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Phase 3A Revision > Neurology > Flashcards

Neurology Flashcards

1
Q

What are the symptoms of a migraine headache?

A

Attacks last 4-72 hours
Two of:
Unilateral
Pulsing
Moderate/severe pain
Aggravated by routine physical activity
At least one of (during headache):
Nausea
Vomiting
Photophobia/phonophobia

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2
Q

What are the symptoms of a tension headache?

A

Attacks can last from 30 minutes to 7 days
No nausea/vomiting/photphobia
At least 2 of:
Bilateral
Tightening pain
Mild/moderate pain
Not aggravated by routine physical activity

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3
Q

What are the symptoms of a cluster headache?

A

Severe or very severe, unilateral, orbital/supraorbital/temporal pain
Lasts 15-180 minutes if not treated
Accompanied by ipsilateral cranial autonomic features (eg.miosis/ptosis, lacrimation) +/- restlessness/agitation

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4
Q

What are the symptoms of trigeminal neuralgia?

A

Occurs in one or more distribution of the trigeminal nerve
At least 3 of:
Unilateral
Severe
Recurring
Electric shock-like pain
Triggered by innocuous stimuli to the affected side of the face (eg. slight breeze of wind)

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5
Q

What are the management steps of migraines?

A
  1. Lifestyle changes –> avoid triggers, stress management, good sleep hygiene etc
  2. Simple analgesia eg. ibuprofen, paracetamol, aspirin
  3. Add a triptan (eg. sumatriptan) alone or with NSAID/paracetamol

(add antiemetic if required)

avoid overprescribing/overmedicating as can cause a medication overuse headache

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6
Q

What medications can be used to prevent recurrent migraines?

A

Topiramate
Propanolol

If unsuitable, gabapentin/amitriptyline

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7
Q

What is the management of a tension headache?

A

Reassurance
Basic analgesia
Relaxation techniques
Hot towels to local area

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8
Q

What is the first line treatment of trigeminal neuralgia?

A

Carbamazepine

Surgery to decompress/damage the trigeminal nerve is an option

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9
Q

What red flags are important to consider with a patient presenting with a headache?

A

Fever/photophobia/neck stiffness –> Meningitis
New neurology –> Haemorrhage/Stroke/Malignancy
Visual disturbance –> Temporal arteritis
Sudden onset –> SAH
Worse on coughing/straining/standing/bending over –> Raised ICP
Trauma –> Haemorrhage
Pregnancy –> Pre-eclampsia

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10
Q

What are triggers for cluster headache?

A

Alcohol
Smoking
Strong smells
Exercise

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11
Q

What is the acute management of a cluster headache?

A

Triptans eg. sumatriptan 6mg SC
High flow 100% oxygen

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12
Q

What medications can be used for prophylaxis of cluster headaches?

A

Verapamil
Lithium
Prednisolone

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13
Q

Which autoimmune condition has a strong link with temporal arteritis (GCA)?

A

Polymyalgia rheumatica

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14
Q

What are the symptoms of temporal arteritis?

A

Severe unilateral headache around temple and forehead
Scalp tenderness
Jaw claudication (jaw fatigue when chewing)
Blurred/double vision
Systemic symptoms such as fever, fatigue, loss of appetite etc

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15
Q

To diagnose temporal arteritis, a temporal artery biopsy is performed. What are the findings in the biopsy if positive?

A

Multinucleated giant cells

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16
Q

What is the initial management of temporal arteritis?

A

Prednisolone 40-60mg OD immediately

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17
Q

What are complications of temporal arteritis?

A

Vision loss
Stroke

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18
Q

What are classic presentations of a stroke?

A

Sudden onset of neurological symptoms
Typically asymmetrical
Limb weakness
Facial weakness
Dysphasia
Visual/sensory loss

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19
Q

What is the definition of a TIA?

A

Transient neurological dysfunction secondary to ischaemia without infarction
Stroke-like symptoms that resolve within 24 hours

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20
Q

What are the risk factors associated with stroke?

A

CVD such as angina, MI and peripheral vascular disease
Previous stroke or TIA
AF
Carotid artery disease
Hypertension
Diabetes
Smoking
Vasculitis
Thrombophilia
COCP

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21
Q

What is the management of stroke?

A

Admit to specialist centre
Exclude hypoglycaemia
CT brain exclude primary intracerebral haemorrhage
Aspirin 300mg immediately and continue for 2 weeks
Thrombolysis with alteplase within 4.5 hours or thrombectomy if indicated

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22
Q

What is the time frame to start thrombolysis with alteplase?

A

4.5 hours

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23
Q

What is the management of TIA?

A

Start aspirin 300mg daily
Start secondary prevention measures for CVD

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24
Q

What is the secondary prevention of stroke?

A

Clopidogrel 75mg OD
Atorvastatin 80mg
Carotid endarterectomy/stenting if carotid artery disease
Treat modifiable risk factors eg. hypertension, diabetes

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25
Q

What is the gold standard imaging used to establish the affected vascular territory?

A

Diffusion-weighted MRI

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26
Q

What are the clinical signs of cerebellar syndrome?

A

Dysdidokinesia
Ataxia
Nystagmus
Intention tremor
Slurred speech
Hypotonia

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27
Q

What are the clinical signs of a frontal lobe disorder?

A

Motor impairment
Expressive aphasia/dysphasia (Broca’s area)
Poor planning and cognition

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28
Q

What are the clinical signs of a parietal lobe disorder?

A

Sensory impairment
Vision problems
Spatial neglect

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29
Q

What are the clinical signs of a temporal lobe disorder?

A

Hearing difficulties
Receptive aphasia/dysphasia (Wernicke’s area)
Impaired memory

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30
Q

What are the clinical signs of a occipital lobe disorder?

A

Visual disturbance

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31
Q

What investigations should be performed if epilepsy is suspected?

A

EEG –> Identify form of epilepsy and support diagnosis
MRI Head –> Rule out other causes or visualise structural problems that could be causing seizures eg. tumours
ECG –> Rule out cardiac cause of seizure/syncope

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32
Q

What is the presentation of a tonic-clonic seizure?

A

Loss of consciousness
Muscle tensing (tonic)
Muscle jerking (clonic)
May be associated tongue biting, incontinence, groaning, irregular breathing
Post-ictal period where the person is confused, drowsy and can feel irritable or depressed

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33
Q

What is the management of tonic-clonic seizures?

A

1st line: Sodium valproate
2nd line or women of child-bearing age: Lamotrigine or Carbamazepine

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34
Q

What are the presentations of a focal seizure?

A

Hallucinations
Memory flashbacks
Deja vu
Hearing problems
Speech problems
Doing strange things on autopilot

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35
Q

What is the treatment for a focal seizure?

A

1st line: Levetiracetam or lamotrigine
2nd line: Sodium valproate or carbamazepine

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36
Q

What is the presentation of an absence seizure?

A

Often in children
The patient becomes blank and tares into space
Abruptly resolves and returns to normal

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37
Q

What is the management of absence seizures?

A

Sodium valproate or ethosuxamide

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38
Q

What is the presentation of an atonic seizure?

A

Limpness
Drop to floor if standing
Eyelids droop
Head nods forward
May drop things held in hand

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39
Q

What is the management of an atonic seizure?

A

1st line: Sodium valproate
2nd line: Lamotrigine

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40
Q

What is the presentation of a myoclonic seizure?

A

Typically happen in children (juvenile myoclonic epilepsy)
Sudden brief muscle contractions
Remains awake

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41
Q

What is the management of a myoclonic seizure?

A

1st line: Sodium valproate
2nd line: Lamotrigine, levetiracetam or topiramate

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42
Q

What are side effects of sodium valproate?

A

Liver damage and hepatitis
Hair loss
Tremor
Teratogenic –> Should be avoided in girls and women unless there is no suitable alternative and strict criteria are met around contraception to ensure they do not get pregnant

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43
Q

What is the definition of status epilepticus?

A

Seizures lasting more than 5 minutes or more than 3 seizures in 1 hour
Medical emergency

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44
Q

What is the management of status epilepticus in hospital?

A

ABCDE
IV lorazepam 4mg, repeated after 10 minutes if symptoms persist
If seizures still persist, IV phenobarbital or phenytoin

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45
Q

What options are available in the community to manage status epilepticus?

A

Buccal midazolam
Rectal diazepam

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46
Q

What suggests non-epileptic attack disorder rather than an epileptic seizure?

A

Can last for 30 minutes
Convulsions are not neuroanatomically accurate (pelvic thrust, wild shaking with arms flexing and extending)
Atypical quick recovery
PMH of childhood trauma, stress or previous unexplained medical symptoms

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47
Q

What are common presentations of narcolepsy?

A

Excessive daytime sleepiness
Sleep attacks (falling asleep suddenly)
Cataplexy (temporary loss of muscle control resulting in weakness and possible collapse)
Sleep paralysis
Excessive dreaming
Frequent night time wakening

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48
Q

What is the management of narcolepsy?

A

Implementing good sleep hygiene
Modafinil/dexamfetamine
SSRIs/SNRIs/TCAs

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49
Q

Korsakoff’s syndrome is caused by a deficiency in which vitamin?

A

Vitamin B1

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50
Q

Wernicke’s encephalopathy is caused by a deficiency in which vitamin?

A

Vitamin B1

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51
Q

What is the difference between Wernicke’s encephalopathy and Korsakoff’s syndrome?

A

Wernicke’s encephalopathy represents the acute stage of B1 deficiency, where Korsakoff’s syndrome represents the disease progressing to a chronic stage

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52
Q

What is the presentation of Wernicke-Korsakoff syndrome?

A

Amnesia
Tremor
Coma
Disorientation
Vision problems
Inability to form new memories

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53
Q

What is the management of Wernicke-Korsakoff syndrome?

A

Thiamine replacement
Providing proper nutrition and hydration
Alcohol cessation

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54
Q

What type of inheritance is seen in Huntington’s disease?

A

Autosomal dominant

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55
Q

What is the presentation of Huntington’s disease?

A

Starts with cognitive, psychiatric or mood problems
Chorea –> involuntary abnormal movements
Eye movement disorder
Speech difficulties
Swallowing difficulties

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56
Q

What is the management of Huntington’s disease?

A

No treatment options
Support the patient and their family
Speech and language therapy
Genetic counselling

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57
Q

What is the classic triad of Parkinson’s disease features?

A

Resting tremor (pill rolling, unilateral, improves with voluntary movement, worsens if patient is distracted)
Rigidity (cogwheel rigidity)
Bradykinesia

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58
Q

What are the other symptoms of Parkinson’s disease?

A

Shuffling gait –> Stooped posture, reduced arm swing
Facial masking
Micrographia
Depression
Sleep disturbance
Loss of sense of smell
Cognitive impairment
Memory problems

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59
Q

What is the first line treatment of Parkinson’s disease?

A

Levodopa –> If motor symptoms are impacting quality of life
Dopamine agonists or MOA-B inhibitors –> If motor symptoms are not impacting quality of life

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60
Q

What are the side effects of levodopa?

A

Dystonia
Chorea
Athetosis –> Abnormal twisting or writhing movements usually in the fingers, hands or feet

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61
Q

What are the causes of raised intracranial pressure?

A

Brain tumours
Intracranial haemorrhage
Idiopathic intracranial hypertension
Abscess or infection

62
Q

What features of headache suggest raised ICP?

A

Constant
Nocturnal
Worse of waking
Worse on coughing/straining/bending forward
Vomiting

63
Q

What are the presenting features of raised ICP?

A

Altered mental state
Visual field defects
Seizures (particularly focal)
Unilateral ptosis
3rd and 6th nerve palsies
Papilloedema

64
Q

What are common cancers that metastasise to the brain?

A

Lung
Breast
Renal cell carcinoma
Melanoma

65
Q

What are the consequences of a pituitary tumour?

A

Bitemporal hemianopia
Acromegaly
Hyperprolactinaemia
Cushing’s disease
Thyrotoxicosis

66
Q

What is the management of a pituitary tumour?

A

Trans-sphenoidal surgery
Radiotherapy
Bromocriptine –> Blocks prolactin-secreting tumours
Somatostatin analogues –> Block GH-secreting tumours

67
Q

What factors are believed to influence the cause of multiple sclerosis?

A

Genetic
EBV
Low vitamin D
Smoking
Obesity

68
Q

What is the pathophysiology of multiple sclerosis?

A

Inflammation of the myelin around neurons and infiltration of immune cells, causing myelin damage and affecting the way signals travel along the neurons

69
Q

What is a characteristic feature of MS lesions?

A

They vary in location and time
“Disseminated in time and space”

70
Q

What are common presentations of multiple sclerosis?

A

Optic neuritis
Abducens nerve abnormalities
Focal weakness –> Bell’s palsy, Horner’s syndrome, limb paralysis, incontinence
Focal sensory problems –> Trigeminal neuralgia, numbness, paraesthesia
Ataxia

71
Q

What is a clinically isolated syndrome in terms of multiple sclerosis?

A

The first episode of neurological signs and symptoms due to demyelination
MS cannot yet be diagnosed as not “disseminated in time and space”

72
Q

What are the classical features of optic neuritis?

A

Central scotoma (enlarged blind spot)
Pain on eye movement
Impaired colour vision
Relative afferent pupillary defect

73
Q

What are other causes of optic neuritis?

A

Sarcoidosis
SLE
Diabetes
Syphilis
Measles
Mumps
Lyme disease

74
Q

What is the treatment of MS relapses?

A

Methylprednisolone

75
Q

What is the treatment of the symptoms of MS?

A

Exercise –> Weakness
Gabapentin/amitriptyline –> Pain
SSRIs –> Depression
Anticholinergic medication –> Incontinence
Baclofen –> Spasticity

76
Q

What is the clinical presentation of Guillain-Barre syndrome?

A

Symmetrical ascending weakness starting in the feet
Reduced reflexes
Peripheral loss of sensation or neuropathic pain
May progress to cranial nerves and cause facial nerve weakness

77
Q

What feature of the PMH suggests Guillain-Barre syndrome?

A

Gastroenteritis

78
Q

What is the management of Guillain-Barre syndrome?

A

IV immunoglobulins (or plasma exchange)
Supportive
VTE prophylaxis –> PE is leading cause of death

79
Q

What are the signs of upper motor neuron disease?

A

Increased tone/spasticity
Brisk reflexes
Upgoing plantar reflex

80
Q

What are the signs of lower motor neuron disease?

A

Muscle wasting
Reduced tone
Fasciculations
Reduced reflexes

81
Q

What is the typical presentation of a patient with MND?

A

Increased fatigue
Clumsiness
Dropping things
Tripping over
Dysarthria

82
Q

What is the management of ALS?

A

No effective treatment for slowing or reversing disease progression
Riluzole used to extend survival by a few months

83
Q

What is neurofibromatosis?

A

A genetic condition causing nerve tumours to develop throughout the body
The tumours are benign but can cause neurological and structural problems

84
Q

What is the diagnostic criteria for neurofibromatosis?

A

Cafe-au-lait spots
Relation with NF1 gene
Axillary or inguinal freckles
Bony dysplasia (bowing of the legs, sphenoid wing dysplasia
Iris hamartomas (Lisch nodules) –> Yellow/brown spots on the iris
Glioma of the optic nerve

CRABING –> At least 2/7 for diagnosis

85
Q

What is the management of neurofibromatosis?

A

No treatment
Control symptoms and monitor

86
Q

What bacteria is involved in meningitis?

A

Neisseria meningitidis
Streptococcus pneumoniae
Group B Streptococcus (neonates)

87
Q

What is the typical presentation of meningitis?

A

Fever
Neck stiffness
Vomiting
Headache
Photophobia
Altered consciousness
Seizures
Non-blanching rash –> In children if meningococcal septicaemia

88
Q

What would the CSF show in bacterial meningitis?

A

Turbid appearance
Raised polymorphs
Raised protein
Low glucose

89
Q

What 2 special tests can be used to diagnose meningitis?

A

Kernig’s test –> Lying on their back, the patient flexes their knee and hip to 90 degrees and then straightens. This would cause spinal pain or resistance to the movement
Brudzinski’s test –> Lying on their back, the patients head and neck are lifted up and the chin is flexed to the chest. This causes involuntary flexion of the hips and knees

90
Q

What is the management of meningococcal septicaemia?

A

IV benzylpenicillin –> In community, unless contraindicated (allergy etc)
Urgent admission to hospital

91
Q

What investigations should be performed in suspected meningitis?

A

Blood culture
Lumbar puncture
Meningococcal PCR

92
Q

What is the management of bacterial meningitis?

A

<3 months = Cefotaxime + amoxicillin
>3 months = Ceftriaxone

93
Q

What are common causes of viral meningitis?

A

HSV
Enterovirus
VZV

94
Q

What are risk factors for intracranial bleeds?

A

Head injury
Hypertension
Aneurysms
Brain tumours
Anticoagulants

95
Q

What is the presentation of an intracranial bleed?

A

Seizures
Weakness
Vomiting
Reduced consciousness

All sudden onset

96
Q

What are the scoring points on the Glasgow Coma Scale?

A

Eyes

Spontaneous = 4
Move to speech = 3
Move to pain = 2
None = 1

Speech

Orientated = 5
Confused conversation = 4
Inappropriate words = 3
Incomprehensible sounds = 2
None = 1

Motor

Obeys commands = 6
Localised to pain = 5
Normal flexion to pain = 4
Abnormal flexion to pain = 3
Extends to pain = 2
None = 1

97
Q

How does a subdural haemorrhage present on a CT scan?

A

Crescent shape not limited by cranial sutures

98
Q

How does a extradural haemorrhage present on a CT scan?

A

Bi-convex shape limited by cranial sutures

99
Q

What are the principles of management with a intracranial haemorrhage?

A

Immediate CT
Check FBC and clotting
Consider surgical treatment

100
Q

What is the main presenting feature of a subarachnoid haemorrhage?

A

Sudden onset thunderclap headache during strenuous activity

Also:
Neck stiffness
Photophobia
Vision changes
Neurological symptoms

101
Q

What are risk factors for subarachnoid haemorrhage?

A

Hypertension
Smoking
Excessive alcohol
Cocaine use
Family history

102
Q

What is a common complication that can occur after a subarachnoid haemorrhage?

A

Vasospasm

103
Q

What is the management of vasospasm?

A

Nimodipine

104
Q

What are the features of benign essential tremor?

A

Fine tremor
Symmetrical
More prominent on voluntary movement
Worse when tired or stressed
Improves with alcohol
Absent during sleep

105
Q

What is the management of benign essential tremor?

A

No definitive treatment
Does not require treatment unless causing functional or psychological problems
Propranolol or primidone to improve symptoms

106
Q

What drugs are used as first line treatment of neuropathic pain?

A

Amitriptyline
Duloxetine
Gabapentin
Pregabalin

107
Q

What is the difference in presentations between UMN and LMN facial palsy?

A

UMN –> Forehead sparing
LMN –> Cannot move forehead on affected side

108
Q

What is the importance in distinguishing between UMN and LMN facial palsies?

A

UMN should be referred urgently as suspected stroke
LMN can be reassured and managed in the community

109
Q

What is the presentation of Bell’s palsy?

A

Unilateral LMN facial nerve palsy

110
Q

What is the management of Bell’s palsy?

A

If presenting within 72 hours, prednisolone 50mg for 10 days

111
Q

What is the presentation of Ramsay-Hunt syndrome?

A

Unilateral LMN facial nerve palsy
Painful and vesicular rash in the ear canal, pinna and around the ear (due to VZV)

112
Q

What is the treatment of Ramsay-Hunt syndrome?

A

Prednisolone and aciclovir

113
Q

At what age does myasthenia gravis typically affect men and women?

A

Women –> Under 40
Men –> Over 60

114
Q

What sort of tumour has a strong link with myasthenia gravis?

A

Thymus gland tumour

115
Q

What is the pathophysiology of myasthenia gravis?

A

ACh receptor antibodies produced
Ab bind to postsynaptic NMJ receptors
Blocks the receptor and prevents stimulation –> muscle weakness

116
Q

What is the presentation of myasthenia gravis?

A

Muscle weakness
Diplopia (extraocular muscles)
Ptosis (eyelid muscles)
Weakness in facial movements
Dysphagia
Fatigue in jaw when chewing
Slurred speech
Weakness worsens as the day progresses

117
Q

Which antibodies are most strongly associated with myasthenia gravis?

A

Anti-ACh-R antibodies

118
Q

What is the treatment for myasthenia gravis?

A

Acetylcholinesterase inhibitors eg. pyridostigmine, neostigmine –> Improves symptoms by increasing ACh in NMJ
Immunosuppression eg. prednisolone, azathioprine –> Suppresses production of Ab
Thymectomy
Monoclonal antibodies eg. Rituximab

119
Q

What is a myasthenic crisis?

A

An acute worsening of myasthenia gravis symptoms, often due to another illness eg. RTI, resulting in weakness of ventilation muscles

120
Q

What is the management of a myasthenic crisis?

A

Invasive/non-invasive ventilation
IV immunoglobulins
Plasma exchange

121
Q

What is Lambert-Eaton syndrome?

A

A more subtle but equally severe form of myasthenia gravis

122
Q

In what disease does Lambert-Eaton syndrome typically occur?

A

Small-cell lung carcinoma

123
Q

What is the management of Lambert-Eaton syndrome?

A

Amifampridine
Immunosuppressants eg. prednisolone, azathioprine
IV immunoglobulins
Plasmapheresis

124
Q

What is the inheritance pattern of Charcot-Marie-Tooth disease?

A

Autosomal dominant

125
Q

What are the classical features of Charcot-Marie-Tooth disease?

A

High foot arches
Distal muscle wasting (“inverted champagne bottle legs”)
Weakness of the lower legs (particularly loss of ankle dorsiflexion)
Weakness in the hands
Reduced tendon reflexes
Reduced muscle tone
Peripheral sensory loss
Peripheral neuropathy

126
Q

What are the causes of peripheral neuropathy?

A

Alcohol
B12 deficiency
Cancer, CKD, Charcot-Marie-Tooth disease
Diabetes, Drugs (isoniazid, amiodarone, cisplatin)
Every vasculitis

ABCDE for other causes of peripheral neuropathy

127
Q

What is the management of Charcot-Marie-Tooth disease?

A

No treatment to alter of prevent progression
Physiotherapy

128
Q

What is the Cushing reflex a response to?

A

Raised intracranial pressure

129
Q

What is the Cushing reflex?

A

Bradycardia
Hypertension with widening pulse pressure
Irregular breathing

130
Q

What is Weber’s syndrome?

A

Midbrain stroke

131
Q

Occlusion of which vessel causes Weber’s syndrome?

A

Posterior cerebral artery

132
Q

What are the signs of Weber’s syndrome?

A

Oculomotor nerve palsy (eye down and out) with contralateral hemiparesis

133
Q

What features must be present to diagnose a total anterior circulation stroke?

A

All three of:
Unilateral weakness (+/- sensory deficit) in the face, arm and leg
Homonymous hemianopia
Higher cerebral dysfunction (dysphasia, visuospatial disorder)

134
Q

What features must be present to diagnose a partial anterior circulation stroke?

A

2/3 of:
Unilateral weakness (+/- sensory deficit) in the face, arm and leg
Homonymous hemianopia
Higher cerebral dysfunction (dysphasia, visuospatial disorder)

135
Q

What is a lacunar stroke?

A

A stroke affecting the perforating arteries around the internal capsule, thalamus and basal ganglia
Presentations are purely motor, purely sensory or ataxic hemiparesis

136
Q

What is lateral medullary syndrome?

A

Occlusion of posterior inferior cerebellar artery

137
Q

What is the presentation of lateral medullary syndrome?

A

Ipsilateral facial numbness, ipsilateral Horner’s syndrome, ataxia and dysphagia but contralateral limb sensory loss

138
Q

What is lateral pontine syndrome?

A

Occlusion of the anterior inferior cerebellar artery

139
Q

What is the presentation of lateral pontine syndrome?

A

Ipsilateral facial pain and temperature loss
Ipsilateral facial paralysis
Ipsilateral deafness
Contralateral limb pain and temperature loss
Ataxia
Nystagmus

140
Q

What would a lesion in the ophthalmic/retinal artery cause?

A

Amaurosis fugax

141
Q

What would a lesion in the basilar artery cause?

A

Locked-in syndrome

142
Q

What are the features of Creutzfeldt-Jakob disease?

A

Rapid onset dementia
Myoclonus

143
Q

What is a pontine stroke a complication of?

A

Chronic uncontrolled hypertension

144
Q

What is the presentation of a pontine stroke?

A

Reduced GCS
Quadriplegia
Miosis
Absent horizontal eye movements

145
Q

What is the ROSIER score?

A

Recognition Of Stroke In the Emergency Room

Used to differentiate between stroke and stroke mimics

146
Q

What is the NIHSS tool?

A

National Institutes of Health Stroke Scale

Used to objectively measure impairment caused by stroke

147
Q

What diagnostic blood test can differentiate between a true and a pseudoseizure?

A

Prolactin

Elevated prolactin 10-20 minutes after an episode in true seizure

148
Q

What is the classic triad for normal pressure hydrocephalus?

A

Urinary incontinence
Dementia
Gait disturbance

149
Q

What does normal pressure hydrocephalus look like on neuroimaging?

A

Ventricular enlargement out of proportion to sulcal enlargement

150
Q

What is syringomyelia?

A

Collection of CSF within the spinal cord

151
Q

What is the presentation of syringomyelia?

A

Cape-like distribution of:
Loss of temperature/pain (spinothalamaic most anterior so first affected)
Intact light touch/proprioception/vibration

Phase 3A Revision (23 decks)

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