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PACES retrieval practice > Neurology > Flashcards

Neurology Flashcards

1
Q

What is internuclear ophthalmoplegia (INO)?

A

A disorder of conjugate lateral gaze in which the affected eye shows impairment of adduction.

When the patient looks contralateral to the affected eye, the affected eye will not adduct. The contralateral eye abducts, but with nystagmus.

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2
Q

List some causes of cerebellar syndrome.

A

Multiple sclerosis
Alcoholic cerebellar degeneration
Posterior fossa SOL
Brainstem vascular lesion
Inherited ataxias (Freidreich’s)
Paraneoplastic syndromes
Phenytoin / other drugs

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3
Q

How would you identify the site of a cerebellar lesion from clinical findings?

A

Cerebellum: divided into midline vermis and two cerebellar hemispheres.

Disease of the vermis: leads to truncal ataxia and ataxic gait.

Disease of a hemisphere: ipsilateral dysmetria, dysdiadochokinesis, intention tremor and fast-beat nystagmus towards the lesion.
MS can cause a global defecit.

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4
Q

What is Freidreich’s ataxia?

A

Autosomal recessive disorder, trinucleotide repeat.

Degeneration of the spinocerebellar tract, resulting in cerebellar signs.

Corticospinal tract damage and peripheral nerve degeneration lead to absent ankle jerks and extensor plantars.

Pes cavus, scoliosis and diabetes are common features. Other features include cardiomyopathy, sensorineural deafness and cataracts.

Will present in a neuro station as a younger patient.

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5
Q

What investigations would you initiate if you thought a patient was having a stroke?

A

Bedside: BP, ECG, 24-hour tape
Bloods: fasting blood glucose / cholesterol
Imaging: neuroimaging in form of CT or MRI, echocardiogram and carotid artery doppler

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6
Q

Management of stroke?

A
  1. Thrombolysis if presents within 4.5h of symptom onset, and SAH is excluded on CT brain first.
  2. High-dose aspirin for 2 weeks (300mg), followed by 75mg clopidogrel lifelong.
  3. NIH stroke scale to assess patient functionality at time of stroke and at regular intervals after.
  4. Secondary prevention: statin + PPI + BP control + BM control.
  5. SLT assessment, PT and OT input.
  6. Psychological and nutritional support.
  7. Measure progress with tools such as Modified Rankin Score to assess prognosis.
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7
Q

What extra investigations are merited in young patients presenting with a proven stroke?

A

Thrombophilia screen
Homocystine levels
Bubble echo (looking for patent foramen ovale)

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8
Q

Do you know of any alternative anticoagulants to warfarin in patients who have suffered a thrombotic stroke and have AF?

A

Factor 10a inhibitors such as apixaban and rivaroxaban.
Direct thrombin inhibitor such as dabigatran (D-D)

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9
Q

What is ‘lateral medullary syndrome’?

A

This is known as Wallenberg’s syndrome. It is caused by a brainstem stroke in the territory of the vertebral or posterior inferior cerebellar artery.

Clinical features - ‘crossed findings’
- Ipsilateral signs: horner’s syndrome, nystagmus, facial sensory impairment, ataxia and diplopia
- Contralateral signs: pain and temperature loss over opposite arm and trunk (spinothalamic tract)

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10
Q

Discuss the advantages and disadvantages of novel anticoagulant therapies versus warfarin.

A

Advantages: rapid onset of action (no need for bridging therapy). Fewer interactions with other meds / foods. Provided the patient is compliant, they are always in the therapeutic window (unlike warfarin). No need for repeated blood tests to monitor INR.

Disadvantages: not safe in renal failure - depends on eGFR

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11
Q

List some complications associated with myotonic dystrophy.

A

(top to toe)

Endocrine: increased risk of diabetes, thyroid dysfunction
Cataracts
Cardiac: dilated cardiomyopathy, arrhythmias
Respiratory: risk of aspiration from muscle weakness
GI: dysphagia, delayed gastric emptying
Reproductive: testicular atrophy

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12
Q

What is the genetic basis of myotonic dystrophy?

A

Autosomal dominant
Trinucleotide-repeat disorder showing genetic anticipation
Affects a gene based on chromosome 19

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13
Q

What problems are associated with general anaesthetic in myotonic dystrophy?

A

Sedatives and neuromuscular blocking drugs may lead to cardiorespiratory complications and delayed recovery from anaesthesia.

Depolarising neuromuscular blocking agents should be avoided (suxamethonium) as this can lead to induced myotonia.

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14
Q

What changes would be detected on EMG in myotonic dystrophy?

A

MD produces high-frequency activity that varies, producing a whining sound on the loudspeaker ‘dive-bomber’.

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15
Q

Describe what is meant by ‘anticipation’?

A

Anticipation is a phenomenon whereby as a genetic disorder is passed onto the next generation, the symptoms of the genetic disorder become more apparent at an earlier age with each generation.

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16
Q

What are the causes of an oculomotor (3rd) nerve palsy?

A

Surgical: these causes generally affect the pupil
- posterior communicating artery aneurysm
- SOL
- haemorrhage

Medical: these causes often do not affect the pupil
- causes of mononeuritis multiplex
- demyelination
- infarction

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17
Q

What are the causes of an abducens (6th) nerve palsy?

A

Causes of mononeuritis multiplex
Vascular lesion
Malignancy
Demyelination
Infection (Lyme, syphilis)
Raised ICP (false localising sign)
Wernicke’s encephalopathy (bilateral abducens nerve palsy)

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18
Q

What are the causes of a complex ophthalmoplegia?

A

Nerve lesions (demyelination, mononeuritis)
Neuromuscular junction: myasthenia gravis
Muscle: Graves’ disease
Mitochondrial disease

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19
Q

What are the causes of an internuclear ophthalmoplegia?

A

Multiple sclerosis
Vascular disease

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20
Q

Causes of Parkinsonism?

A

Parkinson’s disease
Drugs (neuroleptics)
Parkinson’s plus syndromes: PSP, multisystem atrophy
Stroke / SOL affecting basal ganglia
Wilson’s disease
Normal pressure hydrocephalus

21
Q

What are the characteristic features of Parkinson’s disease?

A

Triad of: BRR - bradykinesia, rest tremor, rigidity.
In PD, these features begin asymmetrically and generally affect ULs first.

There is fluctuation in severity, with some days being better than others.

Autonomic dysfunction, loss of postural reflexes and balance and changes in higher mental functioning are also common later on in the illness.

22
Q

What drugs other than L-dopa are used in the management of Parkinson’s disease?

A

Dopamine agonists (ropinirole) used as first-line therapy.
Anticholinergics: useful for tremor.
MAOIs (selegiline) helpful for motor symptoms.
COMT inhibitors (entacapone): helps to shorten the ‘off’ time associated with L-dopa.
Apomorphine: can help with ‘on-off’ effects (can be given via syringe driver).

23
Q

What is the pathology underlying Parkinson’s disease?

A

Degeneration of the substantia nigra dopaminergic neurones in the basal ganglia. The hallmark is the presence of Lewy bodies.

24
Q

Describe the potential problems patients need to be counselled about before starting dopamine agonists.

A

Impulse control disorders: hyper religiosity, gambling, hypersexuality, compulsive eating.

25
Q

What are the differential diagnoses of Parkinsonism?

A

Idiopathic PD
Dementia with Lewy Bodies
Vascular parkinsonism
Multisystem atrophy
Progressive supranuclear palsy
Drug-induced parkinsonism (amiodarone, valproate, metoclopramide)

26
Q

Causes of sensory neuropathy.

A

Diabetes
Alcohol
Vitamin B12 and B1 deficiency
Drugs (platinum-based chemo)
Uraemia

27
Q

Causes of motor neuropathy.

A

Guillain-Barre syndrome
Malignancy
Charcot-Marie-Tooth disease
Porphyria
Lead poisoning

28
Q

What is an autonomic neuropathy?

A

A neuropathy of the autonomic nervous system.
May present alone or in conjunction with a motor or sensory neuropathy. The most common cause is diabetes.
May present with postural hypotension, impotence, urinary retention, diarrhoea / constipation and Horner’s syndrome.

29
Q

What is Charcot-Marie-Tooth disease?

A

A hereditary sensory and motor neuropathy.
Usually starts at puberty with foot drop and weak legs.
The peroneal muscles are the first to atrophy, with UL symptoms appearing at a later stage.
There is muscle wasting, pes cavus and bilateral foot drop (high-stepping gait).
Reflexes absent, sensory loss is variable.
The most common form is autosomal dominant.

30
Q

Which drugs can cause a peripheral neuropathy?

A

Amiodarone
Gold
Isoniazid
Metronidazole
Nitrofurantoin
Phenytoin

31
Q

What is tabes dorsalis? Describe the gait associated with this.

A

Tabes dorsalis is a demyelinating condition affecting the nerves in the dorsal columns of the spinal cord.

These nerves help maintain proprioception, vibration and discriminative touch.

The gait is usually ‘high stepping’ due to loss of proprioception.

32
Q

What is the differential diagnosis of a foot drop?

A

Common peroneal nerve palsy
Peripheral neuropathy (CMT disease)
Sciatic nerve palsy L4/5
Radiculopathy from prolapsed disc
Lumbosacral plexopathy

33
Q

What are the causes of mononeuritis multiplex?

A

WARDS-PLC

Wegener’s granulomatosis
Amyloidosis
Rheumatoid arthritis
Diabetes
Sarcoidosis
Polyarteritis nodosa
Leprosy
Carcinomatosis

34
Q

What are the causes of wasting of the intrinsic muscles of the hand?

A

It will resemble an ulnar nerve lesion, but with thenar wasting and weakness too.

Causes include:
- Anterior horn cell disease (polio)
- Radiculopathy (trauma, slipped disc)
- Plexopathy
- Peripheral nerve lesion
- Muscle disuse atrophy

35
Q

What are the disease variants of motor neurone disease?

A

Amyotrophic lateral sclerosis: 50% of cases, combined UMN and LMN signs.

Primary lateral sclerosis: UMNs only, rare, can later progress to ALS.

Progressive muscular atrophy: 25% of cases, affects anterior horn cells only, signs in distal muscle groups.

Progressive bulbar palsy: 25% of cases, worst prognosis, speech / swallowing issues with increased aspiration risk.

36
Q

What is the prognosis for patients with MND?

A

No known cure, usually fatal within 3-5 years of diagnosis.
Cause of death is usually aspiration pneumonia or ventilatory failure.

37
Q

Differential diagnosis for MND?

A

Degenerative: cervical cord compression, cervical spondylosis.

Inflammatory / traumatic / inherited: syringomelia, spinal muscular atrophy.

Infectious: polio, syphilis.

Malignant or paraneoplastic.

38
Q

What are the causes of absent ankle jerks and extensor plantar reflexes?

A

HSSCC

Hereditary cerebellar ataxias (Freidreich’s, spinocerebellar)
Syphilitic taboparesis
Subacute combined degeneration of the spinal cord
Conus medullaris pathology
Combined pathologies (e.g., peripheral neuropathy with cervical spondylosis)

39
Q

What is multiple sclerosis?

A

MS is a chronic inflammatory demyelinating disease of the CNS. It is autoimmune.

The diagnosis depends on demonstrating at least 2 demyelinating lesions in the brain / spinal cord on MRI, disseminated in time and space.

40
Q

What are Lhermitte’s sign and Uthoff’s phenomenon?

A

Lhermitte’s sign: flexion of the neck causes an ‘electric shock’ down the trunk and limbs.

Uthoff’s phenomenon: increase in severity of symptoms (usually visual) is precipitated by an increase in temperature or by exercise.

41
Q

How is MS classified?

A

Relapsing-remitting: 85% of cases
Primary progressive: 15% of patients, progressive deterioration from the start
Secondary progressive: follows a period of relapsing-remitting

42
Q

What findings on examination would you expect for MS?

A

A combination of spastic paraparesis and cerebellar signs is likely evidence of MS.

43
Q

What malignancies are most likely to cause spinal cord compression?

A

Lung, breast or prostate cancer.
Multiple myeloma should be considered as a cause of MSCC.

44
Q

What is transverse myelitis?

A

Inflammation of the spinal cord characterised by axonal demyelination.
Symptoms come on over a period of hours to weeks.
The most common cause is MS. Viral and other infections can be implicated. Often, no cause is found.
Steroids and plasma exchange may be helpful in management. Neuro-rehab is crucial.

45
Q

What is the pathology in hereditary spastic paraparesis?

A

Axonal degeneration that is maximal in the terminal portions of the longest descending and ascending tracts.

Neuronal cell bodies of degenerating fibres are preserved, and there is no evidence of primary demyelination.

46
Q

What is important to look for when finding a spastic paraparesis?

A

You need to look for a spinal level.

47
Q

What are the causes of a homonymous hemianopia?

A

Vascular: stroke
Trauma
Tumour
Infection: encephalitis
MS

48
Q

What are the causes of an optic nerve lesion?

A

Trauma
Inflammatory: demyelination, optic neuritis
Compression: raised intraocular or ICP
Vascular: acute optic artery ischaemia
Metabolic: vitamin B12 deficiency, alcohol excess, diabetes
Inherited: Leber’s optic neuropathy

49
Q

What are the most common causes of a bitemporal hemianopia?

A

Usually occur due to a lesion of the optic chiasm.

  • Pituitary fossa tumour
  • Craniopharyngioma
  • Suprasellar meningioma

PACES retrieval practice (10 decks)

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