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Neuro and special senses > Neuro > Flashcards

Neuro Flashcards

1
Q

What are the 2 main causes of strokes

A

Inadequate blood supply (ischaemia/infarction)

Intracranial haemorrhage

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2
Q

What is a transient ischaemic attack

A

Transient neurological dysfunction due to ischaemia/infarction

Often come before full strokes

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3
Q

What is a crescendo TIA

A

2 TIAs in 1 week

High risk of developing stroke

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4
Q

How might a stroke present

A

Sudden onset neurological symptoms

Usually asymmetrical

Weakness of limbs

Facial weakness

Dysphasia (slurred speech)

Vision loss

Sensory loss

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5
Q

What are the risk factors for stroke

A

Cardiovascular disease

Previous stroke/TIA

Atrial fibrillation

Carotid artery disease

Hypertension

Diabetes

Smoking

Vasculitis

Thrombophilia

COCP use

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6
Q

How are strokes recognised in the community

A

FAST

Face

Arms

Speech

Time to call 999

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7
Q

How are strokes recognised in A&E

A

ROSIER

Based on clinical features and duration

Stroke likely if score > 0

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8
Q

What specialist imaging is needed in the recognition of strokes

A

Diffusion-weighted MRI: gold standard

Carotid ultrasound: looks for carotid stenosis (if found, consider endarterectomy/stenting)

Used to establish vascular territories affected

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9
Q

What is the initial management for strokes

A

Admit to specialised stroke centre

Exclude hypoglycaemia

Immediate CT brain (exclude haemorrhage)

Aspirin 300mg stat (after CT, continue for 2 weeks)

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10
Q

What are the definitive managements for stroke

A

Alteplase:

  • Tissue plasminogen activator (breaks down clots)
  • After CT has excluded haemorrhage
  • Monitor for haemorrhage (may need repeat CTs)

Thrombectomy
- Depending on location/duration of clot (not used >24 hrs after onset)

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11
Q

How are TIAs managed

A

Aspirin 300mg daily

Secondary prevention for cardiovascular disease

Seen by stroke specialist within 24 hours

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12
Q

What is the secondary prevention for strokes

A

Clopidogrel 75mg OD

Atorvastatin 80mg

Consider carotid endarterectomy/stenting

Treat modifiable risk factors

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13
Q

What percentage of strokes are caused by intracranial bleeds

A

10-20%

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14
Q

What are the risk factors for intracranial bleeds

A

Head injury

Hypertension

Aneurysms

Ischaemic stroke (can progress to haemorrhage)

Brain tumours

Anticoagulants

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15
Q

How might intracranial bleeds present

A

Sudden onset

Headaches

Seizures

Weakness

Vomiting

Reduced consciousness

Sudden onset neurological symptoms

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16
Q

What is the Glasgow coma scale

A

Used to assess levels of consciousness

Involves eyes, verbal response, and motor response

<8, consider need to secure airway

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17
Q

What is involved in the eyes section of the GCS

A

4 - spontaneous

3 - speech

2 - pain

1 - none

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18
Q

What is involved in the verbal response section of the GCS

A

5 - orientated

4 - confused conversation

3 - inappropriate words

2 - incomprehensible sounds

1 - none

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19
Q

What is involved in the motor response section of the GCS

A

6 - obeys commands

5 - localised pain

4 - normal flexion

3 - abnormal flexion

2 - extends

1 - none

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20
Q

What is a subdural haemorrhage

A

Rupture of bridging veins

Between dura mater and arachnoid mater

Crescent shape on CT (not limited by cranial sutures)

Mostly in elderly and alcoholics (due to brain atrophy)

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21
Q

What is an extradural haemorrhage

A

Rupture of middle meningeal artery

In temporo-parietal region

Associated with temporal bone fractures

Between skull and dura mater

Bi-concave shape on CT (limited by cranial sutures)

Usually young patients with traumatic head injury

Get ongoing headaches

Get improved neurological symptoms, then rapid decline

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22
Q

What is an intracerebral haemorrhage

A

Bleeding into brain tissue

Similar presentation to ischaemic stroke

Can be anywhere in brain tissue

Due to: spontaneous event, bleeding into ischaemic infarct/tumour, ruptured aneurysm

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23
Q

What is a subarachnoid haemorrhage

A

Bleeding into subarachnoid space

Between pia mater and arachnoid membrane

Usually due to rupture of cerebral aneurysms

Very high morbidity and mortality

Typical history: sudden onset occipital headache, during strenuous activity, ‘thunderclap headache’

Associated with cocaine use and sickle cell anaemia

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24
Q

What is the management for intracranial bleeds

A

Immediate CT head

Check FBC and clotting

Admit to specialised stroke unit

Consider surgical treatment

Consider intubation/ventilation/ITU admission if have reduced consciousness

Correct clotting abnormalities

Correct severe hypertension (but avoid hypotension)

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25
Q

How might a subarachnoid haemorrhage present

A

Thunderclap headache

Neck stiffness

Photophobia

Visual changes

Neurological symptoms (speech changes, weakness, seizures, loss of consciousness)

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26
Q

What are the risk factors for subarachnoid haemorrhage

A

Hypertension

Smoking

Alcohol

Family history

Black ethnicity

F>M

45-70

Cocaine use

Sickle cell anaemia

Connective tissue disorders

Autosomal dominant polycystic kidney disease

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27
Q

What investigations are needed for a subarachnoid haemorrhage

A

CT head (first line)

Lumbar puncture (if CT head negative): red cell count raised, xanthochromia

Angiography (CT/MRI): locate source of bleeding

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28
Q

What is the management for a subarachnoid haemorrhage

A

Manage in specialised neurosurgical unit

MDT support

Surgery: repair vessel to prevent re-bleeding, coiling/clipping

Nimodipine: CCB, prevents vasospasms (can cause brain ischaemia)

Lumbar puncture/stent: to treat hydrocephalus

Antiepileptics: if having seizures

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29
Q

What is multiple sclerosis

A

Chronic progressive condition

Disseminated in time and space

Demyelination of neurones in CNS

Immune cells attack myelin

Mostly in young adults

F>M

Re-myelination possible in early disease

Linked to: specific genes (MHC-HLA), EBV, low vitamin D, smoking, obesity

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30
Q

How might multiple sclerosis present

A

Optic neuritis

Eye movement abnormalities

Focal weakness

Focal sensory symptoms

Ataxia

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31
Q

Describe the optic neuritis of multiple sclerosis

A

Most common presentation

Demyelination of optic disc

Loss of vision in one eye

Central scotoma (enlarged blind spot)

Pain on eye movements

Impaired colour vision

Relative afferent pupillary defect

Need urgent ophthalmology review

Treat with steroids for 2-6 weeks

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32
Q

Describe the eye movement disorders of multiple sclerosis

A

Double vision (6th nerve lesion)

Internuclear ophthalmoplegia (unilateral lesions)

Conjugate lateral gaze disorder (when looking laterally towards side of lesion, no movement of affected eye)

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33
Q

Describe the focal weakness of multiple sclerosis

A

Bell’s palsy

Horner’s syndrome

Limb paralysis

Incontinence

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34
Q

Describe the focal sensory symptoms of multiple sclerosis

A

Trigeminal neuralgia

Numbness

Paraesthesia

Lhermitte’s sign (electric shock down spine and into limbs when flexing neck)

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35
Q

Describe the ataxia of multiple sclerosis

A

Problems with coordinating movements

Sensory: loss of proprioception, positive Romberg’s test

Cerebellar

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36
Q

What are the disease patterns of multiple sclerosis

A

Clinically isolated syndrome

Relapsing-remitting

Primary progressive

Secondary progressive

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37
Q

Explain what is meant by clinically isolated syndrome of multiple sclerosis

A

First episode of demyelination and neurological abnormalities

Not enough to diagnose MS (symptoms need to be disseminated in time and space)

More likely to progress to MS if lesions seen on MRI

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38
Q

Explain what is meant by relapsing-remitting multiple sclerosis

A

Most common pattern in initial stages

Episodes of disease, then recovery

Symptoms in different areas in different episodes

Active - new symptoms/lesions on MRI

Not active - no new symptoms/lesions on MRI

Worsening - overall worsening disability over time

Not worsening - no worsening disability over time

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39
Q

Explain what is meant by primary progressive multiple sclerosis

A

Worsening from point of diagnosis

No remissions

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40
Q

What is meant by secondary progressive multiple sclerosis

A

Relapsing-remitting at first then progressive worsening with incomplete remission

Symptoms become more and more permanent

Classifications: active/not active, progressing/not progressing

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41
Q

How is multiple sclerosis diagnosed

A

By a neurologist

Based on clinical picture over time (need to have progressive symptoms for > 1 year)

MRI lesions

Oligoclonal bands in CSF on lumbar puncture

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42
Q

What is the management for multiple sclerosis

A

MDT support

Disease modification: disease modification drugs/biological therapies, aim to induce long term remission

Treating relapses: steroids (methylprednisolone)

Symptomatic treatment: exercise, analgesia (amitriptyline, gabapentin), manage depression, manage urge incontinence (oxybutynin), manage spasticity (baclofen, gabapentin)

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43
Q

What is motor neurone disease

A

Umbrella term

Progressive, ultimately fatal condition where motor neurones stop functioning

No effect on sensory neurones

Upper and lower motor neurones affected

Most common type: amyotrophic lateral sclerosis

Progressive bulbar palsy: affects muscles of talking and swallowing

Present in late middle age

M>F

Usually die of respiratory failure or pneumonia

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44
Q

How might motor neurone disease present

A

Insidious, progressive weakness of muscles throughout body

Increased fatigue on exercise

Drop things

Tripping

Dysarthria

Upper motor neurone signs

Lower motor neurone signs

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45
Q

What are some lower motor neurone signs

A

Muscle wasting

Reduced tone

Fasciculations

Reduced reflexes

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46
Q

What are some upper motor neurone signs

A

Increased tone

Spasticity

Brisk reflexes

Up-going plantars

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47
Q

How is motor neurone disease diagnosed

A

Based on clinical presentation and exclusion of differentials

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48
Q

What is the management for motor neurone disease

A

No effective treatment for halting/reversing progression

Riluzole: slows progressing, extends survival

NIV

End of life care planning

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49
Q

What is Parkinson’s disease

A

Progressive reduction of dopamine in basal ganglia

Get disorders of movement

Usually asymmetrical

Classic triad: resting tremor, rigidity, bradykinesia

Typically presents in older men

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50
Q

How might Parkinson’s disease present

A

Unilateral tremor

Cogwheel rigidity

Bradykinesia

Depression

Sleep disturbances

Anosmia (loss of sense of smell)

Postural instability

Cognitive impairment

Memory problems

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51
Q

Describe the unilateral tremor of Parkinson’s disease

A

4-6 Hz frequency

Pill-rolling tremor

More pronounced when resting

Improves with voluntary movement

Worse when distracted

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52
Q

Describe the cogwheel rigidity of Parkinson’s disease

A

Resistance to passive movement

Tension in limbs, gives way to movement in small increments

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53
Q

Describe the bradykinesia of Parkinson’s disease

A

Movements get slower and smaller

Handwriting gets smaller

Shuffling gait

Difficulty initiating movements

Difficulty turning around when standing

Reduced facial movements and expressions

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54
Q

What is Parkinson’s plus syndrome

A

Multiple system atrophy: Parkinson’s symptoms, autonomic dysfunction, cerebellar dysfunction

Dementia with Lewy bodies: dementia with features of Parkinson’s, progressive cognitive decline, visual hallucinations, delusions, fluctuating consciousness

Progressive supranuclear palsy

Corticobasal degeneration

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55
Q

How is Parkinson’s disease diagnosed

A

By a specialist

Based on clinical features

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56
Q

What is the management for Parkinson’s disease

A

Aim to control symptoms and minimise side effects

Levodopa

COMT inhibitors

Dopamine agonists

Monoamine oxidase-B inhibitors

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57
Q

Explain the role of levodopa in the management of Parkinson’s

A

Synthetic dopamine (boosts levels)

Combines with a drug that stops it being broken down before it reaches the brain (carbidopa, benserazide)

Less effective over time (reserved for when other things stop working)

Side effects: dyskinesia (if dose too high)

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58
Q

Explain the role of COMT inhibitors in the management of Parkinson’s

A

Entacapone

Slow breakdown of levodopa (longer duration of effect)

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59
Q

Explain the role of dopamine agonists in the management of Parkinson’s

A

Mimic dopamine, stimulate dopamine receptors

Less effective than levodopa

Side effects: pulmonary fibrosis

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60
Q

Explain the role of monoamine oxidase-B inhibitors in the management of Parkinson’s

A

Selegiline, rasagiline

Prevent breakdown of dopamine

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61
Q

What is benign essential tremor

A

Common condition associated with older age

Fine tremor

Affects all voluntary muscles (most noticeable in hands)

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62
Q

How might benign essential tremor present

A

Fine tremor

Symmetrical features

More prominent on voluntary movements

Worse when tired/stressed/caffeinated

Improves with alcohol

Absent during sleep

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63
Q

What are the differentials for benign essential tremor

A

Parkinson’s disease

Multiple sclerosis

Huntington’s chorea

Hyperthyroidism

Fever

Medications (especially antipsychotics)

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64
Q

What is the management for benign essential tremor

A

No definitive treatment

Only need treatment if causing functional/psychological problems

Propranolol (beta blocker)

Primidone (barbiturate anti-epileptic)

65
Q

What is epilepsy

A

Umbrella term for conditions where there is a tendency to have seizures

66
Q

What are seizures

A

Transient episodes of abnormal electrical activity in the brain

67
Q

What are the investigations for epilepsy

A

EEG (typical patterns in different forms)

MRI brain (diagnose structural problems/tumours)

ECG (exclude cardiac conditions)

68
Q

What are generalised tonic-clonic seizures

A

Loss of consciousness

Muscle tensing, muscle jerking

Associated features: tongue biting, incontinence, groaning, irregular breathing

Prolonged post-ictal period (confused, drowsy, irritable, depressed)

Management

  • First line: sodium valproate
  • Second line: lamotrigine, carbamazepine
69
Q

What are focal seizures

A

Start in temporal lobe

Affect hearing, speech, memory, emotions

Presentation: hallucinations, flashbacks, deja vu, doing strange things on autopilot

Management:

  • First line: carbamazepine, lamotrigine
  • Second line: sodium valproate, levetiracetam
70
Q

What are absence seizures

A

Usually in children, stop as get older

Blank, stare into space, abruptly return to normal

Unaware of surrounding and don’t respond during episodes

Usually last 10-20 seconds

Management:
- First line: sodium valproate, ethosuximide

71
Q

What are atonic seizures

A

Drop attacks

Brief lapses in muscle tone

Last < 3 minutes

Usually begin in childhood

Often indicative of Lennox-Gastaut syndrome

Management:

  • First line: sodium valproate
  • Second line: lamotrigine
72
Q

What are myoclonic seizures

A

Sudden brief muscle contractions

Patient awake during episode

Often part of juvenile myoclonic epilepsy

Management:

  • First line: sodium valproate
  • Second line: lamotrigine, levetiracetam, topiramate
73
Q

What are infantile spasms

A

Start at around 6 months

Get clusters of body spasms

Poor prognosis (1/3 die by 25)

Management:
- First line: prednisolone, vigabatrin

74
Q

What are the maintenance medications for epilepsy

A

Sodium valproate

  • First line for most types of epilepsy
  • Increase activity of GABA
  • Side effects: teratogenic, liver damage, hepatitis, hair loss, tremor

Carbamazepine:

  • First line for focal seizures
  • Side effects: agranulocytosis, aplastic anaemia, induces P450 system

Phenytoin:
- Side effects: vitamin D/folate deficiency, megaloblastic anaemia, osteomalacia

Ethosuximide:
- Side effects: night terrors, rashes

Lamotrigine:
- Side effects: Steven-Johnson syndrome, leukopenia

75
Q

What is status epilepticus

A

Medical emergency

Seizure lasting >5 mins

3 seizures in 1 hour

Management: ABCDE, IV lorazepam (4mg, repeat if needed), if persistent - IV phenobarbital/IV phenytoin

Community management: buccal midazolam, rectal diazepam

76
Q

What is neuropathic pain

A

Abnormal function of sensory nerves

Get abnormal painful signals to brain

77
Q

What are the causes of neuropathic pain

A

Postherpetic neuralgia (from shingles)

Nerve damage from surgery

Multiple sclerosis

Diabetic neuralgia

Complex regional pain syndrome

78
Q

What are the typical features of neuropathic pain

A

Burning

Tingling

Pins and needles

Electric shocks

Loss of sensation to touch

79
Q

What are the investigations for neuropathic pain

A

DN4 questionnaire

Score > 4 indicates neuropathic pain

80
Q

What is the management for neuropathic pain

A

Amitriptyline

Duloxetine

Gabapentin

Pregabalin

Try all 4 in turn if not responding

Other options: tramadol, capsicin cream, physio, psychology input

81
Q

What is complex regional pain syndrome

A

Often triggered by injury to a localised area

Neuropathic pain

Skin flushing

Swelling

Abnormal hair growth

Solar changes

Temperature changes

Abnormal sweating

82
Q

What is facial nerve palsy

A

Isolated dysfunction of facial nerve

Usually presents with unilateral facial weakness

83
Q

What are the branches of the facial nerve

A

Temporal

Zygomatic

Buccal

Marginal mandibular

Cervical

84
Q

How might facial nerve palsies present

A

Upper motor neurone lesions - forehead sparing

Lower motor neurone lesions - forehead affected

85
Q

What is Bell’s palsy

A

Idiopathic cause of facial nerve palsy

Relatively common

Unilateral lower motor neurone lesion

Most recover in a few weeks (can take a year)

Management:

  • If present within 72 hours: prednisolone
  • Lubricating eye drops
  • If develop eye pain, urgent ophthalmology review (exposure keratopathy)
86
Q

What is Ramsay-Hunt syndrome

A

Due to varicella zoster virus

Unilateral lower motor neurone facial nerve palsy

Painful and tender rash in ear canal pinna, around ear

Management:
- If present within 72 hours: prednisolone, aciclovir, lubricating eye drops

87
Q

What are the less common causes of facial nerve palsy

A

Infection: otitis media, malignant otitis externa, HIV, Lyme disease

Systemic disease: diabetes, sarcoidosis, leukaemia, multiple sclerosis, Guillain-Barre syndrome

Tumours: acoustic neuroma, parotid tumours, cholesteatomas

Trauma: direct nerve trauma, damage during surgery, basal skull fracture

88
Q

How might brain tumours present

A

Often asymptomatic

Focal neurological symptoms

Signs of raised ICP (papilloedema, altered mental state, visual field defects, seizures, 3rd/6th nerve palsy)

Headaches (constant, nocturnal, worse on waking, worse on straining/coughing/bending, vomiting)

89
Q

What are the types of brain tumours

A

Secondary metastasis:
- Commonly from lung, breast, renal cell carcinoma, melanoma

Glioma:

  • Tumour of glial cells in spinal cord
  • Subtypes: astrocytoma, oligodendroglioma, ependymoma

Meningioma:

  • Tumour of meninges
  • Takes up lots of space, so raised ICP symptoms

Pituitary tumours:

  • Usually benign
  • Can compress optic chiasma (bitemporal hemianopia)
  • Hormonal imbalance: acromegaly, hyperprolactinoma, Cushing’s, thyrotoxicosis

Acoustic neuroma:

  • Tumour of schwann cells surrounding auditory nerve
  • Classic symptoms: hearing loss, tinnitus, balance issues
  • May have facial nerve palsy
90
Q

What is the management for brain tumours

A

Surgery

Chemotherapy

Radiotherapy

Palliative care

91
Q

What is Huntington’s chorea

A

Autosomal dominant condition

Progressive deterioration of nervous system

Symptoms start at 30 - 50

Genetic mutation in HHT gene

Anticipation effect: each generation gets more repeats of faulty gene

92
Q

How might Huntington’s chorea present

A

Insidious, progressive worsening of symptoms

Cognitive problems

Psychiatric issues

Mood issues

Chorea (involuntary, abnormal movements)

Eye movement disorders

Speech difficulties

Dysphagia

93
Q

What is the management for Huntington’s chorea

A

No treatment to stop/slow progression

Supportive MDT care

Medications to stop abnormal movements (olanzapine, diazepam, tetrabenazine)

94
Q

What is the prognosis for Huntington’s chorea

A

Life expectancy 15-20 years from onset

Death often due to pneumonia

High risk of suicide

95
Q

What is myasthenia gravis

A

Autoimmune condition

Antibodies against ACh receptor (stop action potentials)

Muscle specific kinase (MuSK) antibodies

Progressive muscle weakness with activity

Improves with rest

Women < 40

Men > 60

Strongly linked to thymoma

96
Q

How might myasthenia gravis present

A

Muscle weakness - worse with activity, improves with rest

Proximal muscles affected

Diplopia

Ptosis

Weak facial movements

Dysphagia

Fatigue in jaw when chewing

Slurred speech

Progressive weakness

97
Q

How can the signs of myasthenia gravis be elicited

A

Ptosis on repeated blinking

Diplopia on prolonged upward gaze

Unilateral weakness on abducting arm 20 times

98
Q

What are the investigations for myasthenia gravis

A

Specific antibodies:

  • ACh receptor (ACh R)
  • Muscle-specific kinase antibody (MuSK)
  • Low-density lipoprotein receptor-related protein 4 antibody (LRP4)

CT/MRI thymus

Edrophonium test (give edrophonium chloride, stops breakdown of ACh, levels of ACh in neuromuscular junction increase, temporary relief)

99
Q

What is the management for myasthenia gravis

A

Reversible ACh inhibitors (increase amount of ACh in neuromuscular junctions)

Steroids (suppress production of antibodies)

Thymectomy (even if don’t have thymoma)

Monoclonal antibodies (rituximab)

Plasmapheresis

100
Q

What is myasthenia crisis

A

Severe complication of myasthenia gravis

Slack facial muscles, weak neck, drooling, nasal speech, general weakness, unsafe swallow

Acute worsening of symptoms

Often triggered by infection

Management:

  • NIV/intubation
  • Immunomodulatory therapies (IV immunoglobulins, plasma exchange)
101
Q

What is Lambert-Eaton myasthenic syndrome

A

Progressive muscle weakness with increased use

Damage to neuromuscular junctions

In patients with small cell lung cancer (get antibodies against voltage-gated calcium channels, so impaired release of ACh)

102
Q

How might Lambert-Eaton myasthenic syndrome present

A

Proximal muscle weakness (diplopia, ptosis, slurred speech, dysphagia)

Autonomic dysfunction (dry mouth, blurred vision, impotence, dizziness)

Reduced tendon reflexes (can have post-tetanic potentiation - normal reflexes after strong muscle contractions)

103
Q

What is the management for Lambert-Eaton myasthenic syndrome

A

Amifampridine (more ACh released into neuromuscular junctions)

Immunosuppressants

IV immunoglobulins

Plasmapheresis

104
Q

What is Charcot-Marie-Tooth disease

A

Inherited condition (autosomal dominant)

Affects peripheral motor and sensory nerves

Lots of subtypes

Symptoms start at 10 - 40

105
Q

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

A

High foot arches

Distal muscle wasting

Weakness in lower legs

Loss of ankle dorsiflexion

Weakness in hands

Reduced tendon reflexes

Reduced muscle tone

Peripheral sensory loss

106
Q

What are the causes of peripheral neuropathy

A

Alcohol

B12 deficiency

Cancer

CKD

Diabetes

Vasculitis

107
Q

What is the management for Charcot-Marie-Tooth disease

A

Nothing to stop/slow progression

MDT support

108
Q

What is Guillain-Barre syndrome

A

Acute paralytic polyneuropathy

Affects peripheral nervous system

Get acute, symmetrical, ascending muscle weakness

Usually triggered by infection

Body makes antibodies that attack myelin sheath of nerve cells

Clinical course: symptoms within 4 weeks of infection, peak after 2-4 weeks, resolve over months-years

109
Q

How might Guillain-Barre syndrome present

A

Symmetrical ascending weakness

Reduced reflexes

Peripheral loss of sensation

Peripheral neuropathic pain

Facial weakness

110
Q

What are the investigations for Guillain-Barre syndrome

A

Clinical diagnosis based on Brighton criteria

Nerve conduction studies (reduced signal)

Lumbar puncture (raised protein, normal cell count, normal glucose)

111
Q

What is the management for Guillain-Barre syndrome

A

IV immunoglobulins

Plasma exchange

Supportive care

VTE prophylaxis (PE leading cause of death)

112
Q

What are the complications of Guillain-Barre syndrome

A

Respiratory failure

Pain

VTE

SIADH

Renal failure

Hypercalcaemia

113
Q

What is the prognosis for Guillain-Barre syndrome

A

80% recover

15% left with neurological disability

5% die

114
Q

What is neurofibromatosis

A

Benign nerve tumours throughout nervous system

Autosomal dominant

Defect in gene coding for neurofibromin protein

Types 1 (more common) and 2

115
Q

What is the diagnostic criteria for neurofibromatosis 1

A

Need 2 of 7

CRABBING

Cafe au lait spots

Relative with NF1

Axillary/inguinal freckles

Bony dysplasia

Iris haematomas

Neurofibromas

Glioma of optic nerve

116
Q

What are the investigations for neurofibromatosis

A

Clinical diagnosis

Genetic testing

X-ray of long bones

117
Q

What is the management for neurofibromatosis

A

No treatment

Aim to control symptoms

118
Q

What are the complications of neurofibromatosis

A

Migraines

Epilepsy

Renal artery stenosis

Hypertension

Learning disability

Scoliosis

Loss of vision

Malignant peripheral nerve sheath tumours

GI stromal tumours

Brain tumours

Spinal cord tumours

Increased risk of cancer

119
Q

What is neurofibromatosis 2

A

Development of schwannomas

Get acoustic neuromas

120
Q

What is tubular sclerosis

A

Get hamartomas (benign neoplastic growths of tissues that they come from)

Can affect skin, brain, lung, heart, kidney, eye

Due to mutations in TSC1 or TSC2 genes (get uncontrolled cell size and growth)

121
Q

How might tuberous sclerosis present

A

Mostly children with epilepsy and skin features

Skin signs

Neurological features

Rhabdomyomas in heart

Gliomas

Polycystic kidneys

Retinal hamartomas

122
Q

What are the skin signs of tuberous sclerosis

A

Ash leaf spots (depigmented areas)

Shagreen patches (thickened, dimpled, pigmented patches)

Angiofibromas (skin coloured/pigmented papules)

Subungual fibromata (lumps under nails)

Cafe au lait spots (mild pigmented lesions)

Poliosis (isolated patch of white in head/facial hair)

123
Q

What are the neurological features of tuberous sclerosis

A

Epilepsy

Learning disability

Developmental delay

124
Q

What is the management for tuberous sclerosis

A

Supportive

Monitor and treat complications

125
Q

What are the red flags for headaches

A

Fever, photophobia, stiff neck (meningitis, encephalitis)

New neurological symptoms (haemorrhage, malignancy, stroke)

Dizziness (stroke)

Visual disturbances (temporal arteritis, glaucoma)

Sudden onset occipital headache (subarachnoid haemorrhage)

Worse on coughing or straining (raised ICP)

Postural, worse on lying/bending (raised ICP)

Severe enough to wake from sleep

Vomiting (raised ICP, CO poisoning)

History of trauma (intracranial haemorrhage)

Pregnancy (pre-eclampsia)

126
Q

What are the investigations for headaches

A

Fundoscopy (look for papilloedema)

127
Q

Explain tension headaches

A

Bank-like pattern around head

Frontalis, temporalis, occipital pain

Come on and resolve gradually

Associated with: stress, depression, alcohol, skipping meals, dehydration

Management: reassurance, basic analgesia, relaxation techniques, hot towel to area

128
Q

Explain secondary headaches

A

Non-specific

Due to:

  • Underlying medical condition
  • Alcohol
  • Head injury
  • CO poisoning
129
Q

Explain sinusitis headaches

A

Headaches associated with inflammation of sinuses

Facial pain (behind nose/forehead/eyes)

Tenderness over sinuses

Resolves in 2-3 weeks

Usually viral

Management: steroid nasal spray (if prolonged), consider antibiotics

130
Q

Explain analgesic headaches

A

Due to long term analgesia use

Non-specific features

Management: withdraw analgesia

131
Q

Explain hormonal headaches

A

Related to low oestrogen

Generic, non-specific

Typical timing: 2/3 days before period, around menopause, pregnancy

Improve with COCP use

132
Q

Explain cervical spondylosis

A

Degenerative changes in cervical spine

Get headache and neck pain

133
Q

Explain trigeminal neuralgia

A

Compression of trigeminal nerve

90% unilateral

Linked to multiple sclerosis

Intense facial pain (seconds to hours)

Shooting pains

Triggers: cold weather, spicy food, caffeine, citrus fruits

Management: carbamazepine, surgery to decompress nerve

134
Q

What are the different types of migraines

A

Migraine with aura

Migraine without aura

Silent migraines (with aura, without headache)

Hemiplegic migraine

135
Q

How might migraines present

A

Headache for 4-72 hours

Moderate to severe

Pounding/throbbing sensation

Usually unilateral

Photophobia

Phonophobia

May have nausea and vomiting

136
Q

What is an aura

A

Visual changes associated with migraines

Sparks, blurring, lines, loss of visual fields

137
Q

What are hemiplegic migraines

A

Mimic strokes

Sudden or gradual onset

Hemiplegia

Ataxia

Changes in consciousness

138
Q

What are the triggers for migraines

A

Stress

Bright lights

Strong smells

Certain foods (chocolate, cheese, caffeine)

Dehydration

Menstruation

Abnormal sleep pattern

Trauma

139
Q

What are the stages of a migraine

A

Prodromal: 3 days before headache, yawning, fatigue, mood changes

Aura: up to 60 mins

Headache: 4-72 hours

Resolution: headache fades, relieved by vomiting/sleeping

Postdromal: recovery

140
Q

What is the acute management for migraines

A

Lie down in dark room

Paracetamol

Triptans (sumatriptan as migraine starts)

NSAIDs

Antiemetics

141
Q

What is the prophylactic management for migraines

A

Avoid triggers

Acupuncture

B2 supplements

To reduce frequency and severity: propranolol, topiramate, amitriptyline

142
Q

What are cluster headaches

A

Severe, unbearable, unilateral headaches

Usually around eye

Come in clusters of attacks

Last 15 mins - 3 hours

143
Q

How might cluster headaches present

A

Unilateral symptoms

Red, swollen, watery eye

Pupil constriction

Eyelid drooping

Nasal discharge

Facial sweating

144
Q

What is the management for cluster headaches

A

Acute: triptans (subcut), high flow oxygen

Prophylaxis: verapamil, lithium, prednisolone (breaks cycle during clusters)

145
Q

What are the upper motor neurone lesion signs

A

Increased tone

Clonus

Weakness

Brisk tendon reflexes

Extensor plantars

146
Q

What are the lower motor neurone lesion signs

A

Muscle wasting

Fasciculations

Reduced tone

Reduced/absent tendon reflexes

Flexor plantars

147
Q

What are the side effects of anticholinergics

A

Miosis

SSLUDGE syndrome: salivation, sweating, lacrimation, urinary incontinence, diarrhoea, GI upset, emesis

148
Q

Explain CN 1

A

Olfactory

Sense of smell

149
Q

Explain CN 2

A

Optic

Visual acuity

150
Q

Explain CN 3

A

Oculomotor

Extrinsic eye muscles, LPS, sphincter pupillae

151
Q

Explain CN 4

A

Trochlear

Superior oblique

152
Q

Explain CN 5

A

Trigeminal (branches: ophthalmic, maxillary, mandibular)

Facial sensation

Muscles of mastication

153
Q

Explain CN 6

A

Abducens

Lateral rectus

154
Q

Explain CN 7

A

Facial

Muscles of facial expression

Taste anterior 2/3 tongue

155
Q

Explain CN 8

A

Vestibulocochlear

Hearing

Balance

156
Q

Explain CN 9

A

Glossopharyngeal

Pharyngeal sensation

Taste posterior 1/3 tongue

157
Q

Explain CN 10

A

Vagus

Movement of soft palate, pharynx, laryns

158
Q

Explain CN 11

A

Accessory

Movement of SCM and trapezius

159
Q

Explain CN 12

A

Hypoglossal

Tongue movement

Neuro and special senses (4 decks)

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