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Neurology 3A > Specific Diseases of CNS > Flashcards

Specific Diseases of CNS Flashcards

1
Q

Multiple Sclerosis

A

Inflammatory, autoimmune disease involving demylination of oligodendrites and neurones in the CNS creating plaques. Mediated by T cells. Cell loss, gliosis and demyelination.

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2
Q

Types of multiple sclerosis

A

Relapsing-remitting - periods of exaceration then recovery.
Secondary progressive - initial RRMS but disease progresses to no remission periods.
Primary progressive - Never any remission, constant deterioration.

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3
Q

Pathophysiology of MS

A

T cell mediated demylination. Poor recovery leads to neuronal loss, scarring (plaques).

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4
Q

Risk factors for MS

A 
Genetic
Epstein-barr virus (trigger?)
Female
Smoking
Low vit D
Adolescent obestity
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5
Q

Complications of MS

A 
Fatigue
Spasicity (stiffness + muscle spasm)
Ataxia
Incontinence
Sexual dysfunction
Tremor
Visual impairments (optic neuritis, diplopia)
Pain
Poor mobility
Poor mental health
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6
Q

Differential diagnosis of MS presentation

A

Neuromyelitis optica (worse mortality than MS)
SLE
Sarcoidosis
Lyme disease
Vitamin B12 deficiency
Behcet’s syndrome (+oral and genital ulcers, and uveitis)
Neurosyphilis

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7
Q

Uhthoff’s phenomenon

A

Heat and exercise potentiate ON/MS symptoms (with hot food or in a hot bath vision can decrease)

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8
Q

Optic neuritis symptoms

A

Partial or total unilateral visual loss
Pain behind the eye, particularly on eye movement
Decrease in acuity of eyesight.
‘Washed-out’ colours
Rarely Argyle Robertson type pupil (lesion near edinger-westphal nucleus)

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9
Q

S+S of MS

A

Females between 20 and 30 years
Symmetrical or asymmetrical possible.

Symptoms:
Optic neuritis
Paraesthesia
Weird walking
Urinary urgency/frequency/retention
Constipation
Swallowing problems

Signs:
Weakness
Lhermitte’s sign -neck flexion causes shocking pain through trunk.
Brainstem/Cerebellar - ataxia, diplopia, dysarthria, dysphagia

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10
Q

Diagnosis and investigations for MS

A

Ix = FBC, CRP/ESR, LFT, renal function, HbA1c, TFT, Vit B12, calcium. LP for CSF electrophoresis, CNS MRI, evoked potential test.

MacDonald’s Criteria.

  • 2 episodes of a relapse disseminated in time and space lasting greater than 1hr. MRI scan lesion evidence.
  • Delayed evoked potentials
  • Lumbar puncture CNS has oligocloncal bands of IgG in CSF on electrophoresis.
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11
Q

Treatment of an acute relapse

A

Methylprednisolone to shorten duration.

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12
Q

Long-term treatment and management of MS

A

Interferons 1beta and 1alpha or monoclonal antibodies (Alemtuzumab) to reduce relapse occurrence.
Manage complications e.g. Baclofen for spasticity, self-catheterisation.
Stress-free life
Stop smoking
Regular exercise
Sign post to information to patient and carer.

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13
Q

Ramsay Hunt Syndrome

A

Varicella zoster virus/Herpes simplex 3 reactivated in geniculate ganglion of 7th cranial nerve (facial).
Auricular pain is often the first feature
Ipsilateral facial nerve palsy, forehead NOT spared.
Vesicular rash around the ear/pinna
Vertigo and tinnitus
RX = prednisolone + acyclovir.

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14
Q

Carotid artery stenosis

A

Bruit
Carotid Doppler
Cause anterior circulation stroke
Treat with carotid endarterectomy

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15
Q

Horner’s syndrome

A 
Constricted pupil (miosis), drooping of the upper eyelid (ptosis), absence of sweating of the face (anhidrosis).
Caused by lateral medullary syndrome (from a stroke in posterior inferior cerebral artery), Pancoast tumour in chest, carotid artery dissection.
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16
Q

Pathogenesis of Parkinson’s disease

A

Chronic, progressive neurodegeneration of dopamine-containing cells in the substantia nigra in basal ganglia. Parkinson’s disease becomes apparent at 50% loss neurones.
Lewy bodies present in remaining neurons.
Effects nigro-striatal pathway signalling.

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17
Q

Cause of Parkinson’s

A

Genetic predisposition and environmental factors.

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18
Q

Motor clinical features of Parkinson’s disease

A

Tremor - pill-rolling
Rigidity - cog-wheel in combo with tremor or lead-pipe
Bradykinesia - reduced blinking, swallowing difficulty, difficulty in initiating movements (start hesitation), micrographic handwriting, mask-like expression, drooling, stiff shuffling gait, reduced asymmetrical arm swing, stooped posture, freeze on turning.

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19
Q

Non motor features of Parkinson’s

A 
Constipation
Urinary difficulties
Depression
Dementia
Pressure sores
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20
Q

Management of Parkinson’s

A

MDT
NICE recommends not to start drug until diagnosis confirmed by a specialist.
Vit D supplements
NOTIFY DVLA

L-dopa  + dopa-decarboxylase inhibitor.
Dopamine agonist (Ropinirole)
oral monoamine oxidase B inhibitor
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21
Q

L-dopa

A

+ dopa-decarboxylase inhibitor to prevent peripheral dopamine decarboxylation. Co-carelopa.
Improve motor symptoms but so much tremor and non-motor symptoms.
Efficacy reduces with time (end-of-dose) but up the dose, increase SE. Also get on and off periods of effect.
SE = IMPULSIVITY!! visual hallucinations, drowsy, painful dystonia, nausea and vomiting.

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22
Q

Oral monamine oxidase B inhibitors

A

Selegiline.
Early PD
SE = postural hypotension, AF.

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23
Q

oral dopamine agonists

A

Ropinirole
Delay use of L-dopa so efficacious for longer.
Less effective at improving motor symptoms.
Can get transdermal patches.

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24
Q

Causes of parkinsonism

A 
Lewy body dementia
Wilson's disease
HIV
Repeated head injury (boxers)
Huntington's disease
First generation antipsychotics
Antiemetics
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25
Q

Myasthenia Gravis pathophysiology

A

Autoimmune disease where B cells and T cells target the nicotinic acetylcholine receptor reducing the number of working post-synaptic Ach receptors.

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26
Q

Epidemiology of Myasthenia Gravis and its associated disease

A

Women aged 20-35, more likely to have thymus hyperplasia.

Older men over 60 who are more likely to have thymus atrophy to thymoma tumour.

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27
Q

Differential diagnosis of dysphasia

A 
Stroke.
Bulbar palsy
Pseudobulbar palsy
Myasthenia Gravis
Oesophageal cancer
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28
Q

Clinical features of myasthenia gravis

A

Fatiguability on repeated use of muscles.
Speech and swallow bulbar symptoms common in elderly.
Ocular - ptosis, diplopia
Cranial Nerve - Dysarthria, dysphasia, dysphagia, face and jaw weakness. Causes poor chewing, jaw open when chewing, head drop.
Muscle groups affected - face, trunk, limbs.
Difficulty getting out of chair, SOB when lying down.
Normal reflexes but fatigue on repeated testing.

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29
Q

Exacerbating factors for symptoms of myasthenia gravis

A

Beta-blockers, quinine, opiates, exercise, infection, hypokalaemia, pregnancy, change in climate.

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30
Q

Investigations for myasthenia gravis

A

Tensilon test.
Serum anti-acetylcholine receptor antibodies, serum anti-muscle-specific kinase antibodies.
Thyroid CT and thyroid function test.
Neurophysiology testing - repetitive nerve stimulation gives decreases response.

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31
Q

Management of myasthenia gravis

A

Pyridostigmine - anti-cholinesterase helps control symptoms.
2nd line = prednisolone to help relapses and control symptoms. Give bone density protection.
Consider thymectomy.
Ensure no medications are potentiating the disease.

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32
Q

Complications of myasthenia gravis

A

1) Myasthenia crisis - weakness of respiratory muscles. Life-threatening emergency!!!!!! Immunoglobulins (IV Ig), plasmapheresis and steroids (prednisolone).
2) Cholinergic crisis - too much medication. Muscle fasciculation, pallor, sweating, hypersalivation and small pupils, bradycardia. Rapidly decrease meds.

33
Q

Lambert-Eaton myasthenia syndrome

A

Occurs as autoimmune disease target presynaptic calcium channels or in paraneoplastic small cell lung cancer. No acetylcholine release. Weak proximal muscles = unsteady gait. Autonomic symptoms (constipation, dry mouth). Weakness improves on exercise. Hyporeflexia.

34
Q

Bell’s palsy and treatment

A

Acute, unilateral facial nerve paralysis where the cause is unknown (diagnosis of exclusion).
∆∆ for CN7 palsy but in Bell’s pt can not raise their eye brows as not forehead sparing.
Rx = Prednisolone within 72hrs of onset, lubricate eyes with drops,

35
Q

Causes of facial nerve/CN7 palsy

A 
Ramsay-Hunt syndrome + HSV3.
Lyme disease
Meningitis
Stroke
Tumour
Multiple sclerosis
Gullian-barre syndrome
Parotid gland tumours
36
Q

Symptoms of facial nerve/CN7 palsy

A 
Facial weakness - Unilateral sagging of mouth, saliva drooling, speech difficulty.
Numbness or pain around ear.
Decrease taste
Hypersensitivity to sounds
Forehead sparing - can raise eye browns
37
Q

Bulbar palsy

A

Impairment in nuclei of cranial nerves 9-12 in medulla. Gives lower motor neuron signs in the tongue. Tongue fasciculation, flaccid tongue, quiet, nasal or hoarse voice. Caused by Guillian-barre syndrome, myasthenia gravis, motor neurone disease, brainstem tumour, polio.

38
Q

Pseudobulbar palsy

A

UMN signs due to UMN lesion in muscles of mastication and talking. Slow tongue movements, increase jaw jerk, increase palatal reflex, mood incongruent crying.

39
Q

Example of mononeuropathy and polyneuropathy

A 
Mononeuropathy = Carpal tunnel syndrome (median nerve compression)
Polyneuropathy = Guillian-Barre syndrome (demyelinating polyradiculoneuropathy)
40
Q

Carpel tunnel syndrome associated diseases, clinical features, investigations and management.

A

MEDIAN NERVE COMPRESSION
Associated disease = hypothyroidism, DM, pregnancy, acromegaly, rheumatoid arthritis.
Presentation = Tingling, pain and numbness in lateral 3+1/2 fingers (thumb, index finger, middle finger, and radial half of the ring finger) and palm, can extend up arm.
Wakes patient at night.
Weakness in thenar muscles.
Relieved on shaking arm.
Tinnel’s test (tap on nerve/wrist) & Phalen’s test (flex wrist).
Ix = nerve conduction studies.
Rx = splints, corticosteroid injections, decompression surgery.

41
Q

Guillian-Barre syndrome pathogenesis

A

Post-infection inflammatory, demyelination and axonal loss polyneuropathy.
Commonly post URTI or gastroenteritis of viral cause.

42
Q

Clinical features of Guillian barre syndrome

A

SYMMETRICAL, occuring less than 6 weeks after infection
Ascending weakness and paraesthesia starting in lower limbs
Areflexia of lower limbs
Neuropathic pain in BACK and legs.
Autonomic dysfunction = sweating, tachycardia, hypertension.
Sensory changes may not occur.
Facial weakness = dysarthria and dysphasia.
Death via respiratory muscle weakness.
Apyrexial at presentation.

43
Q

Investigations for gullian barre syndrome

A 
Nerve conduction studies = EMG, slow conduction due to demylination.
Lumbar puncture = high protein in CSF.
Spirometry and FVC.
Antiganglioside autoantidbody,
LFT
44
Q

Treatment of Guillian barre syndrome

A

IV immunoglobulins.
Plasma exchange.
Good prognosis for recovery but may have incomplete with relapsing and remitting disease.

45
Q

Sciatica

A

Compression of lumboscaral nerve roots emerging from spinal canal. Most commonly due to herniated intervertebral disc.
Pain, tingling, and numbness felt in the distribution of the nerve root (dermatome). May be accompanying motor weakness in a corresponding myotomal distribution.

46
Q

Cauda equina syndrome red flags

A

Severe lower back pain.
Weakness, sensory loss and pain commonly bilaterally.
Difficulty in micturition or incontinence.
Saddle paraesthesia
Loss of sensation of rectal fullness (faecal incontinence)
Laxity in anal sphincter
Areflexia of lower limbs.

MRI MRI MRI MRI and urgent neurosurgery.

47
Q

Dementia, apraxia, urinary incontinence + history of subarachnoid haemorrhage =

A

normal pressure hydrocephalus

48
Q

Signs of demyelination or axonal damage on electromyography

A 
Demyelination (in conditions such as MS and GBS) = increased latency, decrease velocity, conduction block.
Axonal damage (in conditions such as VitB12 def and alcohol) = lower amplitude with no change in velocity.
49
Q

Difference between Electroencephalogram and electromyography

A 
EEG = CNS activity recorder.
EMG = peripheral nerve function from anterior horn and below.
50
Q

CV causes of dizziness

A

Postural HTN, dehydration, haemorrhage, tachycardia, arrthymia, anaemia, vasodilation = anxiety, pain, shock (carbamazepine OD, infective shock)

51
Q

Mononeuritis multiplex

A

2 or more peripheral nerves affected by a neuropathy. Subacute presentation. Causes are often systemic: Rheumatoid, DM, Sarcoidosis, leprosy, AIDS

52
Q

Tensilon test

A

Inject edrophonium = transient improvement in muscle function
Can be used to test for a myasthenic crisis from a cholinergic crisis.

53
Q

Features of a third nerve palsy

A

Eye is deviated ‘down and out’
Ptosis
Dilated pupil, if not dilated think PICA stroke!
Eye affected = same side as lesion

54
Q

Ataxic gait

A

Cerebellar disease
Wide based
Loss of heel-toe pattern
increased foot rotation angles.

55
Q

Motor neuron disease pathophys

A

Loss of neurones in the motor cortex, cranial nerve nuclei and anterior horn cells.
Leads to upper and lower motor neuron signs but no sensory loss, eye movement pathology or sphincter disturbance.

56
Q

4 clinical patterns of motor neuron disease

A

Amyotrophic lateral sclerosis
Progressive bulbar palsy
Progressive muscular atrophy
Primary lateral sclerosis.

57
Q

Amyotrophic lateral sclerosis.

A 
Ax = Most common MND. Degeneration of neurones in motor cortex and anterior horn cells. 
CFx = LMN and UMN signs. Stumbling, spastic gait. Foot drop. Weak grip, can't open jars. Aspiration pneumonia.
Dx = El Escorial diagnostic criteria of LMN and UMN signs + EMG results. Exclude other causes with MRI, LP.
Rx = MDT, Riluzole can help with spasticity, BiPAP, supportive and palliative care, carer support.
58
Q

UMN signs

A 
Upgoing plantars/positive Babinski sign.
Muscle weakness
Spasticity 
Hyperreflexia +/- clonus
No muscle wasting
Hypertonia
59
Q

LMN signs

A 
Muscle wasting
Fasciculations
Hypotonia
Hyporeflexia
Flaccidity
60
Q

Split hand sign

A

Seen in ALS

Excessive wasting of muscles around the thumb

61
Q

Factors which make ALS diagnosis worse

A

Older
Bulbar area onset symptoms
Low FVC

62
Q

Diagnosis of amyotrophic lateral sclerosis

A

El Escorial Criteria

63
Q

El Escorial criteria definite ASL

A

LMN and UMN signs in 3 regions

64
Q

Sudden withdrawal of L-dopa

A

Neuroleptic malignant syndrome.

65
Q

Sciatic nerve

A

Roots of L4-S3.

2 branches = tibial and common fibular nerve.

66
Q

Causes of caudal equina

A 
Spinal trauma
Spinal infection or epidural abscess
Birth abnormalities e.g. spina bifida
Tumour - boney mets, lymphomas.
Post lumbar spine operation haematoma
67
Q

What disease is associated with giant cell arthritis and what would the patient complain of

A

Polymyalgia rheumatica. Female patients!
GCA = granulomatous vasculitis, jaw claudication diplopia, headache.
PMR = pain and morning stiffness of neck, shoulder, pelvis. Difficulty rising from seat, joint pain, muscle tenderness.

68
Q

Inheritance of Huntington’s disease

A

Autosomal dominant

Increase in CAG triplet repeats on Huntingtin gene Chr4.

69
Q

What is anticipation in relation to Huntington’s disease?

A

Greater number of CAG repeats.
Earlier age of presentation.
Increased severity of the disease.

70
Q

Presentation of Huntington’s disease

A
  • Start to present around 30-50yrs.
  • Psychotic and behavioural abnormalities, self-neglect, apathy.
  • Clumsiness and fidgeting and eventually chorea.
  • Parkinsonism and dystonia
  • Eye movement disorders, dysphagia, dysarthria.
  • Dementia and cognitive impairment.
71
Q

Ix and Rx for Huntington’s

A

Ix: Head CT (caudate atrophy), Genetic testing.
Rx: MDT, psychological support for pt and family, SALT, Benzos for chorea, levodopa for Parkinsonism, advice on advanced directive/legal power of attorney.

72
Q

Area of brain affected by Huntington’s

A

Putamen and caudate nucleus (aka the striatum)

73
Q

Whats the Gower test for

A

Muscular dystrophy. +ve indicated proximal muscle weakness. Children crawls up using hands to get up from squatting position.

74
Q

Cause of a fixed dilated pupil

A

CN3 palsy, damage to the parasympathetic fibres so can’t constrict pupil.

75
Q

What signs pint towards a Parkinson’s plus syndrome rather than PD?

A

Early falls
Early cognitive decline
Early bladder and bowel dysfunction
Both sides affected equally (in PD, normally one side is worse)

76
Q

Dysarthria and dysphagia definitions and differences

A

Dysarthria is a disorder of speech and articulation. Poor bulbar muscles. Disease of cerebellum.
Dysphasia is a disorder of language. Can be receptive (unable to comprehend but give fluent answers, WERNICKE’S AREA) or expressive (unable to respond, random sounds, Broca’s area).

77
Q

How to differentiate receptive and expressive dysphasia

A

Ask to follow command.

Receptive cant but expressive can.

78
Q

Investigation for neuro causes of breathing difficulty

A

Monitor FVC

79
Q

Medical Mx of a brain tumour and side effect

A

Dexamethasone, insomnia.

Neurology 3A (7 decks)

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