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Year 3 diagnosis and management > Neuroscience > Flashcards

Neuroscience Flashcards

1
Q

Cause of Bell’s palsy?

A

Idiopathic

• 60% preceded by upper respiratory tract infection

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2
Q

Symptoms and signs of Bell’s palsy?

A
  • Prodromal pre-auricular pain
  • Unilateral facial weakness and drop
  • Hyperacusis (stapedius paralysis)
  • Tearing or drying of exposed eye

• Bell’s phenomenon - eyeball rolls up but eyelids remain open when trying to close their eyes

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3
Q

Investigation for Bell’s palsy?

A
  • Clinical diagnosis
  • Serology for Borrelia (Lyme disease)
  • EMG, ENoG
  • Glucose - exclude DM
  • MRI - check for SOL
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4
Q

Management for Bell’s palsy?

A
  1. Corticosteroid - oral prednisolone within 72 hours
    • eye protection
  2. Valaciclovir
  3. Surgical decompression
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5
Q

Differentiation of CNS tumours

A

Low-grade
• Grows slowly
• May or may not be treated
• e.g. meningioma

High-grade
• Grows rapidly and aggresively
• e.g. glioma, medulloblastoma

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6
Q

Presentation of CNS tumours?

A
  • Headache - worse in morning when lying down
  • Seizures
  • Progressive focal neurological deficits
  • Papilloedema
  • Behavioural symptoms
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7
Q

Investigation of CNS tumours?

A
  1. CT - quicker
  2. MRI - gold standard (diagnostic)
  3. Histology
  4. Lumbar puncture
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8
Q

Most common cause of encephalitis in UK?

A

HSV-1

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9
Q

Signs of encephalitis?

A
  • Bizzare encephalopathic behaviours
  • Seizures
  • Pyrexia
  • Signs of meningism (neck stiffness, photophobia, Kernig’s test positive)
  • Signs of raised ICP
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10
Q

Investigations for encephalitis?

A
  • CSF - lymphocytosis, elevated protein
  • PCR - HSV
  • CT
  • MRI - better
  • EEG
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11
Q

Classify the different types of seizure?

A

Partial - focal onset
• Simple - consciousness not affected
• Complex - consciousness affected

Generalised - whole brain
• Tonic-clonic - LOC, stiff then jerk
• Absence
• Myoclonic - sudden jerk
• Atonic
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12
Q

Investigations for epilepsy?

A
  • Bloods - transient increase in prolactin
  • EEG
  • CT/MRI
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13
Q

Management of status epilepticus?

A

(seizure >30min but treatment initated 5-10mins)

  1. Resus and ABC
  2. Thiamine + glucose (if hypoglycaemic)
  3. IV lorazepam
  4. IV phenytoin
  5. IV phenobarbital
  6. GA
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14
Q

Management of partial and generalised seizures?

A

> 2 unprovoked seizures

Partial
1. Carbamazepine

Generalised
1. Sodium valproate or Lamotrigine

Start with one, slowly build up dose. If ineffective, switch to next drug and withdraw first drug when second is established.

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15
Q

Location of epi/extradural, subdural and subarachnoid haemorrhage?

A
  • Epidural - between dura mater and skull
  • Subdural - between dura mater and arachnoid mater
  • Subarachnoid - between arachnoid mater and pia mater
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16
Q

Symptoms and signs of epidural haemorrhage?

A
  • Head injury with temporary LOC
  • Lucid interval
  • GCS deterioration and rising ICP
  • Cushing’s reflex - HTN, bradycardia, irregular breathing
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17
Q

What is Guillain-Barre syndrome?

A
  • Acute inflammatory demyelinating polyneuropathy

* Antibodies after recent infection react with self-antigen on myelin

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18
Q

Presentation of GB syndrome?

A
  • < 1 months of ascending symmetrical limb weakness (lower > upper)
  • Ascending paraesthesia
  • Impaired sensation
  • Autonomic dysfunction - sweating, raised pulse, arrhythmias
  • LMN signs
  • Facial nerve weakness
  • Type II resp failure

Miller-Fisher - eyes affected first, descending, anti-GQ1b

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19
Q

Investigation for GB syndrome?

A
  • Nerve conduction studies - slow
  • LP - elevated protein
  • Spirometry - reduced FVC
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20
Q

Causes and presentation of Horner’s syndrome?

A
  • Brainstem - demyelination, stroke
  • Thoracic outlet - Pancoast’s tumour (apical lung)
  • Disruption to nerve at internal carotid artery entry into skull
  • Ptosis
  • Miosis
  • Anhydrosis
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21
Q

Cause of Huntington’s disease?

A
  • Autosomal dominant CAG repeat on Chr 4

* Atrophy - loss of striatum and cortex

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22
Q

Signs of Huntington’s?

A 
(• Dementia)
• Chorea
• Dysarthria
• Slow voluntary saccades
• Supranuclear gaze restriction
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23
Q

Investigation for Huntington’s?

A
  • Genetic - CAG repeat test (>39 repeats)

* MRI/CT - butterfly dilation of lateral ventricles, symmetrical atrophy of striatum

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24
Q

2 main types/causes of hydrocephalus?

A

Obstructive
• Impaired outflow of CSF from ventricular system
• e.g. Lesions of 3rd/4th ventricle or aqueduct

Non-obstructive
• Impaired CSF reabsorption into subarachnoid villi
• e.g. meningitis

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25
Q

Symptoms and signs of obstructive hydrocephalus?

A
  • Acute drop in conscious level
  • Diplopia
  • Papilloedema
  • 6th nerve palsy (diplopia), - longest intracranial path
  • Neonates: increased head circumference, sunset sign
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26
Q

Symptoms and signs of normal pressure hydrocephalus (non-obstructive)?

A

Triad:
• Dementia
• Gait apraxia
• Urinary incontinence

• Hyperreflexia

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27
Q

Investigations for hydrocephalus?

A
  1. CT head (first line but not diagnostic by itself)
  2. CSF - ventricular drain or LP
  3. LP - contraindicated if raised ICP, therapeutic in normal pressure hydrocephalus
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28
Q

Which layers around the brain are inflamed in meningitis?

A

Pia and arachnoid mater

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29
Q

Most common cause of meningitis?

A
  1. Neisseria meningitidis
  2. Streptococcus pneumonia (more common in > 60)

(• Group B strep. most common in neonates)

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30
Q

Signs of meningitis?

A

Meningism
• Photophobia
• Neck stiffness
• Kernig’s sign (knee extension with flexed hips)
• Brudzinski’s sign (hip flexion with flexed neck)

Infection
• Pyrexia
• Tachycardia
• Hypotension
• Skin rash
• Altered mental state
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31
Q

Investigations for meningitis?

A
  1. CT head - exclude lesion or raised ICP

2. CSF (LP) - high WCC (pleocytosis) - most important, can be no.1 if no focal neurology/raised ICP

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32
Q

Management for meningitis?

A
  1. IV antibiotics - 3rd gen cephalosporin e.g. cefoxatime
    • add ampicillin for listeria if > 55
    • pre-hospital (GP), IM benzylpenicillin
    • add vancomycin if resistant
  2. IV dexamethasone with 1st dose of ABx

Targeted therapy once LP performed and bacterium confirmed

33
Q

What are the subtypes of motor neurone disease?

A
  • Amyotrophic lateral sclerosis (ALS) - UMN and LMN
  • Progressive muscular atrophy variant - LMN
  • Progressive bulbar palsy variant - CN 9-12
  • Primary lateral sclerosis variant - Betz cells in motor cortex
34
Q

Symptoms of motor neurone disease?

A
  • Weakness of limbs - proximal myopathy
  • Speech disturbance
  • Swallowing disturbance
  • Behavioural changes
35
Q

UMN and LMN signs of motor neurone disease?

A

UMN
• Spastic weakness
• Extensor plantar response
• Hyperreflexia

LMN
• Flaccid weakness
• Muscle wasting
• Fasciculations
• Hyporreflexia

Sensory = normal

36
Q

Motor neurone disease investigations (6)

A

Clinical diagnosis

  • Bloods - mild elevation in CK, ESR, positive anti-GM1 ganglioside antibodies
  • Nerve conduction studies
  • EMG - reduced AP, increased amplitude
  • MRI - exclude other things
  • Spirometry - respiratory muscle weakness
37
Q

What is MS?

A

Inflammatory demyelinating disease of CNS

38
Q 
Outline the 4 types of MS:
• Relapsing-remitting
• Clinically isolated syndrome
• Primary progressive
• Marburg variant
A
  • Relapsing-remitting - most common, attacks of demyelination with poor healing in between
  • Clinically isolated syndrome - single clinical attack (does not count as MS)
  • Primary progressive - steady accumulation of disability
  • Marburg variant - severe fulminant variant - advanced disability or death within weeks
39
Q

Symptoms of MS?

A

Depends on site of inflammation, usually monosymptomatic - separated in TIME and SPACE

Most common = optic neuritis

Also sensory, motor, autonomic, psychological, sexual, GI and cerebellar signs.

Uhthoff’s sign - worse symptoms in heat
Lhermitte’s sign - electrical sensation runs down back and into limbs when neck is flexed

40
Q

Signs of MS?

A

• Optic neuritis
- impaired visual acuity (most common)
- loss of coloured vision
• Scotoma - blind spot in normal visual field
• Internuclear ophthalmoplegia - problem with adduction of contralateral eye
• Relative afferent pupillary defect - dilation when light swung to diseased eye
• UMN signs

41
Q

Investigations for MS?

A

McDonald criteria - 2 or more CNS lesions disseminated in TIME and SPACE

  • MRI brain, c + t spine - plaques, Dawson fingers
  • LP - unmatched oligoclonal bands, increased IgG
  • Visual evoked potentials - delayed waveform
42
Q

What is myasthenia gravis?

A
  • Autoimmune disease
  • Affects NM junction
  • Weakness in skeletal muscles
43
Q

What are 2 types of myasthenia gravis?

A

Most common - antibodies against nicotinic ACh receptor (less post-synaptic receptor sites)

Lambert-Eaton syndrome - paraneoplastic sybtype, antibodies against pre-synaptic calcium channels (less ACh release)
e.g. from small cell lung cancer

44
Q

Symptoms of myasthenia gravis?

A
  • Muscle weakeness, worse with repetition or at end of day (improves in LE syndrome), order: extraocular => bulbar => face => neck => limb girdle => trunk
  • Ocular - Drooping eyelids, diplopia
  • Bublar - facial weakness (snarl), hypernasal speech
45
Q

Signs of myasthenia gravis?

A
  • Generalised
  • Bublar (CN 9-12, relating to medulla oblongata)
  • Ptosis, complex ophthalmoplegia - ask patient to look up for 1 min, progressive ptosis
  • Ice on eyelids - improves neuromuscular transmission
  • Voice fades when counting to 50 (bulbar)
  • LE syndrome - gait difficulty before eye signs, autonomic involvement (dry eyes)
46
Q

Investigation for myasthenia gravis?

A
  1. Bloods - CK, serums ACh receptor antibody, or MUSK
  2. Pulmonary function tests
  • Nerve conduction
  • EMG
  • CT thorax/ CXR - thymic hyperplasia (or thymoma)
  • Tensilon test (not used) - short-acting anti-AChase => rapid improvement (risk of bradycardia)
47
Q

What is a neurofibromatosis and the chacterisations of the 2 types?

A

Autosomal dominant disorder affecting cells of neural crest origin => multiple neurocutaneous tumours

Type 1
• Peripheral and spinal neurofibromas
• 5+ cafe au lait spots
• Freckling
• Lisch nodules (hamartomas of iris)
• Pheochromocytomas
Type 2
• Schwannomas 
• Meningiomas
• Gliomas (optic nerve is type 1)
• Cataracts
48
Q

Symptoms of neurofibromatosis?

A

Positive family history

Type 1 
• Skin lesion
• Learning difficulties
• Disturbed vision
• Precocious puberty
Type 2
• Hearing loss
• Tinnitus
• Balance problems
• Facial pain/numbness
49
Q

Investigation for neurofibromatosis?

A
  1. MRI/CT - extent of lesions
  2. PET
  3. Biopsy
  4. Genetic testing - confirms diagnosis, but difficult

• Skull X-ray - sphenoid dysplasia in NF1

50
Q

Parkinson’s characterisations?

A

Bradykinesia
Rigidity
Resting tremor
Postural instability

51
Q

2 causes/types of Parkinson’s?

A

Sporadic/idiopathic
• Most common - unknown cause

Secondary
• Neuroleptic therapy e.g. for schizophrenia
• Vascular insults e.g. in basal ganglia

52
Q

Investigations for Parkinson’s?

A

Diagnosis is clinical - if atypical features or unclear clinical diagnosis:

  1. Dopaminergic agent trial (levodopa)
  2. MRI brain

exlude other things like Wilson’s - serum caeruloplasmin

53
Q

Symptoms and signs of raised ICP?

A

(normal <15mmHg)

  • Headache worse on coughing, leaning forward and in the morning
  • Vomiting
  • History of trauma
  • Poor vision
  • Cushing’s response
  • Cheyne-Stokes respiration - progressively deeper and faster - then gradual decrease, temporary stop, cycle repeats
  • Constriction then dilation of pupil
  • Peripheral visual field loss
  • Papilloedema
54
Q

Investigation for raised ICP?

A
  • Bloods
  • Toxicology screen
  • CXR - source of infection
  • CT head
  • LP if safe - measure opening pressure
55
Q

Investigations for spinal cord compression (inc. cauda equina)?

A
  1. MRI spine - imaging study of choice
  2. CT myelography - useful with CT spine when MRI not available
  3. Spine x-ray - limited value, useful with CT spine in trauma setting

• Gadolinium-enhance MRI spine - choice in infection

56
Q

General cause and presentation of spine radiculopathy and example?

A

Spinal nerve ROOT compression (cervical or lumbar most common)

  • Lumbar/sacral - sciatica
  • Dull reflexes
  • LMN weakness and muscle wasting

(UMN signs below level of affected root suggests CORD compression)

57
Q

Investigations for spine radiculopathy?

A 
(full neurological exam)
• MRI
• x-ray and MRI
• EMG 
• Nerve conduction studies
58
Q

2 main causes of stroke?

A

Infarction (80%)
• Thrombosis, emboli (from carotid dissection), hypotension (watershed zones)

Haemorrhagic (20%)
• Hypertension, trauma

59
Q

Signs of anterior circulation infarction?

A

ACA
• Lower limb weakness (hemiparesis)
• Confusion

MCA (classic stroke)
• Facial weakness
• Upper limb weakness (hemiparesis)
• Hemisensory loss
• Hemineglect
• Left sided - aphasia
60
Q

Signs of lacunar infarcts?

A
  • Internal capsule / pons - pure sensory and/or motor deficit
  • Thalamus - LOC, hemisensory deficit
  • Basal ganglia - hemichorea, parkinsonism
61
Q

Signs of posterior circulation infarcts?

A

PCA
• Hemianopia
• Visual agnosia (unable to recognise things)

AICA (anterior inferior cerebellar artery)
• vertigo
• ipsilateral deafness
• ipsilateral facial weakness

PICA
• veritigo
• ipsilateral Horner’s syndrome
• contralateral spinothalamic sensory loss

Basilar artery
• Cranial nerve pathology
• Impaired consciousness (emergency)

Multiple lacunar infarcts - bascular dementia, urinary incontinence

62
Q

Signs of haemorrhagic stroke?

A

Intracerebral
• Headache
• Focal neurological signs
• Raised ICP

Subarachnoid
• Meningism
• Kernig’s sign

63
Q

Investigations for stroke?

A
  1. CT head (non-contrast) - rule out haemorrhage (from ischaemic)
  2. MRI, diffusion-weighted
  3. CT cerebral angiogram - detects dissections or intracranial stenosis (Doppler AC, this for PC)
  • Serum glucose etc. for exclusion of other causes of focal neurological signs
  • PT
  • ECG - arrhythmia common in ischaemic stroke
64
Q

Management for stroke?

A

Hyperacute stroke (< 4.5 hours from onset)

  1. Alteplase (IV recombinant tissue plasminogen activator)
  2. Aspirin 24 hours later

Acute stroke (> 4.5 hours from onset)
1. Aspirin 300mg to prevent further thrombosis
2. Heparin - emboli prophylaxis
• Swallow assessment

Intracerebral haemorrhage
• Neurosurgical evaluation
• Anti-pyretics
• Blood pressure control - labetolol

Secondary prevention

  1. Clopidogrel
  2. Warfarin if AF

• Exclude haemorrhage with CT-head before treatment (and other contra-indications e.g. trauma)

65
Q

Most common cause of TIA?

A
  • Embolic

* Most common source of emboli - carotid atherosclerosis

66
Q

How long do TIAs last?

A

10-15 mins (but can be between a few mins to 24 hours)

67
Q

Investigation for TIA?

A
  1. Bloods - glucose, FBC etc.
  2. MRI with diffusion - confirms ischaemia
  3. Lipid profile - for statin treatment
  • ECG
  • Carotid doppler

(CT only ordered if MRI not available but it is not useful for ischaemia)

68
Q

Management of TIA?

A
  1. 300mg aspirin immediately and assessed urgently within 24 hours

TIA confirmed

  1. Clopidogrel
  2. High-intensity statin therapy
  3. Ezetimibe in some patients
69
Q

Symptoms and signs of subarachnoid haemorrhage?

A
  • Sudden-onset headache - occipital thunder-crap headache
  • Collapse
  • Seizures
• Meningism
- neck stiffness, Kernig's sign
• Pyrexia
• Raised ICP
• GCS deterioration
70
Q

Investigations for subarachnoid haemorrhage?

A
  1. Emergency CT (non-contrast, thin cuts) - diagnostic
  2. CTA/MRA (angiography) if CT is positive - identify pathology
  3. LP if CT is negative (after 12 hours)
  • ECG - ALL patients - arrythmia
  • Bloods - hyperglycaemia, leukocytosis, elevated troponin I
71
Q

3 top causes of subarachnoid haemorrhage?

A
  1. Rupture of saccular aneurysm at base of brain (85%)
  2. Permesencephalic haemorrhage (10%)
  3. Arteriovenous malformations - dissections (5%)

Associated with HTN

72
Q

Classification of subdural haemorrhage?

A
  • Acute < 72 hours
  • Subacute 3-20 days
  • Chronic > 3 weeks
73
Q

Symptoms of different types of subdural haemorrhage?

A

Acute
• trauma with head injury
• reduced consciousness

Subacute
• Headache worsens 7-14 days after injury
• Altered mental state

Chronic
• Headache
• Gait deterioration
• Focal weakness
• Seizures
74
Q

Signs of acute and chronic subdural haemorrhage?

A

Acute
• Ipsilateral fixed dilated pupil (midline shift)
• Pressure on brainstem - reduced consciousness + bradycardia

Chronic
• Neurological examination may be normal
• Focal neurological signs

75
Q

Investigation for subdural haemorrhage?

A
  1. CT head (non-contrast)
  • MRI - not necessary but higher sensitivity
  • Skull x-ray - skull fractures or intracranial shrapnel
76
Q

Management for subdural haemorrhage?

A

Acute

  1. If small - observation, prophylactic anti-epileptics
  2. If large - burr hole craniotomy = craniotomy

Chronic

  1. Conservative + anti-epileptics
  2. Burr hole
  3. Craniotomy
77
Q

Sign’s of Wernicke’s encephalopathy?

A

Triad:
• Confusion
• Ophthalmoplegia (nystagmus, lateral rectus)
• Ataxia (wide based gait)

  • Mentally alert with vocabulary, comprehension an naming ability maintained
  • Polyneuropathy
  • Reflexes may be decreased
78
Q

What is Korsakoff’s psychosis?

A

Deterioration of Wernicke’s encephalopathy with additional symptoms of amnesia and confabulation

79
Q

Investigations for Wernicke’s encephalopathy?

A
  1. Therapeutic trial of parenteral thiamine

2. Bloods (finger-prick glucose, high MCV, thiamine, ABG hypercapnia and hypoxia confusion)

Year 3 diagnosis and management (9 decks)

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