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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
Consultation - what are the symptoms of multiple sclerosis?
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.
21
What is multiple sclerosis?
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.
22
What examination features would you expect to see in multiple sclerosis?
Optic neuritis Numbness and paraesthesia Altered gait Increased tone Tremor Incontinence (catheter) Limb weakness
22
Given the findings of young patient, altered gait, paraesthesia, increased tone what is your preferred diagnosis and differentials?
Multiple sclerosis DDx: Hereditary spastic paraplegia Cerebral SLE Sarcoidosis AIDS
23
How would you manage a patient with multiple sclerosis?
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.
23
How would you investigate for multiple sclerosis?
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.
24
What are the complications of multiple sclerosis?
Fatigue Mobility problems Pain Visual problems Speech difficulties - dysarthria Spasticity and spasms Incontinence - urinary and faecal Cognitive losses Sexual dysfunction
25
What is the prognosis of multiple sclerosis?
Neurological disability gradually increases over time for most people with MS.
26
Consultation - what are the symptoms of myasthenia gravis?
Muscle fatigue after exercise Diplopia Weakness proximally
27
What examination features would you expect to see in myasthenia gravis?
Fatiguability e.g. on upward gaze or on flapping arms. Bilateral ptosis. Proximal weakness. Normal tone, sensation, and reflexes.
28
Given the findings of normal tone, reflexes, sensation but fatiguability and ptosis what is your preferred diagnosis and differentials?
Myasthenia gravis DDx: Myasthenic syndrome - Lambert-Eaton syndrome MS MND Myalgic encephalomyelitis (ME, chronic fatigue)
29
How would you investigate for myasthenia gravis?
AChR antibodies Thyroid function Serum MuSK antibody if AChR negative Electromyography MR brain Thymus CT or MRI
30
What is myasthenia gravis?
Disorder of neuromuscular transmission due to autoantibodies binding to NM junctions (mostly acetylcholine receptors) causing muscle weakness and fatiguability.
31
How would you manage a patient with myasthenia gravis?
MDT approach Symptomatic treatment with acetylcholinestase inhibition - pyridostigmine Steroids, azathioprine, thymectomy Crisis - immunoglobulins, plasma exchange, steroids, intensive care
31
What are the complications of myasthenia gravis?
Aspiration pneumonia Acute respiratory failure during an exacerbation Myasthenic crisis
32
What is the prognosis of myasthenia gravis?
Near-normal life expectancy with treatment.
33
Consultation - what are the symptoms of myotonic dystrophy?
Weakness - variable Myotonic - inability to relax muscles at will Heart failure symptoms Constipation Dysphagia
34
What examination features would you expect to see in myotonic dystrophy?
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
Given the findings of cataracts, myotonia, slurred speech, and long thin face with hollow templeswhat is your preferred diagnosis and differentials?
Myotonic dystrophy DDx: Myasthenia gravis Hereditary inclusion body myopathy Limb-girdle muscular dystrophy
36
What is myotonic dystrophy?
Muscular dystrophy affecting muscles with progressive muscle degeneration.
37
How would you investigate for myotonic dystrophy?
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
What are the complications of myotonic dystrophy?
Cataracts Arrhytmias Dysphagia with aspiration risk Respiratory muscle weakness
39
How would you manage a patient with myotonic dystrophy?
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
What is the prognosis of myotonic dystrophy?
Variable - worse if symptoms develop earlier. Many have normal life expectancy.
41
Consultation - what are the symptoms of Parkinson's disease?
Insidious onset of impaired dexterity, slowing down, gait disturbance.
42
What examination features would you expect to see in Parkinson's disease?
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
Given the findings of bradykinesia, resting tremor, postural instability, and cogwheeling rigidity what is your preferred diagnosis and differentials?
Parkinson's disease DDx: Drug-induced Parkinsonism benign essential tremor Huntington's disease Wilson's disease CJD Lewy body dementia
44
What is Parkinson's disease?
A movement disorder characterised by tremor at rest, rigidity, and bradykinesia. Due to lack of dopamine production by the substantia nigra.
45
How would you investigate for Parkinson's disease?
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
How would you manage a patient with Parkinson's disease?
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
What are the complications of Parkinson's disease?
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
What is the prognosis of Parkinson's disease?
Variable rate of progression, mortality increased when older 70+ years. 7 year survival if atypical Parkinsonism syndrome (aka Parkinsons plus)
49
Consultation - what are the symptoms of peripheral neuropathy?
Numbness Paraesthesia Altered gait with coordination problems Neuralgia Weakness
50
What examination features would you expect to see in peripheral neuropathy?
Peripheral weakness, muscle wasting, fasciculations, reduced tone, reduced/absent reflexes, reduced sensation.
51
How would you investigate for peripheral neuropathy?
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
Given the findings of hypotonia, hyporeflexia, and sensory loss to the knee what is your preferred diagnosis and differentials?
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
What is peripheral neuropathy?
Damage to the peripheral nerves.
53
How would you manage a patient with peripheral neuropathy?
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
What are the complications of peripheral neuropathy?
Foot ulcers Gait disturbance and falls
55
What is the prognosis of peripheral neuropathy?
Usually permanent, can progress but can improve sometimes. Depends on cause.
56
Consultation - what are the symptoms of post polio syndrome?
Generalised fatigue Joint and muscle pain Muscle weakness and atrophy
57
What examination features would you expect to see in post polio syndrome?
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
What is post polio syndrome?
Deterioration in function 15+ years after recovery from acute poliomyelitis.
59
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?
Post-polio syndrome DDx: MS MND Mysasthenia gravis Polymyalgia rheumatica
60
How would you investigate for post polio syndrome?
MRI spine Nerve conduction EMG
60
What are the complications of post polio syndrome?
Respiratory problems and sleep disorders
60
How would you manage a patient with post polio syndrome?
MDT approach - neurologist reviews, occupational therapists and physiotherapists, neuropsychologist Neuropathic pain - amitriptyline, pregabalin, gabapentin, duloxetine
61
What is the prognosis of post polio syndrome?
Progresses slowly with periods of stability lasting years between.
62
Consultation - what are the symptoms of spastic paraparesis?
Weakness Changed gait and falls Timing of onset of symptoms is important
63
What examination features would you expect to see in spastic paraparesis?
Increased tone Brisk reflexes Upgoing plantars Weakness Reduced sensations
64
How would you investigate for spastic paraparesis?
MRI whole spine - same day if acute Bloods - B12 and copper Genetic screening if hereditary
65
Given the findings of increased tone, hyperreflexia, upgoing plantars, weakness, reduced sensation what is your preferred diagnosis and differentials?
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
What is spastic paraparesis?
Group of disorder with UMN signs.
67
How would you manage a patient with spastic paraparesis?
Depends on cause MDT approach
68
What are the complications of spastic paraparesis?
Falls
69
What is the prognosis of spastic paraparesis?
Generally irreversible

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