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Year 5 Conditions > Neuro 2 > Flashcards

Neuro 2 Flashcards

1
Q

what are the different types of brain tumours

A

glioma (30%) - astrocytoma, oligodendroglioma, ependymoma

Meningioma - benign but can cause mass effect

pituitary tumours

acoustic neuroma

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2
Q

clinical features of pituitary tumours

A

bi-temporal hemianopia

hormonal imbalance

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3
Q

clinical features of acoustic neuroma

A

unilateral hearing loss

tinnitus, balance problems

can be associated with facial nerve palsy

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4
Q

what are some possible tumours that can have mets in the brain?

A

lung
breast
prostate
colorectal

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5
Q

clinical features of brain tumors

A

focal neuro signs - depends of the location of tumours

headaches - worse on the morning

raise ICP - papilloedema, altered mental state, visual fields defects, seizures (particularly focal) unilateral ptosis, 3rd and 6th nerve palsies

if frontal lob - personality change, disinhibition

parietal lobe - dysarthria

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6
Q

investigation and management of brain tumours

A

bloods - coag, blood film for bleeding disorder, hypercalcemia, SIADH - ADH, initial assessment of other possible causes of headaches eg ESR and CRP (elevated in GCA)

CT/MRI scan
PET
biopsy and tumour removal - stereotactic biopsy via skull bur-hole to obtain histology

open exploration (crainotmy) maybe required eg for a symptomatic meningoma

dexamethason - to reduce ICP

  • Palliative, chemo, radio, surgery
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7
Q

a complication of a brain tumour

A

acute haemorrhage into a tumour

bloackage of CSF outflow, causing hydrocephalus

sudden death may occur asa result of obstruction of outflow drainage from 3rd ventricle

sudden inc in ICP = herniation –> high mortaility

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8
Q

definition of encephalitis

A

inflammation of the brain

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9
Q

aetiology of encephalitis

A
  • Viral infection = main cause of encephalitis, herpes = most common
  • bacterial infection can occur  Neisseria meningitides = most common
  • Viral infection e.g. herpes simplex, VZV, mumps, measles, flu.
  • Foreign: Japanese B encephalitis virus, west nile virus, ticks. Sometimes encephalitis can develop with rabies virus infection after an animal bite.
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10
Q

clinical features of encephalitis

A 
high fever 
headaches 
muscle aches/weakness or paralysis 
feeling tired, confused and drowsy 
N+V
beck and back stiffness
photophobia 
change in personality/behaviour 
hallucinations 
seizures 
LOC
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11
Q

IX for encephalitis

A

bloods - FBC, U&E, CRP, swab tests (if blistering skin rash suspecting herpes simplex)

CT/MRI - alternative causes and check for signs of inc ICP in order to perform LP

LP

EEG

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12
Q

mx for encephalitis

A
  • Supportive- fluids, medicine to control seizures, oxygen, pain and high temperature medication.
  • Antiviral medication – acyclovir
  • Antibitoics – cefotamine (cover for meningitis)
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13
Q

complications for encephalitis

A 
speech problems 
weakness and movement disorders 
swallowing problem
seizures 
chronic headaches
personality changes 
memory problems 
behavioural problems 
mood problem, anxiety and depression 
difficulty concentrating
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14
Q

definition of fibromyalgia

A

Chronic pain syndrome diagnosed by the presence of widespread body pain

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15
Q

aetiology of fibromyalgia

A

unknown

CNS - excessive level of pain stimulators or amplifiers in the CNS in response to triggers in the muscles which could not normally cause pain

peripheral and central hyperexcitability in spinal or brainstem level

altered pain perception

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16
Q

risk factor of fibromyalgia

A

female

30-50 yrs old

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17
Q

clinical features of fibromyalgia

A

chronic - over 3 months
pain at multiple sites - low back pain with no radiation, neck and shoulder pain are common presentations

morning stiffness

fatigue

sleep disturbances

paresthesia

feeling of swollen joints - no objective swellings

problem with cognition - memory disturbances, difficulty with words finding - fibro fog

headaches, lightheaded or dizzy, fluctuations in weight, anxiety, and depression

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18
Q

Ix for fibromyalgia

A

bloods - ESR, TFT< ANA - be careful not to over investigate

fibromyalgia questionnaire - used to assess function, it also has a role in review and assessment of treatment interventions

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19
Q

differentials for fibromyalgia

A 
chronic fatigue syndrome 
hypothyroidism 
polymyalgia rheumatica 
inflammatory and metabolic myopathies 
polymyositis
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20
Q

mx of fibromyalgia

A

aim = reduce symptoms and improve quality of life not cure

MDT approach

non-drug - aerobic exercise programmes, CBT, acupuncture

drug - WHO analgesic ladder, antidepressants

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21
Q

definition of hydrocephalus

A

Increase in the volume of CSF occupying the cerebral ventricles. This is usually as a result of impaired absorption, but it may occasionally be due to excessive secretion.

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22
Q

aetiology of hydrocephalus

A
  • Non-communicating/obstructive – flow of CSF obstructed within the ventricles or between the ventricles and the subarachnoid space.
  • Communicating- here is communication between the ventricles and the subarachnoid space and the problem lies outside of the ventricular system (eg, due to reduced absorption or blockage of the venous drainage system). It may also be due to increased CSF production.
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23
Q

clinical features of infant hydrocephalus

A

irritability, vomiting and impaired function

rapid inc in head circumference - HC in 98th centile for he age or greater

the disjunction of sutures dilated scalp veins, tense fontanelle

setting-sun sign - both ocular globes deviate downwards, the upper lids are retracted and the white sclerae maybe visible above the iris

macewen’s sing - a cracked pot sound on percussing the head

inc limb tone

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24
Q

clinical features of older children and adults hydrocephalus

A

acute onset - headache and vomiting, papilloedema and impaired upwards gaze

gradual onset - unsteady gait due to leg spasticity, large head (although sutures are closed, the skull still enlarges due to chronic inc ICP), unilateral or bilateral 6th nerve palsy.

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25
Q

clinical features of adults hydrocephalus

A 
cognitive deterioration 
neck pain 
N+V 
blurred and double vision 
incontinence
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26
Q

investigation of hydrocephalus

A

CT - ventricular enlargement

dilated lateral and 3rd ventricle

with normal 4th ventricle - aqueduct stenosis

with abnor 4th ventricle - fossa mass

generalized ventricular dilation suggesting communicating

US for children - through the anterior fontanelle

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27
Q

differentials for hydrocephalus

A 
brain tumours 
childhood migraine 
frontal lobe syndrome 
epilepsy 
infection
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28
Q

management of hydrocephalus

A

surgical is definitive

  • external ventricular drain
  • ventriculoperitoneal shunt

drugs
- furosemide & acetazolamide inhibits secretion of CSF by the chorotid plexus

  • isosorbide promotes reabsorption of CSF
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29
Q

definition of myasthenia gravis

A

autoimmune condition that causes muscle weakness that gets progressively worse with activity and improves with rest

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30
Q

aetiology of myasthenia gravis

A

85% due to
- Acetylcholine receptor antibodies bind to the post synaptic membrane at NMJ

  • this blocks the receptor preventing acetylcholine stimulant and muscle contraction
  • as receptors are used more and more during activity, there is more muscle weakness and more muscle are used

15% due to
- LRP4 and MuSK antibodies – theses are important in the creation and organisation of acetylcholine receptors, destruction of these proteins by autoantibodies also causes symptoms.

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31
Q

what are the 3 antibodies associated with myasthenia gravis?

A

85% - acetylcholine receptor antibody

15% - LRP4 and MuSK antibodies

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32
Q

what population is most affected by myasthenia gravis

A

<40 - female
male - > 60

common in those with thyoma (benign tumour of the thymus)

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33
Q

clinical features of myasthenia gravis

A

severity greatly varies

symptoms best in the morning and worse at end of day

  • diplopia
  • bilateral ptosis
  • weakness in facial movement
  • difficulty with swallowing
  • fatigue in the jaw when chewing
  • slurred speech
  • progressive weakness with repetitive movements
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34
Q

what is a myasthenia crisis

A

acute worsening of symptosm triggered by illness eg RTI

can lead to resp failure as a result of weakness of muscles of respiration

pt require BiPAP, intubation and ventilation

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35
Q

Ix of myasthenia gravis

A

specific antibody tests - acetylcholine antibodies, muscle-specific kinase antibodies, low-density lipoprotein receptor-related protein 4

CT/MRI thymus

edrophonium test - if diagnostic uncertainty - give IV edrophonium chloride or neostigmine which are acetylcholinesterase inhibitors and temporarily relieves symptoms

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36
Q

mx of myasthenia gravis

A

reversible acetylcholinesterase inhibitor (pyridostigmine, neostigmine)

  • immunosuppression - prednisolone, amabzathioprine

thymectomy

monoclonal antibodies - rituxi

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37
Q

what is the definition of motor neuron disease

A

an umbrella term that encompasses a variety of specific diagnoses

progressive and fatal condition in which eventually the motor nerves stop functioning

38
Q

what are the different types of motor neuron diseaes

A

amyotrophic lateral sclerosis - most common, think Stephen Hawkin

progressive bulbar palsy - affects the muscle of talking and swallowing

progressive muscular atrophy

primary lateral sclerosis

39
Q

RF for motor neuron disease

A

hereditary

smoking, pesticides, heavy metals (carcinogens)

40
Q

clinical features of motor neuron disease

A

insidious progressive weakness of the muscles throughout the body affecting the limbs, trunk, face and speech

  • often complain of tripping, losing grip, inc fatigue when exercising, slurred speech

lower motor neuron disease

  • muscle wasting
  • reduced tone
  • fasciculations
  • reduced reflexes

upper motor neuron disease

  • inc tone or spasticity
  • brisk reflexes
  • upgoing plantar reflexes
    • ve Hoffmans sign - cervical myelopathy/MS - flick nail of middle finger, +ve if flexion of the thumb
41
Q

what are the clinical features of amyotrophic lateral sclerosis

A

LMN signs in arms

UMN signs in legs

42
Q

what are the clinical features of primary lateral sclerosis

A

UMN signs only

43
Q

what are the clinical features of progressive muscular atrophy

A

LMN signs only

44
Q

what are clinical features of bulbar palsy

A

palsy of the tongue, muscles of chewing/swallowing and facial muscles

45
Q

Ix of motor neurone disease

A

clinical diagnosis

46
Q

mx of motor neurone disease

A

no effective treatment of halting or reversing the progression of the disease

riluzole - can help to slow progression and extend survival by few months in ALS

NIV - at night to support breathing

end of life planning is key

47
Q

what is sinus venous thrombus?

A

it is when a thrombus form within the cranial venous drainage system causing damages.

most common place for a sinus venous thrombus to occur would be the cavernous sinus which are behind both eyes

48
Q

what are the important structures within the cavernous sinus

A

internal carotid arteries
CN: 3, 4, 5, 6
postganglionic sympathetic nerve fibre

49
Q

aetiology of sinus venous thrombus

A

local infection - due to nose, sinuses or teeth infection

carotid - cavernous venous fistula - carotid artery dissection in the cavernous sinus

infection in the brain eg meningitis

pituitary adenoma

mets tumours

aneurism of the internal carotid artery within the sinus

50
Q

clinical features of sinus venous thrombus

A

acute onset headache unilateral +/- photophobia

ophthalmoplegia +/- diplopia - due to lesion on 3,4,6, usually unilateral but can later progress to both eyes

seizures

other neuro signs - maybe absence, but can include hemiparesis, lower limb weakness, aphasia or ataxia

facial pain - inc pressure

pulsatile proptosis - carotid artery aneurysm

horner’s syndrome - o Post ganglionic sympathetic nerve fibres being affected

51
Q

investigation for sinus venous thrombus

A

Often low on the headache differential list.
Bloods – FBC, U+Es, CRP, ESR
LP
Imaging – CT (can miss cases), MRI (do a venogram)

52
Q

mx for sinus venous thrombus

A

Refer to neuro.
Consider broad spectrum antibiotics  vancomycin + ceftriaxone
(common causes – staph and step.)
anticoagulation – warfarin and heparin
hydrocortisone/dexamethasone to reduce swelling
surgery

53
Q

clinical features of ataxia

A

This movement disorder affects the part of the brain that controls coordinated movement (cerebellum). Ataxia may cause uncoordinated or clumsy balance, speech or limb movements, and other symptoms.

54
Q

clinical features of cervical dystonia

A

This condition causes long-lasting contractions (spasms) or intermittent contractions of the neck muscles, causing the neck to turn in different ways.

55
Q

clinical features of chorea

A

characterized by repetitive, brief, irregular, somewhat rapid, involuntary movements that typically involve the face, mouth, trunk and limbs.

56
Q

clinical features of dystonia

A

involves sustained involuntary muscle contractions with twisting, repetitive movements. Dystonia may affect the entire body (generalized dystonia) or one part of the body (focal dystonia).

57
Q

clinical features of functional movement disorder

A

may resemble an of the movement disorder but is not due to neurological disease

58
Q

clinical features of Hungtion’s disease

A

this is an inherited progressive, neurodegenerative disorder that causes uncontrolled movements (chorea), impaired cognitive abilities and psychiatric conditons

59
Q

clinical features of multiple system atropy

A

This uncommon, progressive neurological disorder affects many brain systems. Multiple system atrophy causes a movement disorder, such as ataxia or parkinsonism. It can also cause low blood pressure and impaired bladder function.

60
Q

clinical features of Parkinson’s Disease

A

This slowly progressive, neurodegenerative disorder causes tremor, stiffness (rigidity), slow decreased movement (bradykinesia) or imbalance. It may also cause other nonmovement symptoms.

61
Q

clinical feature of Parkinsonism

A

a group of conditions that has symptoms similar to those of Parkinson’s Disease

62
Q

clinical feature of progressive supranuclear palsy

A

This is a rare neurological disorder that causes problems with walking, balance and eye movements. It may resemble Parkinson’s disease but is a distinct condition.

63
Q

clinical feature of restless leg syndrome

A

This movement disorder causes unpleasant, abnormal feelings in the legs while relaxing or lying down, often relieved by movement.

64
Q

clinical feature of tardive dyskinesia

A

This neurological condition is caused by long-term use of certain drugs used to treat psychiatric conditions (neuroleptic drugs). Tardive dyskinesia causes repetitive and involuntary movements such as grimacing, eye blinking and other movements.

65
Q

clinical feature of tourette syndrome

A

This is a neurological condition that starts between childhood and teenage years and is associated with repetitive movements (motor tics) and vocal sounds (vocal tics).

66
Q

what is multiple sclerosis

A

A chronic and progressive condition that involves demyelination of the myelinated neurones in the central nervous system.

67
Q

pathophysiology of multiple sclerosis

A

causes by an inflammatory process involving activation of the immune cells against the myelin.

  • Inflammation around myelin and infiltration of immune cells that cause damage to the myelin.
  • This affects the way electrical signals travel along the nerve leading to symptoms of MS.
  • In early disease remyelination can occur resolving symptoms, in the later stages’ re-myelination is incomplete
  • MS affects different nerves at different times.
68
Q

what are clinical features of MS

A

charcot’s triad

  • dysarthria - difficult or unclear speech due to plagues in brainstem - eating and drinking, swallowing
  • nystagmus - optic neritis (central scotoma, pain on eye movement, impaired colour vision, relative afferent pupillary defect), diplopia
  • intention tremor - plagues along motor pathways (muscle weakness & spams), ataxia

other signs
- Lhermitte’s sign - electric shock down back and radiates to limbs when bend neck

  • +ve hoffman sign - flick nail of middle finger, flexsion of thumb

focal weakness –> bell’s palsy, horner’s syndrome, limb paralysis

plagues in autonomic system

  • bowel and bladder symptoms
  • sexual dysfunction

higher order activities

  • poor concentrations & critical thinking
  • depression and anxiety
69
Q

investigations for multiple sclerosis

A

• Symptoms must progress over a period of 1-year to diagnose primary progressive MS.
• MRI- typical lesions (white matter plagues)
• Anti-neuromyelitis optica antibody – present in neuromyelitis optica
• Lumbar puncture: oligoclonal bands in CSF.
- visual evoked potential - prolonged

70
Q

management of multiple sclerosis

A

• Referral to neurology- they make diagnosis.
• Acute – methylprednisolone +/- plasmapheresis
• Optic neuritis- refer to ophthalmologist: treated with steroids, cyclophosphamide, IVIG, recovery takes 2-6 weeks.
• Plasmaphereisis help to remove any antibodies from blood
• Chronic treatment  recombinant beta interferon + symptomatic control
o Fatigue  Amantadine/modafinil/ armodafinil
o Urinary frequency  oxybutynin
o Pain  TCA
o Inc muscle tone  baclofen
o Tremor  propranolol

71
Q

definition of Parkinson’s Disease

A

progressive reduction of dopamine in the basal ganglia (substantia nigra) leading to movement disorder

72
Q

Causes of Parkinson’s disease

A
  • Unknown  genetic Factor, environmental factor
  • Most commonly sporadic mutation in genes  SNCA, Parkin, PINK-1, DJ-1, TREM2, MHFTR and LRRK2
  • Reduction of dopamine in the BG
73
Q

types of Parkinson’s Disease

A

• 2 subtype
o Juvenile  < 21 yrs
o Young onset – 21-40 yrs

74
Q

clinical features of Parkinson’s Disease

A

triad of resting termor, rigidity & bradykinesia

• Unilateral tremor:
 4/6 hz, pillrollling tremor
 Asymmetrical
 Worse at rest
 Improves wit intentional movement
• Cogwheel ridgitiy
• Bradykinesia: movement gets slower and smaller
 Handwriting gets smaller and smaller
 Take only small steps (shuffling gait)
 Difficulty initiating movements (standing still to walking)
 Difficulty turning around when standing
 Reduced facial movement and facial expression (Hypomania)
• Conjugate gaze disorders  jerky (saccadic) pursuit and falling short of intended target (hypometric saccades)
• Depression
• Sleep disturbance and insomnia
• Loss of the sense of smell (anosmia)
• Postural instability  imbalance or falling
• Cognitive impairment and memory problems  dementia

75
Q

ix for Parkinson’s Disease

A
  • Clinical features are diagnostic
  • Dopaminergic agent trial  Used in diagnostic uncertainty  symptom better
  • MRI Brain  used when diagnostic uncertainty  absence of dorsolateral nigral hyperintensity on 3.0 Tesla susceptibility weighted scan
76
Q

Mx of Parkinsons’ Disease

A

• Monoamine oxidase-B (MAO-B) maybe used as 1st line in very mild symptoms
o Rasagiline for monotherapy or combined use
o Selegiline  adjunct only

• Dopamine agonist 
o pramipexole, ropinirole, transdermal rotigotine
o 1st line in < 70 – less risk with dyskinesia

• Levodopa: Synthetic dopamine combined with drug that stops body breaking down levodopa (carbidopa and bensesarizde)
o 1st line in > 70
o Domperidone for N+V, levodopa can cause N+V

• Anticholinergic agents  only treat mild symptoms * use as adjunct
o Trihexyphenidyl, amantadine

• Combination drugs co-benylidopa (levodopa and benserazide) and co-careldopa (levodopa and carbidopa)

• COMT: prolongs duration of levodopa
o Entacapone, tolcapone, opicapone

• Deep brain stimulation  treat disabling tremor

77
Q

what is tension-type headache

A

• Generalised headache with a predilection for involving the frontal and occipital regions with tight band type headache

78
Q

what are the differernt types of tension headaceh

A
  • Infrequent episodic  less than one day of headache per month.
  • Frequent episodic  at least 10 episodes of headache occurring on average 1–14 days per month for more than 3 months.
  • Chronic  15 or more days of headache per month for 3 or more months.
79
Q

aetiology of tension headache

A
  • Muscle aches in frontails, temporalis and occipitalis
  • Psychological stresses are the most common trigger
  • Distrubed sleep pattern can also be a trigger
80
Q

RF for tension headache

A
  • Stress
  • Depression
  • Alcohol
  • Skipping meals
  • Dehydration
  • Female
  • 20-39 yrs old
81
Q

clinical features of tension headache

A
  • Classical headache which produces a band like pattern around the frontal and occipital region
  • Non-throbbing headache
  • Constricting pain
  • Last minutes to day
  • Not aggravated by daily activities e.g. walking.
  • General muscle tenderness in the head
  • Rare  photophobia or phonophobia, regular analgesic use, anxiety and depression
82
Q

Ix for tension headache

A

• Clinical diagnosis

neuro exam to exclude other red flags

83
Q

Mx of tension headache

A
  • Reassurance
  • Episodic: Basic analgesia: paracetamol, NSAID’s, aspirin
  • Chronic: 10 sessions of acupuncture over 5-8 weeks
  • Relaxation techniques, antidepressants (amitriptyline)
  • Hot towels to local area.
84
Q

what is migraine

A

• chronic, genetically determined, episodic, neurological disorder that usually presents in early to mid-life

85
Q

what are the different types of migraine?

A

• Migraine without aura
 Recurrent headache disorder manifesting in attacks lasting 4 – 72 hours
 Unilateral location, pulsating quality, moderate or severe intensity
 Aggravated by routine physical activity
 Nausea, photophobia and phonophobia
• Migraine with aura
 Recurrent attacks
 Unilateral fully reversible visual lasting minutes precedes headache
• Silent migraine
 aura symptoms without the headache
• Hemiplegic migraine
 Migraine with aura + motor weakness

86
Q

aetiology of migraine

A
  • Unknown

* Related to dilatation and constriction of blood vessels.

87
Q

pathophysiology of migraine

A
  • Neurovascular disorder  neuro event precede and initiate headache
  • Neurogenic inflammation of first division trigeminal sensory neuros which innervate the large vessel and meninges of the brain
88
Q

RF for migraine

A 
•	CHOCOLATE
	CHocolate
	Oral contraceptive
	Caffeine (Or withdrawaL)
	Alcohol
	Travel
	Exercise
89
Q

clinical features of migraine with or without aura

A
  • 4-72 hrs
  • Moderate to severe intensity
  • Worsened by normal activity” walking/bending/climbing stairs.
  • Pounding and throbbing in nature
  • Usually unilateral but can be bilateral
  • photophobia
  • phonophobia
aura 
	Sparks in vision
	Blurring vision
	Lines across vision
	Loss of different visual fields.
	Zig zag
	Scotoma.
	Occur 15-60 minutes before attack caused by reduced blood flow to the occipital cortex before an attack.
	Can also have sensory (pins and needles) and speech aura
•	Nausea and vomitting.
90
Q

clinical features of hemiplegic migraine

A 
•	Hemiplegic migraine
	Mimic stroke and you must exclude this fast
	Typical migraine symptoms
	Sudden or gradual onset
	Hemiplegia
	Ataxia
	Changes in consciousness.
91
Q

what are the different stages of migraine

A

 Premonitory/prodromal (3 days before headache)
 Aura – lasting upto 60 minutes before headache
 Headache -4-72 hrs
 Resolution – headache resolves by sleep/vomiting
 Postdromal or recovery phase.

92
Q

mx for migraine

A

• Acute Medical management
 Paracetamol
 Triptans  sumatriptan
 NSAID’S (ibuprofen/ naproxen)
 Antiemetics if vomiting occurs (metoclopramide)
 Sodium valproate can be used, but not in pregnancy
 Caffeine can also be used to relieve pain

• Prophylaxis
 Propranolol
 Topiramate (not in pregnancy- causes cleft palate)
 Amitriptyline
 Magnesium sulfate
• Acupuncture – Rx and prophylactic
• Supplementation with vitamin B12 – can reduce frequency and severity.
• Menstruation migraine- prophylactic NSAID’s (mefenamic acid) or triptans (fovatriptan or zolmitriptan)

Year 5 Conditions (19 decks)

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