradural haematoma present?

A
  • Often have immediate LOC, followed by period of lucidity, then a progressive decline in consciousness over the next few hours.
  • Headache
  • Nausea & vomiting
  • Confusion
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11
Q

How does an extradural haematoma appear on a CT scan?

A
  • Bi-Convex, lemon-shaped mass
  • Midline shift
  • Brainstem herniation
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12
Q

How does a subdural haematoma present?

A
  • Drowsiness or poor balance & graduate deterioration following head trauma
  • Headache
  • Nausea & vomiting
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13
Q

How does a subdural haematoma show on CT scan?

A
  • Crescent, banana-shaped mass
  • Acute SDH → hyperdense (bright white) appearance
  • Chronic SHD → hypodense (black/grey) appearance
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14
Q

How does a subarachnoid haemorrhage present?

A
  • Sudden onset, severe headache (thunderclap)
  • Nausea & vomiting
  • Photophobia
  • Kernig’s Sign → inability to extend the knee due to pain when the patient is supine & the hip & knee are flexed to 90 degrees
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15
Q

How does a subarachnoid haemorrhage show up on CT scan

A
  • Hyperdensity around the Circle of Willis
  • Hyperdensity in the subarachnoid space
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16
Q

What are the risk factors for idiopathic intracranial hypertension?

A
  • Obesity
  • Female
  • Medications → COCP, tetracyclines, retinoids, lithium
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17
Q

What are the signs & symptoms of Idiopathic Intracranial Hypertension?

A

Symptoms → Chronic & progressive:

  • Headache → non-specific, diffused, sometimes associated with nausea & vomiting. Typically worse in the morning or after bending forwards, or valsalva manoeuvres
  • Transient visual loss / blurring of vision → lasts <30 seconds
  • Pulsatile tinnitus → exacerbated by lying flat
  • Visual disturbance → photophobia, flashes, transient visual darkening or loss

Signs:

  • Bilateral papilloedema seen on fundoscopy
  • Peripheral visual field defects
  • Horizontal diplopia → due to a sixth nerve palsy in some cases
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18
Q

What is the key finding on lumbar puncture for Idiopathic Intracranial Hypertension?

A

elevated opening pressure >250mmH2O

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19
Q

How is Idiopathic Intracranial Hypertension managed?

A

Conservative Management:

  • Weight loss
  • Stop/change any medications which may be causing or worsening the IIH.

Medical Management:

  • Considered in those with Mild-Moderate symptoms.
  • Acetazolamide → carbonic anhydrase inhibitor which reduces the rate of CSF production
    • If not tolerated, then topiramate or furosemide can be used.
  • Serial lumbar punctures can be used short-term to preserve vision in patients with IIH awaiting a surgical procedure.

Surgical Management:

  • Essential for IIH patients with rapidly declining visual function or those who failed medical therapy.
  • CSF diversion procedures
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20
Q

What are the features of an essential tremor?

A
  • Fine tremor (6-12Hz)
  • Symmetrical
  • Most notable in hands, but can affect the head, jaw, voice, tongue, face, lower limbs
  • More prominent with voluntary movement
  • Worse when tired, stressed or after caffeine
  • Improved by alcohol
  • Absent during sleep
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21
Q

How can an essential tremor be medically managed?

A
  • Propranolol → first line, if patient is bothered by symptoms
  • Primidone
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22
Q

What is clinically/radiologically isolated syndrome?

A
  • Clinically IS = an otherwise unexplained clinical episode of neurologic dysfunction
  • Radiologically IS = evidence of white matter pathology on neuroimaging not attributable to any other pathology in the absence of clinical symptoms.
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23
Q

What are the 3 main patterns of MS?

A
  • Relapsing-Remitting MS
    • Most common form of disease at presentation
    • = unpredictable attacks of neurological dysfunction (>24hrs in absence of fever), followed by relief of symptoms, though patients may not return fully to baseline.
  • Secondary Progressive MS
    • Initially presents as relapsing-remitting, then later declines steadily & progressively without remission.
  • Primary Progressive MS
    • Steady, progressive worsening of disease severity from the onset without remission.
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24
Q

What is Lhermitte’s sign?

A

an electric shock sensation that travels down the spine & into the limbs when flexing the neck, indicating disease in the cervical spinal cord, caused by stretching the demyelinated dorsal column.

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25
Q

What are the two key investigations when diagnosing MS?

A
  • MRI brain & spinal cord with gadolinium contrast
    • MS lesions will be apparent as white matter plaques in T2.
    • Need to be disseminated in space & space
  • Oligoclonal bands in CSF & high protein content
    • Reflect various immunoglobulins seen on CSF electrophoresis
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26
Q

How is an acute episode of MS managed?

A
  • High-dose steroid therapy → methylprednisolone
  • Plasmapheresis → if exacerbation is refractory to steroids
  • Exclude any infections
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27
Q

What are the two first-line disease modifying therapies given in MS?

A

beta-inferon or glatiramer (injections)

28
Q

What are the core features of Parkinson’s Disease?

A
  • Bradykinesia → key symptom
    • Movements become slower & smaller
    • Examples
      • Handwriting gets smaller
      • Shuffling gait
      • Difficulty initiating movement
      • Reduced facial movements & expressions (hypomimia)
  • Rigidity
    • Resistance to passive movement of a joint
    • Cogwheel rigidity in the arms
  • Tremor
    • Worse on one side, 4-6 hertz, pill-rolling, worse when resting, improves with voluntary movement. Worse with distraction
  • Gait disturbance
    • Shuffling, reduced arm swing, freezing
29
Q

What are the types of generalised seizure?

A
  • Tonic-Clonic (unconscious, muscle tensing then jerking)
  • Myoclonic (conscious, sudden, brief muscle contractions)
  • Atonic (conscious, sudden loss in muscle tone)
  • Absence (brief vacant episodes, 10-20s
30
Q

What medication is given for generalised tonic-clonic seizures?

A

Men/eligible women -> sodium valproate
Women -> lamotrigine, levetiracetam

31
Q

What medication is given for focal seizures?

A

Lamotrigine or levetiracetam

32
Q

What medication is used for absence seizures?

A

Ethosuximide

33
Q

What medication is used for myoclonic seizures?

A

Men & Eligible women -> sodium valproate
Women -> levetiracetam

34
Q

How is status epilepticus managed?

A

Management:

  • A-E: secure the airway, give high-flow oxygen, check BMs, gain IV access
  • 1st line → benzodiazepine, repeat after 5-10 minutes if the seizure continues
  • 2nd line → IV levetiracetam, phenytoin, sodium valproate
  • 3rd line → general anaesthesia

Benzodiazepine Options:

  • Buccal midazolam (10mg)
  • Rectal diazepam (10mg)
  • IV lorazepam (4mg)
35
Q

What is Bell’s Palsy, and how does it present?

A

= idiopathic syndrome that presents as a lower motor neuron facial palsy.

Presentation:

  • Acute onset of unilateral LMN weakness → entire unilateral facial weakness
  • Mild-moderate postauricular otalgia, which may precede the paralysis.
  • Hyperacusis → disorder in loudness perception, overly sensitive to a range of sounds.
36
Q

How is Bell’s Palsy managed?

A
  • If patient presents within 72hrs of developing symptoms:
    • Prednisolone → 50mg for 10 days, or 60mg 5 days followed by a reducing regime.
  • Lubricating eye drops & tape eye closed at night.
37
Q

What is trigeminal neuralgia?

A

= chronic neuropathic pain, characterised by a sharp shooting sensation affecting the face in the distribution of the trigeminal nerve (CNV).

38
Q

How does trigeminal neuralgia present?

A
  • Unilateral, sharp facial pain → burning, shooting, stabbing
  • Triggers → talking, washing the face, shaving, brushing teeth, exposure to cold air
  • Ophthalmic symptoms occasionally → lacrimation, conjunctival redness, photophobia
39
Q

How is trigeminal neuralgia managed?

A

Medical:

  • Carbamazepine is first line
  • Other choices are phenytoin, lamotrigine, gabapentin

Surgical:

  • Decompression or ablation of nerve.
  • Microvascular decompression
  • Treat any underlying causes such as tumours.
40
Q

What are the features of Chronic Fatigue Syndrome?

A
  • Extreme fatigue, which is not significantly relieved by rest
  • Post-exertional malaise
  • Sleep disturbances → broken or shallow sleep, altered sleep pattern, feeling exhausted, flu-like & stiff on waking.
  • Cognitive impairment
41
Q

How do tension-headaches present?

A
  • Bilateral, non-pulsatile dull pain
  • Constant pressure, like having a tight band around the head.
  • Scalp muscle tenderness -> around the scalp, neck, or shoulder muscles on palpation
  • Triggers: stress, depression, alcohol, skipping meals, dehydration.
42
Q

How are tension headaches managed?

A
  • Reassurance
  • Simple analgesia
  • Stress management
  • Physio: massage or muscle relaxation exercises.
  • Amitriptyline for chronic or frequent tension headaches.
43
Q

What is cervical spondylosis? How does it present?

A

= age-related degeneration of the cervical spine, leading to pain & disability.
- Neck pain, made worse by movement
- Headaches
- Radiculopathy: due to compression of nerve roots, leading to flaccid upper limb paralysis.

44
Q

What are cluster headaches? How do they present?

A

= a primary headache disorder that presents with severe unilateral headaches associated with a number of autonomic symptoms.
- Severe, unilateral, intra or supra-orbitally. Patients need to rock or sway to distract themselves from the pain.
- Red, swollen, watering eye
- Miosis (pupil constriction)
- Ptosis
- Nasal discharge
- Facial sweating

45
Q

How are cluster headaches managed?

A

Prophylaxis -> verapamil 1st line, topirimate, lithium

Acute attack -> triptans (subcut or nasal), high-flow 100% oxygen

46
Q

How is an acute migraine managed?

A
  • NSAIDs
  • Paracetamol
  • Triptans -> avoid in patients with ischaemic heart disease, as triptans cause vasoconstriction.
  • Antiemetics

NB: opiates may make the condition worse.

47
Q

What prophylactic management is given for migraines?

A
  • avoid triggers
  • Propranolol - 1st line
  • amitriptyline
  • topiramate
48
Q

What is myasthenia gravis?

A

= an autoimmune condition affecting the neuromuscular junction (NMJ), causing muscle weakness that progressively worsens with activity & improves with rest.

49
Q

What is the pathophysiology of myasthenia gravis?

A
  • Acetylcholine receptor (AChR) antibodies are found in most patients with MG.
  • These antibodies bind to the postsynaptic ACh receptors, blocking them & preventing stimulation by ACh.
  • The more the receptors are used during muscle activity, the more blocked they become.
  • There is less effective stimulation of the muscle with increased muscle activity.
  • With rest, the receptors are cleared & the symptoms improve.
  • These antibodies also activate the complement system within the NMJ, leading to cell damage at the postsynaptic membrane, further worsening symptoms
50
Q

How does myasthenia gravis present?

A

Muscle weakness that worsens with use, improves with rest

  • Commonly proximal muscles of limbs & small muscles of head/neck.
  • Difficulty climbing stairs, standing from seat, raising hands above head
  • Diplopia → extraocular muscle weakness
  • Ptosis → eyelid weakness
  • Weakness in facial movements
  • Difficulty swallowing
  • Fatigue in jaw when chewing
  • Slurred speech
51
Q

What test can be performed when there is diagnostic uncertainty with myasthenia gravis? How is it performed?

A

Edrophonium Test:

  • Give IV edrophonium chloride (or neostigmine).
  • Normally cholinesterase enzymes in NMJ break down acetylcholine → edrophonium blocks these enzymes, reducing the breakdown of ACh.
  • Therefore ACh level rises at the NMJ, temporarily relieving the weakness.
  • A positive result suggests a diagnosis of MG.
52
Q

How is myasthenia gravis managed?

A
  • Pyridostigmine → cholinesterase inhibitor, prolongs action of ACh & improves symptoms
  • Immunosuppression → eg, prednisolone, azathioprine, suppresses the production of antibodies
  • Thymectomy → can improve symptoms, even in patients without a thymoma
  • Rituximab → monoclonal antibody against B cells
53
Q

What is a myasthenic crisis & how is it managed?

A

= A potentially life-threatening complication of MG

  • Causes an acute worsening of symptoms, often triggered by another illness, such as an URTI.
  • Respiratory muscle weakness can lead to respiratory failure → patients may require non-invasive ventilation or mechanical ventilation.
  • Treat with IV immunoglobulins & plasmapheresis
54
Q

What are the components of GCS?

A

Eye (4)
4 - spontaneous
3 - sound
2 - pressure
1 - no response

Verbal (5)
5 - orientated
4 - confused
3 - words
2 - sounds
1 - no response

Motor (6)
6 - obey commands
5 - localising to pressure
4 - normal flexion (withdraws to pain)
3 - abnormal flexion
2 - abnormal extension
1 - no response

55
Q

What is the most common cause of encephalitis?

A

HSV-1

56
Q

How is encephalitis managed?

A
  • 2g IV ceftriaxone BD
  • High dose IV acyclovir:
    • 10mg/kg TDS
    • Continue for 14 days then repeat LP
    • If HSV PCR negative, stop further treatment. If positive, then give a further 7 days and repeat LP.
57
Q

How does a brain abscess present?

A

Classic Triad:

  • Headache
  • Fever
  • Focal neurological signs

Other Presentations:

  • Nausea & vomiting
  • Meningism
  • Papilloedema
58
Q

How is a brain abscess managed?

A
  • Neurosurgical intervention for drainage
  • Empirical antibiotics → IV ceftriaxone & IV metronidazole
59
Q

At what vertebral level does spinal cord compression become referred to as cauda equina syndrome?

A

L3 onwards, as the spinal cord ends around L2

60
Q

How does spinal cord compression present?

A
  • Back pain → delayed diagnosis
    • Localised, gradually increasing, worse on straining, waking up from sleep.
  • Weakness (UMN pattern)
    • Hyper-reflexia, increased tone, muscle weakness.
    • Different to cauda equina syndrome which shows a LMN pattern
  • Sensory loss
  • Bladder & bowel dysfunction
    • Urinary retention
61
Q

How is spinal cord compression managed?

A
  • Immediate practical measures → lie flat, neutral spine alignment, analgesia, high dose steroids.
  • Palliative mostly → indicative of advanced metastatic cancer
  • Definitive → radiotherapy (symptom control), surgery (laminectomy), chemotherapy
62
Q

How does cauda equina syndrome present?

A

Symptoms:
- Severe back pain
- Bilateral sciatica
- Perianal anaesthesia
- Bowel & bladder dysfunction (urinary retention)
- Sexual dysfunction

Symptoms (LMN signs):
- Hypotonia
- bilateral or unilateral weakness
- areflexia
- abnormal sensory changes
- reduced anal sphincter tone/loss of anal squeeze

63
Q

How does an UMN lesion present?

A

An UMN lesion will be in the CNS (brain & spinal cord).

  • The CNS is involved in suppressing pathway activity → helps in the conscious inhibition of muscle
  • If we damage UMNs, there is a loss of inhibitory tone of muscles, leading to constant contraction.

On examination:

  • Minimal atrophy
  • Increased tone (spasticity/rigidity)
  • Ankle clonus
  • Pyramidal pattern of weakness → extensors weaker than flexors in arms, vice versa in legs
  • Hyper-reflexia
  • Upgoing plantars → babkinski sign
64
Q

How does a LMN lesion present?

A

An LMN lesion affects anywhere from the anterior horn cell to the muscle.

  • If LMNs are damaged/lost, there is nothing to tell the muscles to contract.

On examination:

  • Marked atrophy
  • Fasciculations
  • Reduced tone
  • Variable patterns of weakness
  • Reduced or absent reflexes
  • Downgoing plantars or absent response.
65
Q

What are the two most common times of MND?

A
  • Amyotrophic lateral sclerosis (ALS) → most common & well-known type of MND
  • Progressive bulbar palsy → second most common form, and primarily affects the muscles of talking & swallowing.
66
Q

How does MND present?

A

Typically manifests as a combination of upper & lower motor neuron signs.

  • If there are any sensory changes, an alternative diagnosis should be considered.

Symptoms:

  • Insidious, progressive weakness of the muscles throughout the body
    • Limbs, trunk, face, speech
    • Increased fatigue when exercising
  • Clumsiness, dropping things more often, tripping over
  • Slurred speech → dysarthria

Signs:

  • LMN disease
    • Muscle wasting
    • Reduced tone
    • Fasciculations
    • Reduced reflexes
  • UMN disease
    • Increased tone or spasticity
    • Brisk reflexes
    • Upgoing plantar reflex
67
Q

How is MND managed?

A

There are no effective treatments for halting or reversing the progression of MND.

Supportive:

  • MDT input
  • Symptom control → pain relief, baclofen for muscle spasticity, antimuscarinic for excessive saliva
  • Benzodiazepines → for breathlessness worsened by anxiety
  • Palliative care

Medical:

  • Non-invasive ventilation → to support breathing when the respiratory muscles weaken
  • Riluzole → can slow the progression of disease & extend life by an average of 3 months.