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3rd Year Conditions > Neurology > Flashcards

Neurology Flashcards

1
Q

What is encephalitis?

A

inflammation of brain parenchyma by infection or autoimmune response

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2
Q

Describe the aetiology/risk factors of encephalitis

A
  • usually viral infection
  • HSV, mumps, adenovirus, coxsackie, EBV, HIV,
  • Non-viral = syphilis, Staph.a
  • autoimmune
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3
Q

Presenting symptoms of encephalitis

A
  • self-limiting and mild
  • subacute onset (hours to days)
  • headache
  • fever
  • vomiting
  • behavioural changes
  • history of seizures
  • focal neurological symptoms
  • usually preceded by infectious prodrome (fever, rash, lymphadenopathy, cold sores, conjunctivitis)
  • Travel history
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4
Q

Signs of encephalitis on examination

A
  • reduced consciousness
  • bizarre behaviour
  • deteriorating GCS
  • seizures
  • pyrexia
  • meningism
  • raised ICP (cushing’s response, papilloedema)
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5
Q

Investigations for encephalitis

A
  1. Bloods (high lymphocytes)
  2. MRI/CT to exclude mass lesion
  3. Lumbar puncture (high lymphocytes, high monocytes, high protein)
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6
Q

What is MS?

A

Chronic and progressive condition that involves demyelination of the myelinated neurones in the CNS. Caused by an inflammatory process involving activation of immune cells against myelin.

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7
Q

Causes of MS

A

Unclear but probably influenced by a factor of: multiple genes, EBV, low vitamin D, smoking, obesity

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8
Q

Signs and Symptoms of MS

A
  • optic neuritis (enlarged blind spot, pain on eye movement, impaired colour vision)
  • focal weakness (bells, horners, limb paralysis, incontinence)
  • focal sensory symptoms (trigeminal neuralgia, numbness, paraesthesia)
  • ataxia (sensory or cerebellar)
  • relapsing remitting then progressive or just always progressive
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9
Q

Investigations for MS

A

MRI scans to detect lesions

Lumbar puncture to detect oligoclonal bands

Evoked potentials show delayed conduction velocity

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10
Q

What is a SAH?

A

bleeding into the subarachnoid space, where CSF is located, between the pia mater and the arachnoid membrane. Usually the result of a ruptured cerebral aneurysm.

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11
Q

Presentation of a SAH

A
  • sudden onset occipital headache
  • during strenuous activity
  • neck stiffness
  • photophobia
  • vision changes
  • neurological symptoms
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12
Q

Risk factors for SAH

A
  • hypertension
  • smoking
  • alcohol
  • cocaine
  • family history
  • black
  • female
  • 45- 70
  • sickle cell anaemia
  • connective tissue disorders
  • neurofibromatosis
  • autosomal dominant polycystic kidney disease
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13
Q

Investigations for SAH

A
  • CT head!!!
  • hyperattenuation in subarachnoid space
  • Lumbar puncture - increased red cell count, xanthochromia
  • Angiography to locate source once SAH confirmed
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14
Q

What is epilepsy?

A

Condition where there is a tendency to have seizures

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15
Q

Investigations done for epilepsy

A
  1. EEG shows typical patterns
  2. MRI brain to view structural problems associated with seizures and other pathology
  3. ECG to exclude problems in the heart
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16
Q

Types of seizure found in epilepsy

A
  1. Generalise tonic-clonic seizures - loss of consciousness and tonic and clonic, usually tonic before clonic, prolonged post-ictal period where person is confused, drowsy and irritable or depressed
  2. Focal seizures - start in temporal lobes, affect hearing, speech, memory and emotions, hallucinations, memory flashbacks, Deja vu, doing strange things on autopilot
  3. Absence seizures - children, becomes blank, stares into space and then abruptly returns to normal. Unaware of surroundings and won’t respond. Usually just 10-20 seconds. Usually don’t happen as you get older.
  4. Atonic seizures - drop attacks, brief lapses in muscle tone, usually up to 3 mins, may indicate Lennox-Gastaut syndrome
  5. Myoclonic seizures - sudden, brief muscle contractions, like a sudden jump. Patient remains awake
  6. Infantile spasms - west syndrome. In infants. Clusters of full body spasms. 1/3 due by age 25 but 1/3 are seizure free.
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17
Q

Treatment for epilepsy

A
  1. Sodium valproate - except for focal seizures, has a relaxing effect on the brain by increasing the activity of GABA, avoid in girls and women as it’s teratogenic
  2. Carbamazepine - for focal seizures
  3. Phenytoin
  4. Ethosuximide
  5. Lamotrigine
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18
Q

What is status epilepticus a day how is it treated?

A

Medical emergency where a seizures lasts more than 5 mins or more than 3 seizures in an hour

ABCDE approach

IV lorazepam 4mg repeated after 10 mins if seizure continues

IV phenobarbital or phenytoin if lorazepam doesn’t work

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19
Q

What are tension headaches?

A

the most basic, normal type of headache

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20
Q

What triggers tension headaches?

A 
stress
anxiety
poor posture
fatigue
dehydration
missing meals
bright sunlight
noise
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21
Q

Presenting symptoms of tension headache

A
  • Mild-moderate severity
  • Pressure around head like a band
  • Bilateral
  • Non-pulsatile
  • gradual onset
  • responds to over-the-counter meds
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22
Q

Management for tension headaches

A
  • reassure
  • address triggers
  • avoid meds that cause med-induced headaches
  • simple analgesia
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23
Q

What is trigeminal neuralgia?

A

neuralgia involving one or more of the branches of the trigeminal nerves

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24
Q

Risk factors and aetiology for trigeminal neuralgia

A
  • compression of the trigeminal nerve by artery or vein loop

- could also be secondary to MS or skull base malformation

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25
Q

Presenting symptoms of trigeminal neuralgia

A
  • sudden, unilateral, brief stabbing pain in the distribution of one or more branches of the trigeminal nerve
  • recurrent
  • pain last from a few seconds to a couple of mins
  • triggered by vibration, skin contact, eating, talking, dental prostheses, brushing teeth, exposure to wind
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26
Q

Investigations for trigeminal neuralgia

A
  • diagnosis is clinical

- MRI to exclude secondary causes

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27
Q

What is a subdural haemorrhage?

A
  • collection of blood that develops between the surface of the brain and the dura mater
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28
Q

Causes and risk factors of a subdural haematoma

A
  • Trauma, usually due to rapid acceleration/deceleration of the brain, may have been up to 9 months ago
  • Falls, low ICP, dural metastases, old age, anticoagulation
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29
Q

Presenting symptoms of a subdural haemorrhage

A
  • Acute - history of trauma, reduced conscious level
  • Subacute - worsening headache, 7-14 days after injury, altered mental state

Chronic - headache, confusion, cognitive impairment, gait deterioration, focal weakness, seizures, sleepiness

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30
Q

Signs of subdural haemorrhage on examination

A

Acute - reduced GCS, ipsilateral fixed dilated pupil, reduced consciousness, bradycardia

Chronic - neurological exam may be normal, focal neurological signs

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31
Q

Investigations for subdural haemorrhage

A
  • CT head
  • MRI brain - higher sensitivity than CT
  • Will show clot +/- midline shift
  • crescent shaped collection of blood
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32
Q

Management of subdural haemorrhage

A
  • Watch out for cervical spine injury
  • if raised ICP consider osmotic diuresis
  • surgical for irrigation/evacuation
  • burr hole
    address any causes of the trauma
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33
Q

What is myasthenia gravis?

A

autoimmune disease affecting the NMJ producing weakness in skeletal muscles

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34
Q

Describe the epidemiology of myasthenia gravis

A

Females under 40 or males over 60

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35
Q

Aetiology and risk factors for myasthenia gravis

A
  • autoantibodies against the nicotinic acetylcholine receptor
  • Lambert-Eaton Syndrome where autoantibodies are against the pre-synaptic calcium channels, leading to impaired acetylcholine release
  • associated with thymoma
36
Q

Presentation of myasthenia gravis

A
  • muscle weakness that worsens with repetitive use or towards the end of the day
  • ocular symptoms: drooping eyelids, diplopia
  • bulbar symptoms: facial weakness, hyper nasal speech, difficulty swallowing, chewing, smiling
37
Q

Examination findings for myasthenia gravis

A
  • ptosis when asking them to blink many times
  • upwards gaze will result in worsening of diplopia and ptosis
  • reading aloud: voice fades
  • repeated abduction will cause fatigue quickly
38
Q

Investigations for myasthenia gravis

A
  1. Bloods - CK to exclude myopathies

Serum acetylcholine receptor antibody

MUSK antibodies

  1. Tensilon Test - increases acetylcholine levels and causes a rapid and transient improvement in clinical features
39
Q

Treatment of myasthenia gravis

A
  1. Acetylcholinesterase inhibitors - pyridostigmine or neostigmine
  2. Immunosuppression - steroids or azothioprine
  3. Thymectomy
40
Q

What is Parkinson’s disease?

A
  • neurodegenerative disease of the dopaminergic neurons of the substantia nigra
  • characterised by resting tremor, bradykinesia and rigidity
41
Q

Epidemiology of Parkinson’s

A
  • very common

- 1-2% of over 60s

42
Q

How does Parkinson’s present

A
  • insidious onset
  • resting tremor (one side worse)
  • stiffness and slowness of movements
  • mental slowness
  • shuffling gait
  • micrographia (small hand writing)
  • insomnia
  • anosmia
43
Q

Signs of Parkinson’s on examination

A
  • unilateral pill-rolling tremor, 4-6Hz and decreased on action
  • Rigidity (cogwheel)
  • stopped, shuffling gait with no arm swinging
  • postural instability
  • hypomimia
44
Q

Investigations for Parkinsons

A
  • based on clinical findings
  • levodopa trial (dopamine precursor given and then do a walking test)
  • CT or MRI to rule of other causes of gait decline
45
Q

Management of Parkinson’s

A
  1. Levodopa (synthetic dopamine, given with drug to stop it being broken down before getting to the brain, carbidopa or benserazide)
  2. Dopamine agonists (too much will cause pulmonary fibrosis)
  3. COMT inhibitors (prevent metabolism of levodopa)
  4. Monoamine oxidase B inhibitors
46
Q

What is Wernicke’s Encephalopathy?

A

presence of neurological symptoms caused by biochemical lesions of the CNS system following exhaustion of vitamin B (particularly thiamine/B1) reserves

47
Q

Causes and risk factors of Wernicke’s encephalopathy

A
  • chronic alcohol consumption resulting in thiamine deficiency (inadequate nutritional, decreased absorption, impaired utilisation)
  • eating disorders, malnutrition, prolonged vomiting, GI malignancy, chronic subdural haematoma, AIDS
48
Q

Symptoms of wernicke’s encephalopathy

A
  • diplopia, eye movement abnormalities, ptosis
  • unsteady gait
  • loss of memory
  • inability to form new memories
  • hallucinations
49
Q

Signs of wernicke’s encephalopathy on examination

A
  • confusion, ophthalmoplegia, ataxia
  • abnormal gait and coordination
  • reflexes may be decreased
  • eye abnormalities
  • low temperature
  • rapid pulse
50
Q

Investigations for Wernicke’s encephalopathy

A
  • based on history and exam
  • FBC (high MCV in alcoholics)
  • U&Es
    LFTs
  • Glucose

CT head

51
Q

Treatment of Wernicke’s encephalopathy

A

IV thiamine injection

52
Q

What is an essential tremor?

A
  • progressive, mainly symmetrical, rhythmic, involuntary oscillation movement disorder of the hands and forearms
  • usually absent at rest and present during posture and intentional movements
53
Q

What is motor neuron disease?

A
  • progressive neurodegenerative disorder of cortical, brainstem and spinal motor neurons (lower and upper motor neurons)
  • doesn’t affect sensory neurons
54
Q

How does motor neuron disease present?

A
  • late to middle aged man
  • insidious, progressive weakness of muscles throughout the body affecting the limbs, trunk, face and speech
  • increased fatigue when exercising
  • clumsiness, dropping things, tripping over, dysarthria
55
Q

Signs of motor neuron disease on examination

A
  1. Lower motor neuron signs: muscle wasting, reduced tone, fasciculations, reduced reflexes
  2. Upper motor neuron signs: increased tone or spasticity, brisk reflexes, upgoing plantar responses
56
Q

Investigations for motor neuron disease

A
  • diagnosis made by experienced neurologist based on clinical findings
  • mild elevation in CK
  • normal nerve conduction studies
  • MRI to exclude cord compression and brainstem lesions
57
Q

Treatment for motor neuron disease

A
  • Riluzole may give you a few extra months

- NIV

58
Q

What is a normal ICP in adults?

A

<15mmHg

59
Q

What can cause a raised ICP and what are some risk factors?

A
  • primary or metastatic tumour
  • head injury
  • haemorrhage
  • infection
  • hydrocephalus
  • cerebral oedema
  • status epilepticus
60
Q

Symptoms of raised ICP

A
  • headache which is worse on coughing and leaning forwards, worse in morning
  • vomiting
  • altered GCS
  • poor vision
61
Q

Investigations for raised ICP

A

U&Es, FBC, LFT, glucose, clotting, blood culture

CT head

LP if no chance of coning

62
Q

What is a spinal cord compression?

A
  • pressure injury to the spinal cord with neurological symptoms dependent on the site and extent of the injury
  • cauda equina syndrome is due to damage to the bundle of nerves below the end of the spinal cord (L2)
63
Q

Causes and risk factors of spinal cord compression

A
  • usually trauma and tumours

- trauma, malignancy, osteoporosis, metabolic bone disease, vertebral disc disease

64
Q

Symptoms of cord compression

A

history of trauma or malignancy

pain, weakness, sensory loss, disturbance of bowel and bladder function

65
Q

Signs of spinal cord compression on examination

A
  • normal above level of lesion
  • diaphragmatic breathing
  • reduced anal tone
  • hyporeflexia
  • weakness or paralysis
  • LMN below lesion, UMN above lesion
66
Q

Investigations for spinal cord compression

A

Radiology - X-ray or MRI

Bloods

CXR for primary lung malignancy

67
Q

What is radiculopathy?

A

spinal nerve root compression - usually lumbar or cervical

68
Q

Causes and risk factors of radiculopathy

A
  • herniated disc
  • spinal stenosis
  • degenerative disc disease
  • osteoarthritis
  • facet joint degeneration
  • age
  • overweight
  • poor posture
  • improper lifting technique
69
Q

Primary symptoms of radiculopathy

A

lumbar or sacral radiculopathy is primary cause of sciatica

  • pain/electrical sensations in arms or fingers at compression level
  • dull reflexes
  • LMN weakness and muscle wasting
  • UMN signs below level of affected root suggest cord compression
70
Q

What is Bell’s Palsy?

A

Unexplained episode of facial muscle weakness or paralysis. Begins suddenly and worsens over 48 hours. Damage to facial nerve.

71
Q

Symptoms of Bell’s palsy

A

Unilateral lower motor neurone facial palsy

Forehead affected, ptosis, loss of nasolabial fold

Drooling, dry mouth, loss of taste, eye irritation

72
Q

Who is affected by Bell’s palsy?

A

Pregnant women
Diabetics
Influenza, cold or other upper respiratory sufferers
Middle aged

73
Q

Treatment for Bell’s palsy

A

Prednisolone

50mg for 10 days OR 60mg for 5 days followed by reducing regime of 10mg a day

Lubricating eye drops if can’t close eye

74
Q

Typical symptoms of a migraine headache

A
  • moderate to severe intensity
  • pounding or throbbing
  • usually unilateral
  • photophobia
  • phonophobia
  • possibly auras
  • nausea and vomiting
75
Q

Describe the auras in migraines

A
  • sparks in vision
  • blurring vision
  • lines across vision
  • loss of different visual fields
76
Q

What is a hemiplegic migraine and how does it present?

A
  • mimics a stroke
  • typical migraine symptoms
  • sudden or gradual onset
  • hemiplegia
  • ataxia
  • changes in consciousness
77
Q

Triggers of migraines

A
  • stress
  • bright lights
  • strong smells
  • certain foods
  • dehydration
  • menstruation
  • abnormal sleep patterns
  • trauma
78
Q

What are the stages of a migraine?

A
  • Prodromal stage
  • Aura stage
  • Headache
  • Resolution
  • Resolution
79
Q

How should migraines be managed with medication?

A
  • paracetamol
  • triptans (5HT receptor agonists)
  • NSAIDs
  • antiemetics
80
Q

How can we prevent migraines?

A
  • avoid triggers
  • headache diary
  • propranolol
  • topiramate (teratogenic so not for pregnant / people who want to become pregnant)
  • amitriptyline
81
Q

What are TIAs?

A
  • rapidly developing focal disturbance of brain function of presumed vascular origin that resolved completely within 24 hours
82
Q

What usually causes TIAs?

A
  • usually embolic
  • most common source is carotid atherosclerosis
  • can also arise from atrial fib, mitral valve disease, atrial myxoma
83
Q

Risk factors for TIAs

A
  • hypertension
  • smoking
  • diabetes
  • heart disease
  • peripheral arterial disease
  • polycythaemia rubra vera
  • COCP
  • hyperlipidaemia
  • alcohol
  • clotting disorders
84
Q

Presentation of a TIA

A
  • any patient presenting with acute neurological symptoms that resolve completely within 24 hours should be given 300mg aspirin and assessed within 24 hours
  • usually last 10-15 minutes
  • depends on area of brain affected but it’s same as stroke
85
Q

How should TIAs be investigated?

A
  • Primary care = the usual

Secondary = CT to check for haemorrhage, ECG, doppler US of carotid and vertebral arteries

86
Q

How should TIAs be managed?

A
  • 300mg aspirin immediately and assess within 24 hours
  • Confirmed TIA = clopidogrel 300mg then 75mg thereafter, statins
  • Antiplatelets, antihypertensives, lipid-modifying treatments, manage AF

3rd Year Conditions (16 decks)

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