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Neurology cases Flashcards

1
Q

Consultation - what are the symptoms of cerebellar syndrome?

A

Balance problems, gait disorders, incoordination.

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2
Q

What examination features would you expect to see in cerebellar syndrome?

A

Dysdiadochokinesia
Ataxia
Nystagmus
Intention tremor
Staccato speech
Hypotonia

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2
Q

Given the findings of truncal ataxia, scanning speech, hypotonia, preserved power, normal reflexes and sensation, dysdiadochokinesis what is your preferred diagnosis and differentials?

A

Cerebellar syndrome.
Causes for cerebellar syndrome would include (PASTRIES) paraneoplastic, alcohol, sclerosis, tumour, rare (Friedrich’s ataxia), iatrogenic (phenytoin), endocrine (hypothyroid), stroke.

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3
Q

What is cerebellar syndrome?

A

Dysfunction of cerebellum leading to DANISH signs.

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3
Q

How would you manage a patient with cerebellar syndrome?

A

Based on the underlying aetiology of the cerebellar syndrome.
MDT approach to retain function and independence - e.g. physio to help with mobility and preserve strength, occupational therapists for adaptations to home and mobility aids for independence.

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3
Q

How would you investigate for cerebellar syndrome?

A

MR imaging (better than CT for posterior fossa visualising).

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4
Q

What are the complications of cerebellar syndrome?

A

Falls, paralysis.

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4
Q

What is the prognosis of cerebellar syndrome?

A

Depends on cause, probs shortened.

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5
Q

Consultation - what are the symptoms of Charcot-Marie-Tooth?

A

Slow insidious onset of weakness at the feet and ankles usually by the age of 10 (CMT1)

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6
Q

What examination features would you expect to see in Charcot-Marie-Tooth?

A

Depressed/absent tendon reflexes
Weak foot dorsiflexion
Bilateral foot drop
Symmetrical atrophy of the muscles below the knee
Pes cavus
Atrophy of intrinsic hand muscles
Sensory loss distally

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7
Q

Given the findings of foot drop, pes cavus, distal muscle wasting, absent reflexes, reduced sensation what is your preferred diagnosis and differentials?

A

Charcot-Marie-Tooth
DDx:
Friedrich’s ataxia
Acquired peripheral neuropathies e.g. alcohol, B12 deficiency, hypothyroidism, diabetes
Vasculitis
Amyloidosis

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8
Q

What is Charcot-Marie-Tooth?

A

Heterogeneous group of inherited peripheral neuropathies that causes distal limb muscle wasting and sensory loss, with proximal progression over time.

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9
Q

How would you manage a patient with Charcot-Marie-Tooth?

A

MDT approach - rehabilitation, neurologist, geneticist, orthopaedic surgeon, physiotherapist and occupational therapist.

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9
Q

How would you investigate for Charcot-Marie-Tooth?

A

Exclude other causes of neuropathy - bloods including TFTs, vitamin B12 and folate; MRI brain and spinal cord, lumbar puncture.
Genetic studies.
Nerve conduction studies - low conduction velocities.
Can do nerve biopsies but rarely needed.

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10
Q

What are the complications of Charcot-Marie-Tooth?

A

Due to loss of sensation distally, risk of foot ulcers and cellulitis.
Ankle sprains and fractures.
Pregnancy - higher risk of complications during delivery.

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11
Q

What is the prognosis of Charcot-Marie-Tooth?

A

Usually normal remaining ambulatory throughout life but disease progresses with some disability.

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12
Q

Consultation - what are the symptoms of hereditary spastic paraplegia?

A

Lower limb weakness, spasms, stiffness.

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13
Q

What examination features would you expect to see in hereditary spastic paraplegia?

A

Increased tone
Brisk reflexes
Upgoing plantars
Weakness
Reduced sensation

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14
Q

Given the findings of increased tone, brisk reflexes, upgoing plantars, weakness, reduced sensation what is your preferred diagnosis and differentials?

A

Hereditary spastic paraplegia.
If acute - compressive pathology e.g. intravertebral disc herniation; or vascular e.g. spinal stroke
If subacute - inflammatory e.g. MS transverse myelitis; infective e.g. VZV
If chronic - metabolic e.g. vitamin B12 deifciency; tumour; neurodengerative e.g. primary lateral sclerosis.

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15
Q

What is hereditary spastic paraplegia?

A

Group of rare inherited disorders causing progressive weakness and stiffness in the lower limb.

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16
Q

How would you investigate for hereditary spastic paraplegia?

A

Bloods including viatmin B12 and copper
Most importantly - MRI whole spine
Genetic testing

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17
Q

How would you manage a patient with hereditary spastic paraplegia?

A

MDT approach - physiotherapy, occupational therapy, orthotics.
May need antispasmotics for pain or botulinum injections.
Surgery to release tendons or shortened muscles.

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18
Q

What are the complications of hereditary spastic paraplegia?

A

Shortening of calves.
Back/knee pain from gait disturbance.
Psychological burden - stress and depression.

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19
Q

What is the prognosis of hereditary spastic paraplegia?

A

Variable - mobility aids vary from mobility aids to wheelchairs.

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20
Q

Consultation - what are the symptoms of multiple sclerosis?

A

Neurological symptoms under the age of 50 with previous neurological symptoms.
Loss/reduction of vision in one eye with painful eye movements.
Double vision.
Ascending sensory disturbance and/or weakness.
Altered sensation or pain down the back and into limbs when bending neck forwards.
Progressive difficulties with balance and gait.

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21
Q

What is multiple sclerosis?

A

Acquired, chronic, immune-mediated, inflammatory condition of the central nervous system. The inflammatory process causes areas of demyelination, gliosis, and neuronal damage in the CNS.

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22
Q

What examination features would you expect to see in multiple sclerosis?

A

Optic neuritis
Numbness and paraesthesia
Altered gait
Increased tone
Tremor
Incontinence (catheter)
Limb weakness

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22
Q

Given the findings of young patient, altered gait, paraesthesia, increased tone what is your preferred diagnosis and differentials?

A

Multiple sclerosis
DDx:
Hereditary spastic paraplegia
Cerebral SLE
Sarcoidosis
AIDS

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23
Q

How would you manage a patient with multiple sclerosis?

A

Refer to neurology.
MDT approach - MS nurses, consultant neurologists, physiotherapists and occupational therapists, speech and language therapists, psychologists, dieticians, continence specialists.
DVLA - must notify but can continue to drive as long as able to safely control vehicle at all times.
Relapse - oral methylprednisolone 0.5g for 5 days or IV.
Disease-modifying therapy -(not to be used within 12 months of becoming pregnant) interferon beta and glatiramer acetate, alemtuzumab.
Secondary progressive - interferon beta.
Vitamin D replacement.
Symptomatic management - neuropathic pain, antispasmodics, continence nurse.

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23
Q

How would you investigate for multiple sclerosis?

A

Baseline bloods to help exclude differentials including FBC, inflammatory markers, TFT, glucose, HIV, B12.
Electrophysiology - demyelination with characteristic delays.
MRI brain and spine.
CSF fluid - raised proteins, increased immunoglobulin concentration and oligoclonal bands.
Diagnosis with McDonald criteria: 2+ relapses and either clinical evidence (MRI, oligoclonal bands) of 2+ lesions or 1 lesion + historical evidence of previous relapse.

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24
Q

What are the complications of multiple sclerosis?

A

Fatigue
Mobility problems
Pain
Visual problems
Speech difficulties - dysarthria
Spasticity and spasms
Incontinence - urinary and faecal
Cognitive losses
Sexual dysfunction

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25
Q

What is the prognosis of multiple sclerosis?

A

Neurological disability gradually increases over time for most people with MS.

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26
Q

Consultation - what are the symptoms of myasthenia gravis?

A

Muscle fatigue after exercise
Diplopia
Weakness proximally

27
Q

What examination features would you expect to see in myasthenia gravis?

A

Fatiguability e.g. on upward gaze or on flapping arms.
Bilateral ptosis.
Proximal weakness.
Normal tone, sensation, and reflexes.

28
Q

Given the findings of normal tone, reflexes, sensation but fatiguability and ptosis what is your preferred diagnosis and differentials?

A

Myasthenia gravis
DDx:
Myasthenic syndrome - Lambert-Eaton syndrome
MS
MND
Myalgic encephalomyelitis (ME, chronic fatigue)

29
Q

How would you investigate for myasthenia gravis?

A

AChR antibodies
Thyroid function
Serum MuSK antibody if AChR negative
Electromyography
MR brain
Thymus CT or MRI

30
Q

What is myasthenia gravis?

A

Disorder of neuromuscular transmission due to autoantibodies binding to NM junctions (mostly acetylcholine receptors) causing muscle weakness and fatiguability.

31
Q

How would you manage a patient with myasthenia gravis?

A

MDT approach
Symptomatic treatment with acetylcholinestase inhibition - pyridostigmine
Steroids, azathioprine, thymectomy
Crisis - immunoglobulins, plasma exchange, steroids, intensive care

31
Q

What are the complications of myasthenia gravis?

A

Aspiration pneumonia
Acute respiratory failure during an exacerbation
Myasthenic crisis

32
Q

What is the prognosis of myasthenia gravis?

A

Near-normal life expectancy with treatment.

33
Q

Consultation - what are the symptoms of myotonic dystrophy?

A

Weakness - variable
Myotonic - inability to relax muscles at will
Heart failure symptoms
Constipation
Dysphagia

34
Q

What examination features would you expect to see in myotonic dystrophy?

A

Inability to relax muscles at will e.g. release a clenched fist.
Weakness.
Arrhythmias, heart failure.
Cataracts.
Myotonic face - long face with hollow temples, early balding.

35
Q

Given the findings of cataracts, myotonia, slurred speech, and long thin face with hollow templeswhat is your preferred diagnosis and differentials?

A

Myotonic dystrophy
DDx:
Myasthenia gravis
Hereditary inclusion body myopathy
Limb-girdle muscular dystrophy

36
Q

What is myotonic dystrophy?

A

Muscular dystrophy affecting muscles with progressive muscle degeneration.

37
Q

How would you investigate for myotonic dystrophy?

A

Genetic test - CTG repeats in DMPK gene.
Electromyogram.
Slit lamp examination for posterior subcapsular cataracrts.
ECG for arrhythmias.
Muscle biopsy - rarely needed.
MRI brain.

38
Q

What are the complications of myotonic dystrophy?

A

Cataracts
Arrhytmias
Dysphagia with aspiration risk
Respiratory muscle weakness

39
Q

How would you manage a patient with myotonic dystrophy?

A

MDT approach - neurology consultant, specialist nurses, geneticists, chest physiotherapists for cough assist, physiotherapy and occupational therapy.
Avoid general anaesthetics.
OSA management.
Modafinil for daytime somnolence.
Pacemaker/ICD for various arrhythmias.

40
Q

What is the prognosis of myotonic dystrophy?

A

Variable - worse if symptoms develop earlier. Many have normal life expectancy.

41
Q

Consultation - what are the symptoms of Parkinson’s disease?

A

Insidious onset of impaired dexterity, slowing down, gait disturbance.

42
Q

What examination features would you expect to see in Parkinson’s disease?

A

Bradykinesia (slow to initiate voluntary movement with progressive reduction in speed and amplitude of repetitive actions) plus muscular rigidity or 4-6Hz resting tremor or postural instability.
Unilateral onset, rest tremor, progressive disorder, persistent asymmetry affecting the side of onset most, good response to L-dopa, hyposmia, visual hallucinations.

43
Q

Given the findings of bradykinesia, resting tremor, postural instability, and cogwheeling rigidity what is your preferred diagnosis and differentials?

A

Parkinson’s disease
DDx:
Drug-induced Parkinsonism
benign essential tremor
Huntington’s disease
Wilson’s disease
CJD
Lewy body dementia

44
Q

What is Parkinson’s disease?

A

A movement disorder characterised by tremor at rest, rigidity, and bradykinesia. Due to lack of dopamine production by the substantia nigra.

45
Q

How would you investigate for Parkinson’s disease?

A

Clinical diagnosis but can investigate with:
CT or MRI brain if not responding to L-dopa/to rule out rarer causes
SPECT if ?IPD vs ?essential tremor.

46
Q

How would you manage a patient with Parkinson’s disease?

A

Referral to specialist for diagnosis.
MDT approach - specialist consultants, specialist nurses, physiotherapists and occupational therapists, SALT if applicable, dieticians.
DVLA - need to be informed.
Initial drug treatment - levodopa if motor symptoms, dopamine agonists (ropinirole) if motor symptoms not significant, MAO-BIs (selegiline).
Needs escalating with time due to wearing off phenomenon and on-off fluctuations.

47
Q

What are the complications of Parkinson’s disease?

A

Dementia - 20-40%
Depression - 45%
Autonomic dysfunction.
Progressive supranuclear palsy (paresis of conjugate gaze with problems looking up and down).
Multiple system atrophy (cerebellar symptoms and autonomic ones at presentation).

48
Q

What is the prognosis of Parkinson’s disease?

A

Variable rate of progression, mortality increased when older 70+ years.
7 year survival if atypical Parkinsonism syndrome (aka Parkinsons plus)

49
Q

Consultation - what are the symptoms of peripheral neuropathy?

A

Numbness
Paraesthesia
Altered gait with coordination problems
Neuralgia
Weakness

50
Q

What examination features would you expect to see in peripheral neuropathy?

A

Peripheral weakness, muscle wasting, fasciculations, reduced tone, reduced/absent reflexes, reduced sensation.

51
Q

How would you investigate for peripheral neuropathy?

A

Bedside for diabetes - fundoscopy for diabetic retinopathy, urinalysis for glucose, blood glucose measurement
Bloods - FBC, U+Es, LFTs, thyroid, B12, ESR for inflammatory causes, immunoglobulins and electrophoresis, Hb1Ac
Nerve conduction studies and EMG

51
Q

Given the findings of hypotonia, hyporeflexia, and sensory loss to the knee what is your preferred diagnosis and differentials?

A

Peripheral neuropathy, causes for this include:
Diabetes
Metabolic - thyroid disease, uraemia, B12 deficiency
Toxic - chemotherapy, antibiotics
Inflammatory - chronic inflammatory demyelinating polyneuropathy, sarcoidosis, vasculitis, rheumatoid arthritis
Paraneoplastic - lung cancer

52
Q

What is peripheral neuropathy?

A

Damage to the peripheral nerves.

53
Q

How would you manage a patient with peripheral neuropathy?

A

MDT approach - physiotherapy and occupational therapy, specialist nurse if diabetic, orthotics and podiatry for foot care.
Manage the underlying cause e.g. if diabetes tight glycaemic control.

54
Q

What are the complications of peripheral neuropathy?

A

Foot ulcers
Gait disturbance and falls

55
Q

What is the prognosis of peripheral neuropathy?

A

Usually permanent, can progress but can improve sometimes. Depends on cause.

56
Q

Consultation - what are the symptoms of post polio syndrome?

A

Generalised fatigue
Joint and muscle pain
Muscle weakness and atrophy

57
Q

What examination features would you expect to see in post polio syndrome?

A

Walking aids and splints
Multiple scars from prior surgeries
Leg length discrepancy with wasting on shorter leg, reduced power, hypotonia and hyporeflexia
Normal sensation
Pes cavus

58
Q

What is post polio syndrome?

A

Deterioration in function 15+ years after recovery from acute poliomyelitis.

59
Q

Given the findings of leg length discrepancy with hypotonia/reduced power/hyporeflexia in affected limb with normal sensation what is your preferred diagnosis and differentials?

A

Post-polio syndrome
DDx:
MS
MND
Mysasthenia gravis
Polymyalgia rheumatica

60
Q

How would you investigate for post polio syndrome?

A

MRI spine
Nerve conduction
EMG

60
Q

What are the complications of post polio syndrome?

A

Respiratory problems and sleep disorders

60
Q

How would you manage a patient with post polio syndrome?

A

MDT approach - neurologist reviews, occupational therapists and physiotherapists, neuropsychologist
Neuropathic pain - amitriptyline, pregabalin, gabapentin, duloxetine

61
Q

What is the prognosis of post polio syndrome?

A

Progresses slowly with periods of stability lasting years between.

62
Q

Consultation - what are the symptoms of spastic paraparesis?

A

Weakness
Changed gait and falls
Timing of onset of symptoms is important

63
Q

What examination features would you expect to see in spastic paraparesis?

A

Increased tone
Brisk reflexes
Upgoing plantars
Weakness
Reduced sensations

64
Q

How would you investigate for spastic paraparesis?

A

MRI whole spine - same day if acute
Bloods - B12 and copper
Genetic screening if hereditary

65
Q

Given the findings of increased tone, hyperreflexia, upgoing plantars, weakness, reduced sensation what is your preferred diagnosis and differentials?

A

Spastic paraparesis with various causes:
Acute - compressive (disc herniation), vascular (spinal stroke)
Days - inflammatory (MS, transverse myelitis), infective (VZV)
Longer - metabolic (B12 deficiency), slow growing tumour, neurodegenerative like primary lateral sclerosis
Family history - hereditary

66
Q

What is spastic paraparesis?

A

Group of disorder with UMN signs.

67
Q

How would you manage a patient with spastic paraparesis?

A

Depends on cause
MDT approach

68
Q

What are the complications of spastic paraparesis?

A

Falls

69
Q

What is the prognosis of spastic paraparesis?

A

Generally irreversible

0 PACES top cases (7 decks)

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