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Neuro Flashcards

0
Q

How can the lesions in MS be described?

A

Disseminated in space and time

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1
Q

What is Lhermitte’s sign and in which disease is it seen?

A

Seen in MS. It is when electric shock-like pain occurs in trunk and limbs when the neck is flexed

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2
Q

What is the mean age of onset of MS?

A

30

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3
Q

What kind of symptoms occur with MS?

A

Sensory- pins and needles, Lhermitte’s sign, trigeninal neuralgia, reduced vibration sense

Motor: myelitis, spastic weakness

Sexual/GU: erectile dysfunction, anorgasmia, urine retention

GI: constipation, swallowing disorder

Cerebellum: ataxia, intention tremor, monotonous speech

Eye: diplopia, hemianopia, INO, optic neuritis, pupil defects

Cognitive decline

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4
Q

What is the pathogenesis of MS?

A

Autoimmune disease attacking myelinated axons

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5
Q

What worsens MS symptoms?

A

Heat/exercise

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6
Q

What is the lifetime risk of MS in the UK?

A

1:1000

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7
Q

How is MS diagnosed?

A

Clinical diagnosis:
Past episodes e.g. Brief unexplained vision loss
Attacks lasting more than 1 hr with more than 30 days between attacks

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8
Q

What is seen in the CSF of MS patients

A

Oliclonal bands of IgG in >90% of patients

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9
Q

What can be used to identify a demyelinating event?

A

Evoked potentials

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10
Q

What are the differential diagnoses for MS?

A

Spinal cord neoplasms, subacute combined degeneration of the cord, transverse myelitis, progressive multifocal leukoencephalitis

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11
Q

What is the treatment for MS?

A 
Steroids (for acute attacks)
DMDs (to reduce number of relapses):
-interferon alpha and beta
-monoclonal antibodies (alemtuzumab and Natalizumab)
-azathioprine
-glatiramer acetate
Treatment of spasticity- baclofen, gabapentin
Treatment of tremor-Botox
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12
Q

What is the definition of a relapse?

A

Appearance of new symptoms or the return of old symptoms for a period of 24 hours or more in the absence of a change in core body temperature or infection

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13
Q

What are the 4 types of MS?

A

Relapsing-remitting
Secondary progressive
Primary progressive
Progressive-relapsing

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14
Q

What is CJD caused by

A

Prions- midfielder forms of normal proteins which can transform other proteins into prion proteins

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15
Q

What kind of changes do prion proteins cause in the brain?

A

Spongiform changes- cavities and tubulivesicular structures in the brain

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16
Q

What are the 2 types of CJD

A

Variant CJD- transmitted in BSE contaminated beef

Classic CJD- occurs spordically due to mutation

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17
Q

What is the mean age of onset for classic CJD and variant CJD?

A

Classic: 68
Variant: 28

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18
Q

What is the mean duration of illness for classic and variant CJD?

A

Classic: 4-5 months
Variant: 13-14 months

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19
Q

What are the symptoms of CJD?

A 
Progressive dementia
Focal neuro signs
Myoclonus
Depression
Eye signs
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20
Q

What is Guillain-Barré syndrome?

A

Acute inflammatory demyelinating neuropathy

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21
Q

What are the triggers for Guillain-Barré syndrome?

A

Campylobacter jejuni, CMV, mycoplasma, HZV, HIV, EBV, vaccinations

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22
Q

What is the treatment for Guillain-Barré?

A

Plasma exchange
IV immunoglobulin
Supportive therapy

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23
Q

What are the symptoms of Guillain-Barré?

A

Acute ascending paralysis with glove-and-stocking weakness
Progressive weakness of all 4 limbs (days- weeks)
Arreflexia
CN palsies
Paresthesiae
Autonomic dysfunction (sweating, ⬆️pulse)

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24
Q

What is the prognosis for Guillain-Barré?

A

85% make a full recovery

10% unable to walk at 1 year

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25
Q

Differential diagnosis for Guillain-Barré?

A

Acute myelopathy
Chronic inflammatory demyelinating polyneuropathy
HIV peripheral neuropathy
Spinal cord compression

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26
Q

Signs and symptoms of spinal cord compression

A 
Leg weakness
Sensory loss
Spinal/root pain may precede this
Urine/faecal incontinence 
LMN signs at level 
UMN signs below level (but tone and reflexes reduced in acute cord compression)
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27
Q

What are the main causes of spinal cord compression?

A
  1. Vertebral body neoplasms
  2. Disc and vertebral lesions (trauma, degenerative disease)
  3. Inflammatory (epidural abscess, TB)
  4. Spinal cord neoplasms
  5. Rarities- Paget’s disease, epidural haemorrhage , bone cysts
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28
Q

Differential diagnoses for cord compression

A 
Transverse myelitis
MS
carcinomatous meningitis
Cord vasculitis (syphillis)
Trauma
Guillain-Barré 
Dissecting aneurism
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29
Q

What is the most common cause of cauda equina syndrome?

A

Lumbar disc prolapse at L4/L5 and L5/S1

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30
Q

Signs and symptoms of cauda equina lesion

A 
Bladder and bowel dysfunction 
Mixed UMN/LMN leg weakness- ASYMMETRICAL
Saddle numbness 
Back pain
Erectile dysfunction 
Arreflexia
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31
Q

What are the causes of foot drop?

A 
Diabetes
Common peroneal nerve palsy
Stroke
Prolapsed disc 
MS
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32
Q

What causes leg weakness with no sensory loss?

A

Motor neurone disease
Polio
Parasaggital meningioma

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33
Q

What causes chronic spastic paraparesis?

A 
MS
Cord tumour 
Motor neurone disease
SCDC
Syringomyelia
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34
Q

What causes chronic flaccid paraparesis?

A

Peripheral neuropathy

Myopathy

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35
Q

What causes absent knee jerks and extensor plantars?

A

Motor neurone disease/myeloradiculitis
Friedrich’s ataxia
SCDC
Tabes dorsalis

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36
Q

What are the differential diagnoses for blackouts?

A
  1. Epilepsy
  2. Postural hypotension
  3. Syncope
  4. Cardiac causes
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37
Q

What is syringomyelia?

A

Fluid-filled cavity in the spinal cord

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38
Q

What is syringobulbia?

A

Fluid-filled cavity in the brainstem

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39
Q

What is the most common cause of syringomyelia and syringobulbia?

A

Blockage of CSF flow from the 4th ventricle (due to Arnold-Chiari malformation)

Other causes: SAH, post infection, masses, post trauma, post AVM rupture

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40
Q

What is an Arnold-Chiari malformation?

A

Congenital herniation of the cerebellar tonsils through the foramen magnum

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41
Q

What is the normal presentation of syringobulbia or syringomyelia?

A

Presentation in 3rd/4th decade of life with pain and sensory loss (pain+temperature only) in the upper limbs and upper trunk only

Damage to pyramidal tracts, anterior horn cells and medulla cause wasting in the hands and claw hand

Spastic paraplegia
nystagmus
Horner’s syndrome
Charcot’s joints

Syringobulbia: nystagmus, tongue atrophy, pharyngeal/palatal weakness, facial sensory loss

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42
Q

What is the treatment for syringomyelia and syringobulbia?

A

Decompression of the foramen magnum

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43
Q

What is Friedreich’s ataxia?

A

Progressive degeneration of the cerebellum and spinocerebellar tracts
–> cerebellar ataxia, dysarthria, nystagmus
Tendon reflexes absent (peripheral n. damage)
Loss of dorsal columns–> absent joint position and vibration sense
Loss of corticospinal tract–> weakness and up going plantar
Pes cavus
Optic atrophy
Death by middle age

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44
Q

What is motor neurone disease?

A

Destruction of UMNs and anterior horn cells in brain and spinal cord

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45
Q

What is the life expectancy for MND and what do patients die of?

A

3 years- die of resp failure due to bulbar palsy and pneumonia

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46
Q

Is MND more common in men or women? Is it familial?

A

Men
Most cases sporadic (not familial)
Familial cases can be due to mutations in SOD-1 (responsible for clearing up free radicals)

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47
Q

What are the 4 clinical patterns of MND?

A
  1. Progressive muscular atrophy
  2. Amyotrophic lateral sclerosis
  3. Progressive bulbar and pseudobulbar palsy
  4. Primary lateral sclerosis
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48
Q

What is progressive muscular atrophy?

A

LMN lesion of the cord

Hands and arms- weakness, wasting, fasciculation

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49
Q

What is amyotrophic lateral sclerosis?

A

Disease of lateral corticospinal tracts and anterior horn cells
Progressive spastic tetra paresis/paraparesis
LMN signs

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50
Q

What is progressive bulbar and pseudobulbar palsy?

A

Destruction of UMN (pseudobulbar palsy) and LMN (bulbar palsy) in cranial nerves
Dysarthria+dysphagia
Wasting and fasciculation of tongue

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51
Q

What is primary lateral sclerosis?

A

Affects corticospinal tract in arms, legs and face

Progressive tetra paresis

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52
Q

What symptom is characteristic of MND?

A

Fasciculation

Weakness in arms and legs

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53
Q

What’s the differential diagnosis for MND?

A

Cervical spine lesion

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54
Q

What is the management of MND?

A

Riluzole- Na channel blocker that inhibits glutamate release (slows disease progression)

Ventilator support

PEG feeding

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55
Q

What is spinal muscular atrophy?

A

Group of rare disorders
Anterior horn cells destroyed
Symmetrical wasting and weakness of limbs

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56
Q

What percentage of over-65s and over-80s are affected by dementia?

A

10% of over-65s

20% of over-80s

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57
Q

What are the most common dementias?

A

Alzheimer’s (65% of all dementias)
Fronto-temporal dementia
Vascular dementia
Dementia with Lewy bodies

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58
Q

What is the disease progression and symptoms of Alzheimer’s?

A 
Progresses over years 
Short term memory loss 
Disintegration of personality and intellect
Difficulty with language
Apraxia
Agnosia
Visuospatial skills
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59
Q

What is the pathophysiology of Alzheimer’s?

A

Neurofibrillary tangles

Amyloid plaques

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60
Q

Which investigations are done in dementia?

A 
MMSE
FBC
LFTs
TFTs
Measure B12 And folate 
Brain CT
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61
Q

Management of Alzheimer’s?

A

AChE inhibitors- rivastigmine, donepezil, galantamine

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62
Q

What is the prognosis for Alzheimer’s?

A

Average survival= 8-10 years

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63
Q

What is the progression of vascular dementia?

A

Stepwise deterioration

Hx of TIAs or strokes

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64
Q

What is the disease course of dementia with Lewy bodies?

A

Fluctuating cognition with profound variation in attention and alertness
Memory loss may not occur in early stages
Impaired attention and visuospatial ability
Visual hallucinations
Parkinsonism
Depression and sleep disorders

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65
Q

What are the general causes of mononeuropathy?

A

Compression
Entrapment
Direct damage

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66
Q

What is carpal tunnel syndrome?

A

Entrapment neuropathy

Median nerve is compressed as it passes through carpal tunnel

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67
Q

What’s the cause of carpal tunnel?

A

Mostly idiopathic

Associated with: hypothyroidism, diabetes, pregnancy, obesity, RA, acromegaly

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68
Q

What are the features of carpal tunnel?

A

Pain and parenthesiae in the hand
Worse at night
Hanging the hand out of the bed and shaking it out can relieve pain
Tinnel’s sign: tapping on carpal tunnel is painful
Weakness+wasting of the bar muscles
Sensory loss- palm and palmar aspects of radial 3.5 fingers

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69
Q

Treatment for carpal tunnel?

A

Nocturnal splints
Local steroid injections
Surgical decompression

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70
Q

What is mononeuritis multiplex

A

Multiple mononeuropathy

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71
Q

What are the causes of mononeuritis multiplex?

A 
Indicates systemic disease:
Diabetes
Leprosy
Vasculitis
Sarcoidosis
Anyloidosis
Malignancy
Neurofibromatosis
HIV
Guillain-Barré
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72
Q

What are the differential diagnoses for Parkinson’s disease?

A

Drug-induced Parkinsonism (prochlorperazine)
Parkinson-plus syndromes (progressive supra nuclear palsy and multiple system atrophy)
Dementia with Lewy bodies
Post-encephalitic Parkinson’s
Normal pressure hydrocephalus
Vascular Parkinson’s

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73
Q

What kind of symptoms may occur in a poly neuropathy?

A

Sensory- paraesthesiae, numbness ‘glove and stocking’ distribution, pain in extremities, unsteadiness
Motor- weakness
Autonomic- postural hypotension, urinary retention, erectile dysfunction, diarrhoea, ⬇️sweating, cardiac arrhythmias, impaired pupillary responses

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74
Q

Name some causes of poly neuropathy

A 
Guillain-Barré
Drugs e.g. Isoniazid, phenytoin
Diabetes
Thyroid disease
Amyloidosis
Vitamin deficiency : B1, B12, B6
Alcohol, lead, arsenic 
Chronic inflamm. demyelinating polyn.
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75
Q

Which investigations should be done in a patient with polyneuropathy?

A 
FBC
ESR
Serum B12
BM
U&E
LFTs
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76
Q

What is Miller Fisher syndrome

A

Variant of Guillain-Barré which affects ten cranial nerves to the eye
Characterised by ophthalmoplegia and ataxia

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77
Q

Which test is done to confirm diagnosis of Guillain- Barré?

A

Nerve conduction study

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78
Q

What is the consequence of vitamin B1 (thiamin) deficiency?

A

Wernicke-Korsakoff syndrome
Polyneuropathy
Cardiac failure

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79
Q

What causes thiamin deficiency?

A

Alcholism, beriberi, starvation

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80
Q

What is the consequence of vitamin B6 (pyridoxine) deficiency?

A

Sensory neuropathy

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81
Q

What can cause vitamin B6 deficiency?

A

Isoniazid therapy

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82
Q

What is the consequence of vitamin B12 deficiency?

A

Subacute combined degeneration of the cord

Distal sensory loss, absent ankle jerks, exaggerated knee jerks, up going plantars

83
Q

Give an example of a hereditary sensorimotor neuropathy and explain the symptoms

A

Charcot-Marie-Tooth (common peroneal nerve palsy)
Progressive distal limb wasting and weakness
Loss of sensation and reflexes in legs

84
Q

What is the difference in clinical

Presentation between a neuropathy and a muscle disease?

A

Reflexes and sensation normal in muscle disease but not neuropathy

85
Q

What are polymyosotis and dermatomyositis?

A

Acquired muscle diseases

Polymyositis- inflammation and necrosis of skeletal muscle fibres
Dermatomyositis- when skin is involved

86
Q

Symptoms of Polymyositis and dermatomyositis

A

Symmetrical progressive muscle weakness and wasting of proximal muscles of shoulder and pelvic girdle

Difficulty rising from a chair and raising hands above head

Dysphagia, dysphonia

Dermatomyositis- purple discolouration of eyelids, erythema over knuckles, arthralgia, dysphagia

87
Q

How is myosotis treated?

A

Prednisolone

88
Q

What condition is associated with myasthenia gravis in 70% of patients under 40?

A

Thymic hyperplasia

89
Q

What is the clinical presentation of myasthenia gravis?

A

Weakness and fatiguability of ocular, bulbar and proximal limb muscles (weakness improves after rest)
Ptosis
Diplopia
Difficulty in talking, chewing, swallowing, breathing
Ask pt to sit with arms outstretched and look for slow downward drift

90
Q

Which antibodies are specific for myasthenia gravis?

A

Anti-AChR autoantibodies

91
Q

Which investigations are done in suspected myasthenia gravis?

A

Nerve stimulation tests- decrease in evoked potential

CT/MRI of mediastinum to look for thymoma

92
Q

What is the differential diagnosis for myasthenia gravis

A 
Thyroid ophthalmopathy
Myotonic dystrophy
Brainstem cranial nerve lesions 
Botulism
Lambert-Eaton myasthenic myopathic syndrome
93
Q

Treatment for myasthenia gravis

A

Anticholinesterases
Azathioprine
Plasmapherisis and IV Ig (for myasthenic crisis)
Thymectomy (for thymoma)

94
Q

What is myasthenic crisis?

A

When respiratory and bulbar muscles become weak

95
Q

What is myotonia? What are examples of some myotonic conditions?

A

Delayed muscle relaxation after contraction (e.g. Difficulty releasing grasp after shaking hands)
Examples: dystrophia myotonica, myotonia congenita

96
Q

How does Duchenne muscular dystrophy present and what is the disease course?

A

Presents with weak proximal leg muscles- clumsy walking and difficulty standing
Progresses to other muscle groups- resp failure
Severe disability and death in late teens

97
Q

What are symptoms of dystrophia myotonica?

A

Progressive distal muscle weakness with myotonia, ptosis, facial muscle weakness and wasting

98
Q

What are the symptoms of myotonia congenita?

A

Mild isolated myotonia accentuates by rest and cold

99
Q

What are the causes of low CSF opening pressure

A

CSF leak

Recent lumbar puncture

100
Q

Which invesitgations are done in syringomyelia?

A

MRI

101
Q

What are the causes of high CSF opening pressure?

A

Meningitis
Tumour
Intracranial haemorrhage
Benign intracranial hypertension

102
Q

What does cloudy/purulent CSF

signify?

A

Meningitis

103
Q

What does bloody CSF signify?

A 
Traumatic tap (hit a blood vessel during lumbar puncture)
Subarachnoid haemorrhage
104
Q

What are the causes of raised CSF protein?

A 
Meningitis 
Brain abscess
Infra cerebral haemorrhage 
Neoplastic disease
Guillain-Barré
MS
105
Q

CSF glucose should be …..% that of the level in the blood

A

40-60%

106
Q

What are the signs of type 1 neurofibromatosis?

A

Cafe ah lair spots
Freckling in skin-folds
Nodular neurofibromas
Lisch nodules

107
Q

Which dural venous sinus is the most commonly thrombosed?

A 
Sagittal sinus (47% of cases)
Transverse sinus (35% of cases)
108
Q

What are the signs of sagittal sinus thrombosis?

A

Headache, vomiting, seizures, decreased vision, papilloedema

109
Q

What are the signs of transverse sinus thrombosis?

A

Hedache +/- mastoid pain, focal CNS signs, seizures, papilloedema

110
Q

What are the symptoms of cortical vein thrombosis?

A

Symptoms: Thunderclap headache, seizures.
Signs: encephalopathy, slowly evolving focal deficits (paresis, speech disorders, decreased cognition, decreased vision)
Usually occurs with sinus thrombosis
Galen thrombosis=rare cause of CVT associated with vascular malformation

111
Q

What are the differential diagnosis for intracranial venous thrombosis?

A

SAH, meningitis, encephalitis, intracranial abscess, arterial infarction

112
Q

Which investigations are done in intracranial venous thrombosis?

A

CT/MRI venography, LP

113
Q

What is the treatment for intracranial venous thrombosis?

A

Heparin

Streptokinase

114
Q

What are some causes of intracranial venous thrombosis?

A

Pregnancy, OCP, head injury, dehydration, intracranial malignancy, extracranial malignancy (hypercoagulation), recent LP, hyperthyroidism, meningitis/TB, androgens…

115
Q

When should you suspect an extradural haemorrhage?

A

If, after head injury, conscious level falls after a lucid interval

116
Q

What is the most common cause of extradural haemorrhage?

A

Fracture of temporal/parietal bone causing laceration of middle meningeal artery
(can also be caused by tearing of dural venous sinuses)

117
Q

What are the differential diagnoses for extradural haemorrhage?

A

Epilepsy, Carotid dissection, carbon monoxide poisoning

118
Q

What are the signs and symptoms of an extradural haemorrhage?

A

Raised ICP, decreased GCS, headache, vomiting, confusion, seizures, ipsilateral pupil dilatation, bilateral limb weakness, deep and irregular breathing (brainstem compression)

119
Q

What is pseudobulbar palsy caused by?

A

Damage to the corticobulbar tracts.

MND, MS, stroke, brainstem disorders, neurosyphilis, head injury.

120
Q

What are the signs and symptoms of pseudobulbar palsy?

A

Donald Duck speech, paralysed tongue, exaggerated jaw jerk, dysphonic, dysphagic, facial muscles paralysed

121
Q

What happens to speech in myasthenia gravis?

A

Soft, slurred, monotonous speech which gets worse the longer the patient talks.

122
Q

When should subdural haematoma be suspected?

A

Fluctuating conscious level, insidious physical/intellectual slowing, sleepiness, headache, personality change, unsteadiness
Risk factors: falls (alcoholics, epileptics), anticoagulation

123
Q

What are the causes of subdural haematoma?

A

Bleeding from bridging veins between cortex and venous sinuses
Note: does not have to be trauma!
Intracranial HYPOtension, dural metastases

124
Q

What is a cause of the following presentation:

  • bilateral facial palsy
  • uveitis
  • parotitis (swollen parotid glands)
  • fever
A

Heerfordt’s syndrome (a presentation of sarcoidosis)

Resolves spontaneously in a few weeks

125
Q

Can myasthenia gravis and Lyme disease cause bilateral facial palsies?

A

Yep

126
Q

What is Ramsay-Hunt syndrome?

A

Facial palsy associated with HZV

  • LMN facial palsy (forehead sparing)
  • Pain around ear
  • Vesicles in and around external auditory meatus
127
Q

Give 3 examples of mainly motor polyneuropathies

A

Guillain-Barre syndrome, Lead poisoning, Charcot-Marie-Tooth syndrome

128
Q

Give 3 examples of mainly sensory polyneuropathies

A

Diabetes mellitus, Renal failure, leprosy

129
Q

What are some causes of autonomic neuropathy?

A

Sjogren’s syndrome, HIV, SLE, leprosy, Guillain-Barre, paraneoplastic syndrome, diabetes

130
Q

What are the signs of parasympathetic neuropathy?

A

erectile dysfunction, nocturnal diarrhoea, urine retention, Holmes-Adie pupil

131
Q

What are the signs of sympathetic neuropathy?

A

Ejaculatory failure, postural hypotension, decreased sweating, Horner’s syndrome

132
Q

What is cervical spondylosis?

A

Chronic cervical disc degeneration with herniation of disc material, calcification and osteophytic outgrowths

133
Q

What are the signs and symptoms of cervical spondylosis

A 
Can cause cord compression --> progressive spastic quadraparesis with sensory loss below neck
Painful neck movement
Neck stiffness
Crepitus (cracking) on moving neck
Stabbing/dull arm and wrist pain
Signs of cord compression:
-Spastic leg weakness (often one leg is worse)
-weakness and clumsiness in hands
-heavy legs
-numb hands
-foot drop/poor walking
-incontinence
134
Q

What are the signs and symptoms of radiculopathy?

A

Pain (electrical sensations) in arms or fingers at level of compression
Dull reflexes
Sensory disturbance (numbness, tingling, reduced pain and temp sensation)
LMN effects in muscles innervated by affected root
UMN affected below level

135
Q

Where is pain referred to in:

a) Trapped nerve at C3-C4
b) Trapped nerve at C5
c) Trapped nerve at C6
d) Trapped nerve at C7
e) Trapped nerve at C8

A

a) Neck and trapezius pain
b) Shoulder pain and pain in arm to below the elbow
c) Pain worse on wrist flexion
d) Pain down arm into 3rd finger
e) Pain down arm into 4th and 5th fingers

136
Q

What are the motor + sensory defects associated with:

a) C5 root involvment
b) C6 root involvement
c) C7 root involvement
d) C8 root involvement

A

a) Weak deltoid+supraspinatus, reduced supinator jerk, numb elbow
b) Weak biceps+brachioradialis, reduced biceps jerk, numb thumb and index finger
c) Weak triceps+finger extension, reduced triceps jerks, numb middle finger
d) Weak finger flexors+small hand muscles, numb 4th and 5th fingers

137
Q

What are differential diagnoses for cord compression?

A

MS, nerve root neurofibroma, SCDC, bone/cord tumour, intramedullary spinal sarcoidosis

138
Q

What are the management options for cervical spondylosis?

A

Neck collar
Surgical root decompression (laminectomy or laminoplasty)
Transforaminal steroid injection

139
Q

What is the difference between laminectomy and laminoplasty?

A 
Laminectomy= portion of bone removed
Laminoplasty= screws and plates
140
Q

What are the features of myopathies/muscular dystrophies

A

Gradual onset of symmetrical proximal weakness (also distal in myotonic dystrophy)

Specific muscle groups affected

Tendon reflexes preserved

No paraesthesiae/bladder problems

141
Q

What are the symptoms and signs of fascioscapulohumeral dystrophy?

A 
Weakness of face ('ironed out' expression)
Cannot puff out cheeks
Cannot raise arms
Winging of scapula
Foot drop
Scoliosis
Horizontal clavicals
Anterior axillary folds
142
Q

What are the signs and symptoms of Becker’s muscular dystrophy?

A

Similar to Duchenne’s, but later presentation

143
Q

What is the inheritance pattern of:

a) Duchenne’s
b) Becker’s
c) fascioscapulohumeral

A

a) X-linked recessive
b) X-linked recessive
c) autosomal dominant

144
Q

What do myotonic disorders cause? What is the most common one?

A 
Tonic muscle spasm (myotonia)
Most common= dystrophia myotonica (autosomal dominant chloride channelopathy)
Signs+symptoms:
-hand/foot drop
-weak sternocleidomastoids
-myotonia
-facial weakness
-cataracts
-male frontal baldness
-diabetes
-testis/ovary atrophy
-cardiomyopathy
145
Q

Give examples of acqured myopathies (late onset)

A

Part of systemic disease:

Cushing’s, hyperthyroid, malignancy, hypocalcaemia, hypercalcaemia

146
Q

Give an example of an inflammatory myopathy

A

Inclusion body myositis:

  • weakness in quads, finger flexors and pharyngeal muscle
  • intranuclear inclusions seen in histology
147
Q

What are the complications of type 1 neurofibromatosis? How common are they?

A

Occur in 30% of cases
Mild learning disability
Local effects of neurofibromas (nerve root compression, GI bleeds and obstruction, bone lesions, ⬆️BP, sarcoidosis)
Malignancy (in 5% of pts)- optic glioma, sarcomatous change in neurofibroma

148
Q

What is the management of type 1 neurofibromatosis

A

Yearly management of BP

Can excise neurofibromas

149
Q

What is the prevalence of type 1 and type 2 neurofibromatosis?
How are they inherited?

A

Type 1: 1 in 2500
Type 2: 1 in 35000

Both autosomal dominant

150
Q

What are the characteristic signs of type 2 neurofibromatosis?

A

Bilateral vestibular Schwannoma (acoustic neuroma)

Schwannonatosis (multiple tender Schwannomas without the bilateral vestibular Schwannomas)

Juvenile posterior subcapsular lenticular opacity (type of cataract)

152
Q

What are the differential diagnosis for NF1?

A

McCune-Albright syndrome
Multiple lentigenes
Urticaria pignentosa

153
Q

What is the differential diagnosis for NF2?

A

NF1

Schwannomatosis

154
Q

What neurological problems can HIV cause?

A 
Meningitis (fungal/TB)
Toxoplasmosis 
Dementia 
Encephalomyelitis
Cord problems 
Mononeuritis multiplex
Guillain-Barré syndrome
155
Q

What is HTLV-1 myelopathy/tropical spastic paraplegia?

A

Slowly progressing spastic paraplegia
Paraesthesiae
Sensory loss
Disorders of micturation

156
Q

What is the treatment of Parkinson’s disease?

A

L-dopa (dopamine precursor which can cross the BBB)
Entacapone (dopamine decarboxylase inhibitor- reduced SEs by stopping peripheral conversion of L-dopa)
Selegiline (MAO-B inhibitors- increases effect of L-dopa)
Bromocriptine, ropinirole cabergoline (dopamine agonists)
Benzatropine (muscarinic antagonists- reduce tremor and drooling)

157
Q

How does LEMS (Lambert-Eathon myasthenic syndrome) differ from myasthenia gravis?

A

MG- normal/brisk reflexes

LEMS- hyporeflexia

158
Q

What are the symptoms of temporal lobe epilepsy?

A

Automatisms
Abdominal rising sensation/pain beforehand
Deja vu
Dysphasia
Impaired awareness and little memory of the event
Hallucinations

159
Q

What are the symptoms of frontal lobe epilepsy?

A 
Motor features e.g. posturing
Jacksonian march
Behavioural disturbances
Dysphasia
Todd's palsy post-seizure
160
Q

What are the symptoms of parietal lobe epilepsy?

A 
Sensory disturbances
Motor symptoms (if seizure spreads to pre-central gyrus)
161
Q

What kind of epilepsy do childhood febrile convulsions predispose to?

A

Temporal lobe epilepsy

162
Q

What is a common cause of temporal lobe epilepsy?

A

Hippocampal sclerosis

163
Q

What are the symptoms of an anterior cerebral artery infarction?

A

Weak/numb contralateral arm and leg
No facial involvement
Bilateral infarction–> akinetic mutism

164
Q

What are the symptoms of a middle cerebral artery infarction?

A

Contralateral hemiparesis
Contralateral hemisensory loss
Dysphasia (dominant hemisphere lesions)
Apraxia (non-dominatnt hemisphere lesions)

165
Q

What are the symptoms of a posterior cerebral artery infarction

A

Contralateral homonymous hemianopia

166
Q

What are the symptoms of lacunar infarcts?

A

Pure motor/pure sensory symptoms
Ataxic hemiparesis
Dysarthria
Clumsy hand

167
Q

What are the symptoms of infarction of the vertebrobasilar circulation?

A 
hemianopia
cortical blindness
diplopia
vertigo
nystagmus
ataxia
dysarthria
dysphasia
hemiplegia
unilateral/bilateral sensory symptoms
168
Q

What is the clinical difference between conus medullaris/cauda equina lesion and lesions higher up in the cord?

A

Conus medullaris/cauda equina- weakness is flaccid and arreflexic
Lesions higher up in spinal cord: weakness is spastic and hyperreflexic

169
Q

What is the most common cause of weak legs and cord compression?

A

Secondary malignancy (breast, lung, prostate, thyroid, kidney) in the spine

170
Q

What are the symptoms of conus medullaris lesions?

A 
Mixed UMN/LMN leg weakness
Early urinary retention
Constipation
Back pain
Sacral sensory disturbance
Erectile dysfunction
171
Q

What are the causes of a resting tremor? How is a resting tremor abolished?

A

Parkinsonism

Abolished by movement

172
Q

What are the causes of postural tremor? When is it present?

A

Benign essential tremor (improves with alcohol)
Thyroxicosis
Anxiety
Beta-agonists

Tremor is present on maintained posture and may persist on movement

173
Q

What is re-emergent tremor?

A

Postural tremor developing after a delay of 10 seconds (e.g. in Parkinsons)
DBS may help

174
Q

What are the causes of chorea?

A

Huntington’s disease

Sydenham’s chorea (occurs after rheumatic fever. Spontaneous remission within weeks)

175
Q

What are the causes of hemiballismus?

A

Vascular lesion of subthalamic nucleus (hemiballismus occurs contralateral to lesion)

176
Q

What is athetosis and what are the causes?

A

Athetosis consists of slow, confluent, purposeless movements
Most common cause= cerebral palsy

177
Q

Tics occur in which syndrome?

A

Tourette’s syndrome

178
Q

What are the causes of myoclonus?

A 
CJD
Metabolic problems (metabolic flap- liver/kidney failure, thalamic stroke (unilateral flap), hyponatraemia, hypercapnia)
179
Q

What are the treatments for benign essential myoclonus?

A

valproate, clonazepam, piracetam

180
Q

What is the cause of tardive dyskinesia

A

Chronic extposure to dopamine agonists (antipsychotics, antiemetics)

181
Q

What is dystonia?

A

Prolonged muscle contractions causing abnormal posture or repetitive movements

182
Q

What is idiopathic generalized dystonia and how is it treated?

A 
Childhood onset
Starts in one leg and spreads along that side of the body
Progresses over 5-10 years
Autosomal dominant
Treatment: Trihexyphenidyl, DBS
Exclude Wilson's disease
183
Q

What is the treatment for focal dystonias (e.g. writer’s cramp, blepharospasm)

A

Botox

184
Q

What are the causes of acute dystonia? What are the signs and symptoms?

A

Caused by drugs:

  • antipsychotics
  • antiemetics (cyclizine)

Signs and symptoms:

  • torticollis (head pulled back)
  • oculogyric/oromandibular spasm (eyes drawn up and mouth movements
185
Q

What is the treatment for acute dystonic reactions?

A

anti-cholinergics

186
Q

What is the mortality rate after the first stroke?

What is the incidence of stroke?

A

12%

1/1000 per year incidence

187
Q

What are the 4 main causes of stroke?

A

Small vessel occlusion or thrombosis in situ
Cardiac emboli
Atherothromboembolism (e.g. from carotids)
CNS bleeds (SAH, carotid artery dissection)

188
Q

Which genetic diseases predispose to stroke?

A

CADASIL (cerebral autosomal dominant arteriopathy with subcortical infarcts and leucocencephalopathy)

Antiphospholipid syndrome (predisposes to clots)

189
Q

What is a watershed stroke?

A

A stroke that occurs in the zone between 2 cerebrovascular territories

190
Q

What are the modifiable risk factors for stroke?

A

Hypertension, smoking, diabetes, heart disease (valvular, ischaemic, AF), peripheral vascular disease, past TIA, carotid bruit, OCP, increased lipids, alcohol, increased clotting, syphilis

191
Q

What are the signs of a haemorrhagic stroke?

A

Meningism, coma within hours, severe headache, decreased GCS

192
Q

What is the plan of action in the first hour after a stroke?

A
  1. Pulse, BP, ECG (do they have AF?, Cannot thrombolyse if the blood pressure is too high). Stop HRT if patient is on it.
  2. Blood glucose- aim for 4-11 mmol/L
  3. Urgent CT/MRI: Diffusion weighted MRI shows acute infarct. CT shows haemorrhage
  4. Thrombolysis (if symptoms begain under 4.5 hours ago)
  5. Nil by mouth- hydrate by IV
  6. Antiplatelet agents if haemorrhagic stroke is excluded (aspirin)
193
Q

What are the contraindications for thrombolysis?

A 
Major infarct or haemorrhage on CT
Mild/non-disabling deficit
Recent birth, surgery, trauma or artery/vein puncture
Past CNS bleed
AVM/aneurysm
Severe liver disease, varices or portal hypertension
Seizures
Anticoagulants or INR above 1.7
Platelets below 100
BP> 220/130
194
Q

What is the differential diagnosis for stroke?

A 
Head injury
Transient global amnesia
Epilepsy (Todd's paresis)
Space-occupying lesion
Migraine (N.B. migraines can cause stroke)
Demyelination
Hypo/hyperglycaemia
Infections
Electrolyte disturbance
Hypertensive encephalopathy
Wernicke's encephalopathy
Posterior reversible encephalopathy syndrome (PRES)
Cerebral reversible vasoconstrictive syndrome (CRVS)
195
Q

Which drug is used for thrombolysis?

A

Alteplase (tissue plasminogen activator)

196
Q

How are ADC and DWI images used to identify stroke?

A

ADC- dark= new stroke
light= old stroke
DWI- dark=old stroke
light=new stroke

If bright on both ADC and DWI–> think demyelination or tumour

197
Q

What is malignant MCA syndrome?

A

MCA occlusion
Massive oedema
Midline shift

198
Q

What are the primary preventative measures for stroke (i.e. preventing a stroke in the first place)?

A

Control risk factors
Folate supplements
Lifelong anticoagulation for AF, prosthetic valves, rheumatic heart valves

199
Q

What are the secondary preventative measures for stroke (i.e. preventing further strokes)

A

Control risk factors
Antiplatelet agents- clopidogrel
Anticoagulation after stroke from AF- warfarin

200
Q

Which tests and investigations should be done after a stoke?

A

Tests for HTN- retinopathy, nephrpathy, enlarged heart on CXR
ECG- to look for AF, valvular lesions after endocarditis etc.
Carotid doppler- to look for carotid artery stenosis
Hypo/hyperglycaemia
Hyperlipidaemia
ESR- to look for vasculitis
Clotting screen- to look for thrombophilia
Hyperviscosity- polycythaemia, SCD
Thrombocytopenia
Genetic tests- CADASIL

201
Q

AF increases chance of stroke by how much?

A

4.5% per year

202
Q

What is used for prevention of stroke in patients with AF?

A

Warfarin or dabigatran

203
Q

What are the cardiac causes of stroke?

A

Non-valvular atrial fibrillation
External cardioversion
Prosthetic valves
Acute MI (emboli arise in 10% of patients in the next 6-12 months)
Paradoxical systemic emboli
Cardiac surgery
Valve vegetations from infective endocarditis

204
Q

what is the death rate in stroke?

A

20-25%

205
Q

What is lateral medullary syndrome?

A 
Most common brainstem vascular syndrome
Caused by occlusion of posterior inferior cerebellar a.
Sudden vomiting and vertigo
Ipsilateral:
Horner's syndrome
Facial numbness
Cerebellar signs
Palatal paralysis
Diminished gag reflex

NOP (3 decks)

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