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neuro Flashcards

1
Q

GBS: define and aetiology

A

an acute (quick onset) paralytic polyneuropathy → affects PNS

An acute inflammatory demyelinating ascending polyneuropathy affecting the PERIPHERAL NERVOUS SYSTEM (SCHWANN CELLS TARGETED) following an upper respiratory tract infection of GI infection

triggered by infection

  • Campylobacter jejuni
  • Cytomegalovirus (CMV)
  • Epstein-Barr virus (EBV)
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2
Q

GBS: pp?

A
  • GBS is usually triggered by infection e.g. Campylobacter jejuni, EBV or cytomegalovirus (CMV)
  • infectious organisms share the same antigens as those on the Schwann cells (PNS) so the antibodies made (by B cells) against the infectious organisms will also WORK AGAINST the schwann cells or against axon itself - MOLECULAR MIMICRY→ leading to autoantibody mediated nerve cell damage formation via molecular mimicry
  • Nerve cell damage consists of damage to the SCHWANN CELLS and thus demyelination resulting in the reduction in peripheral nerve conduction resulting in an acute polyneuropathy
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3
Q

GBS: symptoms?

A
  • 1-3 weeks post infection
    • symptoms peak within 2-4wks
    • slow recovery per
    • iod lasting months-yrs
  • a SYMMETRICAL ASCENDING MUSCLE WEAKNESS starts - this may advance quickly, affecting all limbs at once and
    can lead to paralysis
  • can also affect sensory nerves = → sensory neuropathy - can be peripheral loss of sensation or neuropathic pain
  • Reduced reflexes bc its a peripheral neuropathy- Reflexes are lost early in the illness
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4
Q

GBS: investigations?

A

made clinically - no specific test

  • brighton criteria

supported by:

  • Nerve conduction studies (NCS):
    • DIAGNOSTIC if matches with clinical examination
    • Show slowing of conduction, prolonged distal motor latency +/- conduction block - baso shows reduced signal throughout the nerve
  • Lumbar puncture - done at L4:
    • CSF has raised protein but normal white cell count
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5
Q

GBS: management?

A
  • IV IMMUNOGLOBULIN for 5 days:
    • Decreases the duration and severity of paralysis
    • Contraindicated in patients with IgA deficiency!! - in whom it can cause a severe allergic reaction - screen for deficiency BEFORE treatment
  • Plasma exchange
  • Supportive care
  • venous thromboemblism prophylaxis ie Low-molecular weight heparin e.g. SC ENOXAPARIN and compression stockings to reduce risk of venous thrombosis - to prevent them from getting blood clots bc PE is major causse of death in GBS

If FVC < 1.5L/80% / if there is respiratory failure then ventilate and admit to ICU- MONITOR FVC 4 HOURLY!

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6
Q

ACA stroke: symptoms?

A
  1. Lower limb weakness and loss of sensation to the lower limb.
  2. Gait apraxia (unable to initiate walking).
  3. Incontinence.
  4. Drowsiness.
  5. Difficulty initiating speech
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7
Q

PCA stroke: symptoms?

A
  1. Visual field defects.
  2. Cortical blindness.
  3. Visual agnosia.
  4. Prosopagnosia.
  5. Dyslexia.
  6. Unilateral headache.
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8
Q

MCA stroke: symptoms?

A

CONTRALATERAL ARM & LEG WEAKNESS
• CONTRALATERAL sensory loss
• Hemianopia
• Aphasia (inability to understand or produce speech)
• Dysphasia (deficiency in speech generation)
• Facial droop

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9
Q

Meningitis: management?

A
  • children seen in community/primary care w suspected meningitis AND non-blanching rash
    • URGENT STAT INJECTION (IM or IV) of benzylpenicillin
  • IF YOU SUSPECT BACTERIAL MENINGITIS - START ANTIBIOTICS BEFORE TESTS COME BACK!!(steroids then ab?)
    • < 3 months–IV cefotaximeplusamoxicillin(the amoxicillin is if its listeria monocytogenes - to cover listeria contracted during pregnancy from the mother)
    • > 3 months–IV ceftriaxone

Vancomycin- for return travellers

ORAL Dexamethasone— Steroidsare also used in bacterial meningitis to reduce the frequency and severity ofhearing lossandneurological damage/cerebral oedema.

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10
Q

Meningitis: prevention?

A

Post exposure prophylaxis is guided bypublic health. The usual antibiotic choice for this is asingle doseofciprofloxacin!!!

prophylaxis is only EFFECTIVE AGAINST N.meningitidis.

This risk of highest for people that have had close prolonged contact within the7 daysprior to the onset of the illness. T

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11
Q

Meningitis: investigations

A
  • Physical exam
  • Blood cultures BEFORE LUMBAR PUNCTURE
  • Blood tests; FBC, U&E, CRP, serum glucose, FOR SEROLOGY + PCR
  • Throat swabs (bacterial + viral)
  • Lumbar puncture at L4 - measure pa and analyse WBC, protein and glucose - if unable to perform within 30 mins give empirical antibiotics!:
    . It makes sense that bacteria swimming in the CSF will release proteins and use up the glucose. Viruses don’t use glucose but may release a small amount of protein. The immune system releases neutrophils in response to bacteria and lymphocytes in response to viruses.

CT head:
• To exclude lesions e.g. tumour

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12
Q

Meningitis: symptoms? triad?

A

Headache + neck stiffness + fever

in acute bacterial infection:
Onset is typically sudden
- Papilloedema:
- fever (pyrexia) rigors, severe headache, photophobia and vomiting - within hours
or minutes
- Neck stiffness, positive Kernig’s & Brudzinski’s
sign can appear within hour

  • Meningococcal septicaemia is associated with a
    NON-BLANCHING PETECHIAL (test using glass
    test) + PURPURIC SKIN RASH
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13
Q

Meningitis: aetiology

A

most common cause of viral meningitis = Enterovirus.

bacteria and viruses → = ACUTE meningitis

fungi = CHRONIC MENINGITIS

Adults and children:
• Neisseria meningitides - gram-NEGATIVE DIPLOCOCCI - transmitted by droplet spread
• Streptococcus Pneumoniae/Pneumococcus

  • Pregnancy women/older adults:
    • Listeria monocytogenes - found in cheese, why pregnant women told to AVOID
    • also strep menominiae

Neonates:
• Escheria coli
• Group B Haemolytic streptococcus

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14
Q

Encephalitis: management?

A

If viral e.g. herpes simplex or varicella zoster then IMMEDIATE TREATMENT with anti-viral e.g. IV ACICLOVIR - even BEFORE the investigation results are available

  • Anti-seizure medication e.g. PRIMIDONE
  • If meningitis is suspected then EMERGENCY IM BENZYLPENICILLIN
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15
Q

Encephalitis: investigations?

A
  • Lumbar puncture:
    • Lymphocytosis (raised lymphocytes).
    • Raised protein.
    • Normal glucose.

MRI:
• Shows areas of inflammation and swelling, generally in the temporal
lobes in HSV encephalitis

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16
Q

Encephalitis: symptoms? triad?

A

triad: Fever + Headache + Altered mental status/Behavioural Change +/- lethargy

  • Begins with features of viral infection:
    • Fever, headaches, myalgia, fatigue and nausea
  • Progresses to:
    • Personality and behavioural changes - common early manifestation
    • Decreased consciousness, confusion, drowsiness

Seizures#

  • Focal neurological deficit:
    • Hemiparesis and dysphasia

WHOLE BRAIN AFFECTED - THUS problems with consciousness (global defect in higher functioning as well as drowsiness etc.) compared to meningitis

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17
Q

Encephalitis: define and aetiology? and epidemiolgy?

A
  • Infection and inflammation of the brain parenchyma
  • Usually viral

epidemiology =

  • Infections are most frequent in children and elderly - mainly viral cause
  • More common in immunocompromised
  • Mainly viral:
    • Herpes simplex virus 1 & 2
    • Varicella zoster, Epstein Barr, Cytomegalovirus, HIV, mumps, measles
  • Non-viral:
    • Bacterial meningitis
    • TB
    • Malaria
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18
Q

Huntington’s: typical age and pp?

A

Patients are usually asymptomatic until symptoms begin around aged 30 to 50.

Huntington’s is a cause of chorea and is a neurodegenerative disorder
characterised by the LACK of the inhibitory neurotransmitter GABA
Huntington’s chorea is anautosomal dominantgenetic condition that causes a progressive deterioration in the nervous system.

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19
Q

Huntington’s: symptoms?

define chorea

A

A continuous flow of jerky, semi-purposeful movements, flitting from one
part of the body to another
• They may interfere with voluntary movements but cease during sleep

BEGINS:
- cognitive,psychiatric ormood, or behavioural problems

  1. Irritability.
  2. Depression.
  3. Personality change.

FOLLOWED BY:

  • Chorea(involuntary, abnormal movements)
    • Relentlessly progressive, jerky, explosive, rigidity INVOLUNTARY
      movements - CEASES when sleeping
    • Can’t sit still
    • May begin as general restlessness, unintentionally initiated
      movements and lack of coordination
  • Eye movement disorders
  • Speech difficulties (dysarthria)
  • Swallowing difficulties (dysphagia)
  • Dementia: Impaired cognitive abilities and memory
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20
Q

Huntington’s: management?

A

SUPPORTING PERSON AND FAMILY:

There is no treatment to prevent progression

MEDS - for SYMPTOMATIC RELIEF:

  • Symptomatic management of chorea:
    • BENZODIAZEPINES EG diazepam
    • Antipsychotics (e.g. olanzapine) • SULPIRIDE - neuroleptic - depresses nerve function
    • TETRABENAZINE - dopamine depleting agent
  • Antidepressants such as selective serotonin reuptake inhibitors (SSRI’s)
    e.g. SEROXATE
  • Counselling to patient and family, genetic counselling to any children of
    patients
  • Speech and language therapywhere there are speech and swallowing difficulties
  • Advanced directivesto document the patients wishes as the disease progresses
  • End of lifecare planning
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21
Q

Parkinson’s: define and triad of symptoms?

A

Degenerative movement disorder caused by a REDUCTION IN DOPAMINE IN THE SUBSTANTIA NIGRA (in the basal ganglia of the brain)

Characterised by the triad of:

  • Rigidity
  • Bradykinesia (slow to execute movement)
  • Resting tremor
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22
Q

Parkinson’s: 2 histopathological signs of Parkinson’s disease.
also pp?

A
  1. Lewy bodies.
  2. Loss of dopaminergic neurones in the substantia nigra.
    - The substantia nigra produces DOPAMINE→ In Parkinson’s disease, there is a gradual but progressive fall in the production of dopamine.There is a loss of dopamine producing neurones in the substantia nigra.
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23
Q

Parkinson’s: symptoms?

A

Onset is ASYMMETRICAL - ONE SIDE ALWAYS WORSE THAN THE OTHER

Characterised by the triad of:
- Rigidity
pain, problems turning in bed
is a resistance to passive movement of a joint.

Bradykinesia (slow to execute movement)can only take small steps when walking (“shuffling gait”)
reduced facial movements and expressions - expressionless face (hypomimesis)

  • Resting tremor
    • Improved by voluntary movements and made worse by anxiety/if pt is distracted
      requency of 4-6 Hz, meaning it occurs 4-6 times a second - pill rolling tremor”

REM sleep disorders
Depression is common, psychiatric problems, dementia
Stooped posture,
loss of sense of smell

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24
Q

Parkinson’s: management?

A

Main treatment aim is to compensate for the loss of dopamine - ie to increase dopamine levels

Due to all the above complications, L-Dopa should only be started until
ABSOLUTELY NECESSARY - when other treatments are ineffective

—— BUT dopamine can’t cross BBB so given PO L-DOPA or LEVODOPA which is a synthetic dopamine that can cross BBB but does have s/e

  • —- usually combined with peripheral decarboxylase inhibitors - Examples arecarbidopa andbenserazide
  • Co-benyldopa (levodopaand***benserazide
  • Co-careldopa (levodopaand***carbidopa

ENTACAPONE - COMT Inhibitors!!! These are inhibitors ofcatechol-o-methyltransferase(COMT) - These inhibit COMT which breaks down dopamine

Dopamine Agonist - eg Bromocryptine, Pergolide, Carbergoline
usually used to delay the use of levodopa and are then used in combination with levodopa

Monoamine Oxidase-B Inhibitors - eg selegiline, rasagiline

physiotherapy

Physical activity

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25
Q

Dementia: define

and aetiology?

A

A set of symptoms that may include memory loss and difficulties with thinking, problem solving or language. There is a progressive decline in cognitive function.

  1. Alzheimer’s disease (65%).
  2. Fronto-temporal.
  3. Vascular.
  4. Lewy bodies.
  5. Vitamin deficiency e.g. B12.
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26
Q

Dementia: investigations?

A

PRIMARY CARE

  • History (of symptoms) - assess cognitive functions by asking various questions
  • Mini Mental State Examination (MMSE) commonly used to screen for cognitive function:
  • **Six-item Cognitive Impairment Test (6CIT)
  • Blood tests:- To look at the vitamin levels that may suggest a reversible cause e.g. dementia due to B12 deficiency.

SECONDARY CARE

  • imaging - eg CT or MRI - for VASCULAR DEMENTIA - showing multiple cortical or subcortical infarcts or atrophy of cortex - MRI - to see extent of atrophy
  • Amyloid and tau histopathology.
  • PET scans and functional MRI.
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27
Q

Dementia: management?

A

No specific therapy

Medication:
• Acetylcholinesterase inhibitor in Alzheimer’s to increase ACh e.g.
ORAL DONEPEZIL or ORAL RIVASTIGMINE
• Blood pressure control to reduce further vascular damage, particularly
in vascular dementia such as ACE-inhibitors e.g. RAMIPRIL

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28
Q

Dementia: AD - define and pp?

A

Alzheimer’s disease (AD) is the COMMONEST CAUSE of dementia, but not all
dementias is due to AD

Degeneration of the cerebral cortex, with cortical atrophy

Accumulation of beta-amyloid peptide, a degradation product of
amyloid precursor protein, results in progressive neuronal damage,
neurofibrillary tangles, increases in the number of amyloid plaques and
the loss of ACh (neurotransmitter)

amyloid precursor protein (APP) gets chopped up by beta-secretase → beta amyloid PROTEIN

its chemically sticky → so forms beta amyloid placqes

can get between neurons

neurofibrillary tangles

neurons w tangles and plaques can’t signal as well and end up undergoing apoptosis

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29
Q

Dementia: AD - symptoms?

and complications of AD?

A

Insidious onset with steady progression over years

Short-term memory loss

Decline in language

impaired ability to carry out skilled motor tasks

long-term memory loss

Around 25% of all patients with AD will develop PARKINSON’S!!

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30
Q

Dementia: frontotemporal define and symptoms?

A

Specific degeneration/atrophy of the frontal and temporal lobes of the brain

  1. Behaviour variants: personality and behavioural change.

2. Language variants.

  1. Often there is overlap with MND.
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31
Q

Dementia: fronto-temporal - - Which disease is fronto-temporal dementia often associated with?

A

Motor neurone disease.

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32
Q

dementia: lewybody - define? and pp?

A
  • 3rd most common cause of dementia
  • Deposition of abnormal protein within neurons in the brain stem and neocortex
    ASSOCIATED WITH PARKINSONS!!!!

not fully understood - alpha-synuclein → gets misfolded

→ aggregates to form lewy bodies inside neurones

→ as disease progresses, more and more neurons get deposits of lewy bodies and die!!!

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33
Q

dementia: lewybody - symptoms?

A

early symptoms:

  • mostly cognitive like difficulty w focusing and attention, poor memory, visual hallucinations, disorganised speech, depression - SIMILAR TO AD

later symptoms:

  • more motor symptoms like resting tremors, stiff and slow movements, reduced facial expressions - similar to PARKINSON’S
  • Prominent or persistent memory loss may not occur in the early stages
  • have difficulty learning new info
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34
Q

dementia: lewybody - management?

A

motor symptoms: drugs used to treat parkinson’s → LEVODOPA (dopamine analogue)

cognitive symptoms: - drugs used to treat AD → DONEPEZIL

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35
Q

headaches: classification?

A

Primary:
• No underlying cause relevant to the headache
• Examples include; migraine (20% of population), cluster and tension
headache (affect 99% in lifetime)

Secondary baso red flag headaches
• There is an underlying cause
• These are the ones where you need to identify the underlying cause e.g.
giant cell arteritis which can cause headache
Red flags for secondary headache
- Thunderclap headache (think subarachnoid haemorrhage!)
- Seizure and new headache
- Suspected meningitis
- Suspected encephalitis
papilloedema

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36
Q

migraine: aetiology?

A

CHOCOLATE:

  • Chocolate
  • Hangovers
  • Orgasms
  • Cheese
  • Oral contraceptives
  • Lie-ins
  • Alcohol
  • Tumult - loud noise
  • Exercise

ALSO -

  • Brain chemical imbalance may be cause
  • May be caused by changes in the brainstem and its interactions with the
    trigeminal nerve
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37
Q

migraine: symptoms?

A
  • Migraine without aura:
    • Attacks last 4-72 hours
    • Two of the following:
  • Unilateral (70%) and upper half!!
  • gradual onset
  • crescendo pattern - increasing in intensity!!!
  • moderate-severe intensity pain in head
  • During headache at least one of:/Associated symptoms:
    • Nausea and/or vomiting during headache
    • Photophobia (light sensitive) and phonophobia (sound sensitive)
      during headache (these are not attributable to another disorder)
    • aura (feeling that something is about to happen)
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38
Q

migraine: management?

A
  • Reduce triggers e.g. avoid dietary factors
  • simple analgesia eg paracetomol
  • Acute:
    • DO NOT OFFER ERGOTS e.g.ergotamine or OPIODS
    • Triptans e.g. SUMATRIPTAN:
      • Selectively stimulate 5-hydroxytryptamine receptors in brain
      • Contra-indicated in ischaemic heart disease, coronary spasm and
        uncontrolled high BP
      • S/E; arrhythmias or angina +/- MI
    • NSAIDs** e.g. **KETOPROFEN, NAPROXEN or ASPIRIN - good since less
      chance of developing medication overuse headache
      • Avoid paracetamol or ibuprofen
    • +/- anti-emetic e.g. PROCHLORPERAZINE
    • and HYDRATION
39
Q

tension headaches: define

A

MOST CHRONIC DAILY & RECURRENT HEADACHES are tension headaches

40
Q

tension headaches: symptoms?

A

Bilateral
- Tight band-like sensation around forehead/eyes
- which waxes and wanes
Headaches can last from 30 mins to 7 days
usually WITHOUT associated symptoms - Without vomiting or sensitivity to head movement, no aura

41
Q

tension headaches: management?

A

SIMPLE ANALGESICS
• ASPIRIN
• PARCETAMOL

42
Q

cluster headaches: define

A

Most disabling of the primary headache disorders

associated w trigeminal neuralgia

43
Q

cluster headaches: symptoms?

A
  • unilateral normally
  • around eye/orbit area
  • Abrupt onset
  • Rapid onset of CONTINUOUS, EXPLOSIVE AND EXCRUCIATING pain AROUND ONE EYE, TEMPLE or FOREHEAD
  • Ipsilateral cranial autonomic features:
    • Eye may become watery and bloodshot with lid swelling, lacrimation,
    • Facial flushing
    • Rhinorrhea (blocked nose)
    • Miosis (excessive pupil constriction) +/- ptosis (drooping or falling of
    upper eyelid    ) - seen in 20% of attacks
    • nasal discharge
44
Q

cluster headaches: management?

A
  • Analgesics are unhelpful!!!!
  • 100% 15L OXYGEN for 15mins via non-rebreathable mask (not if COPD)
  • Triptan (selective serotonin (5HT) agonist) e.g. SC SUMATRIPTAN:
    • Triptans are serotonin receptor agonists - this reduces vascular
      inflammation
    • BUT TRIPTANS ARE CONTRAINDICATED IN PT W CAD or CVS or cerebrovascular disease
45
Q

drug overuse headache: diagnostic criteria

A
  1. Headache present for >15 days/month.
  2. Regular use for >3 months of >1 symptomatic treatment drugs.
  3. Headache has developed or markedly worsened during drug use.
46
Q

Cauda Equina: define and pp eg functions?

A

MEDICAL EMERGENCY
compression, trauma or damage to the peripheral nerves protruding from the bottom of the spinal cord - cauda equina
= formed by the nerve roots caudal (distal) to the level of the termination of the spinal cord at L1/L2

Cauda Equina functions: carries motor innervation for:

  • genitals!
  • internal and external ANAL sphincters
  • detrusor vesicae - muscle in bladder that contract during urination
  • and muscles of leg
  • knee and ankle reflexes
  • skin sensations of legs and pelvis
47
Q

Cauda Equina: aetiology?

A

Herniation of lumbar disc - most common cause of CES - MOST COMMONLY at L4/5 and L5/S1 – Trauma

  • Poor posture
  • Physical Activity
  • strong rotational movement

Tumours/Metastases

Infection

Trauma

Spinal Stenosis

Spondylolisthesis

48
Q

Cauda Equina: symptoms?

A

Cauda equina presents with lower motor neuron signs (reduced tone and reduced reflexes). The nerves being compressed are lower motor neurons that have already exited the spinal cord.

  • Bilateral sciatica
    • sciatic pain - sharp pain going down back and legs
    • (pain radiates down the leg to the foot).
  • Saddle anaesthesia
    • loss of sensation in saddle area - includes buttocks, inner surface of thigh and perineum
  • Bladder/bowel dysfunction
    • • Faecal incontinence
    • • Loss of sensationin thebladderandrectum(not knowing when they are full)
    • • Urinary retentionorincontinence
    • due to decreased tone of anal sphincters and muscle wall of bladder
  • Erectile dysfunction/decreased sexual function
  • **Variable leg weakness that is FLACCID & AREFLEXIC (LMN
    signs) **
49
Q

Cauda Equina: investigations?

A

sually CLINICAL - based on pattern of sensory and motor nerve findings

  • MRI to localise lesion - TO CONFIRM !!!!!!!!!!!!!!!!!!!!
  • OR CT scan to confirm
50
Q

Cauda Equina: management?

A

Refer to neurosurgeon ASAP to RELIEVE PRESSURE or risk irreversible
paralysis/sensory loss/incontinence!!!!:

  • SURGICAL decompression - within 48 hrs
    • symptoms will appear suddenly if due to disc herniation, trauma, tumours, or abscess
  • antibiotics- to treat abscesses

BUT IF DEGENERATIVE DISEASE (symptoms will appear more gradually):

  • ANTI-INFLAMMTORY meds and corticosteroids
51
Q

Spinal Cord Compression: aetiology

A
  • Vertebral body neoplasms - MOST COMMON CAUSE OF ACUTE
    COMPRESSION:!!!
    • Secondary malignancy commonly from lung, breast, prostate,
      myeloma, lymphoma
  • Disc herniation:
    • When centre of disc (nucleus pulposus) has moved out through the annulus (outer part of disc) resulting in pressure on nerve root and pain
  • Disc prolapse:
    • When nucleus pulposus moves and presses against the annulus but it doesn’t
      escape outside the annulus

Rarer:
• Infection e.g. epidural abscess
• Haematoma e.g. warfarin
Primary spinal cord tumour e.g. glioma, neurofibroma

52
Q

Spinal Cord Compression: symptoms?

A

When the spinal cord is being compressed higher up by metastatic spinal cord compression, upper motor neuron signs (increased tone, brisk reflexes and upping plantar responses) will be seen.

  • back pain weeks before any neurological symptoms appear
    • first symptom - progressively worsening - changes w position
  • weakness )motor weakness)
    • abnormal gait
    • upper or lower extremity dysfunction
  • sensory changes
    • less common - clinically useful tho

Bladder (and anal) sphincter involvement is late and manifests as
hesitancy, frequency and later as painless retention

53
Q

Spinal Cord Compression: investigations? and gold ?

A

DO NOT DELAY IMAGING, AT ANY COST!!!! - since irreversible paraplegia
may follow if the cord is NOT DECOMPRESSED!!!!

MRI:!!!!!
• GOLD STANDARD
• Identifies the cause and site of cord compression AND MRI BRAIN if mets suspected

CT scan with contrast is useful when time-limited but may be limited w
in trauma - combine SPINAL XRAY W CT

Biopsy/surgical exploration may be required to identify the nature of any
mass

Screening blood tests: FBC, ESR, B12, U&E’s, syphilis serology, LFT, PSA

54
Q

Spinal Cord Compression: mx?

A

If malignancy then give IV DEXAMETHASONE glucocorticoid (reduces inflammation/oedema around malignancy and improves outcome) and consider more specific therapy e.g. radiotherapy or chemotherapy(most lesions are chemo-resistant) or surgery

  • Epidural abscess must be surgically decompressed and antibiotics given
    • Refer to neurosurgeons!!:!!!
      • Epidural steroid injection - effective for leg pain
      • Surgical decompression of cord:
      • LAMINECTOMY - removal of the lamina/spongy tissue between discs to
        relieve pressure and thus symptoms
      • MICRODISCECTOMY - removal of herniated tissue from disc
55
Q

Primary brain tumours: types?

A

below = 3 gliomas:
- astrocytomas - (glioblastoma multiformeis the most common)
—-> sooo glioblastomas
highly malignant = Grade IV

  • Oligodendroglioma - relatively rare - genetic defects in chromosomes in 1 and 19 - - typically form in frontal lobes
  • relatively slow-growing and can become malignant - Grade II-Grade III
  • Ependymoma

THEN MENINGIOMA - arise from the arachnoid mater and may grow to a large size, usually over years - pushing into the brain - graded I-III - relatively slow growing - They are usually benign, however they take up space and this mass effect can lead to raised intracranial pressure and neurological symptoms.

  • PITUITARY ADENOMA - formed in pituitary gland by hormone-secreting cells of ANTERIOR pituitary
    • typically benign - no WHO class

HAEMANGIOBLASTOMA - derived from cells w blood vessel origins

- usually found in cerebellum
- slow-growing - typically **Grade 1**
56
Q

Primary brain tumours: grades of WHO classification?

A
  1. Grade 1: benign paediatric tumour.
  2. Grade 2: pre-malignant tumour.
  3. Grade 3: ‘anaplastic astrocytoma’ - cancer.
  4. Grade 4: glioblastoma multiforme (GBM).
57
Q

Primary brain tumours: symptoms?

A

Symptoms of raised ICP:

  • Progressive headache:
  • —-worse on waking - cluster headache - Pain is increased by coughing, straining and bending forwards - +/-

Vomiting and nausea -

CARDINAL SIGN IS PAPILLOEDEMA - key finding on fundoscopy - Swelling of the optic disc due to obstruction of venous return
from the retina due to the raised ICP bc sheath around optic nerve is connected w the subarachnoid space

seizures (particularly focal)

  • unilateral ptosis
  • altered mental status
  • 3rd and 6th nerve palsies

Progressive neurological deficit: - Significantly altered consciousness, memory, confusion.

58
Q

Primary brain tumours: investiagtions what is contra-indicated?

A

LUMBAR PUNCTURE IS CONTRAINDICATED when there is any possibility
of a mass lesion since withdrawing CSF may PROVOKE IMMEDIATE
CONING - that is herniation of the brain through the foramen magnum
resulting in BRAINSTEM COMPRESSION as it passes through foramen
magnum and POTENTIAL DEATH

  • CT & MRI:
    • MRI is superior for posterior fossa lesions
    • Determine the size and location of lesions
    • High grade tumours have irregular edges and high growth rate
  • Blood tests e.g. FBC, U & Es, LFT’s, B12 etc.
  • Biopsy:
    • Via skull burr-hole
    • To determine cancer grade and confirm!!
59
Q

Secondary brain tumours: Commonest neoplasms to metastasise to CNS in order?

A

Commonest neoplasms to metastasise to CNS in order:

  • Non small cell LUNG - MOST COMMON
  • Small cell LUNG
  • Breast
  • Renal cell
  • Melanoma
  • GI
60
Q

epilepsy: define

A

Epilepsy is an umbrella term for a condition where there is a tendency to have seizures.

The recurrent tendency to spontaneous, intermittent, abnormal electrical activity in part of the brain, manifesting in seizures

A CHRONIC DISORDER i.e. need at least 2 seizures to be defined as epileptic

61
Q

epilepsy: primary generalised ?

A

when both hemispheres are affected
(sometimes will start out as partial seizure → then will quickly develop into generalised seizure → = SECONDARY GENERALISED SEIZURES)

  • Tonic Seizures
    • where muscles become stiff and flexed - tensecan cause pt to fall - often BACKWARDS
  • Atonic Seizures
    • where muscles suddenly relax and become floppy
    • can cause pt to fall - often BACKWARDS
  • Clonic Seizures
    • w violent muscle contractions aka convulsions - muscle JERKING
  • Generalised Tonic-Clonic Seizures→ most common generalised seizures
    • loss of consciousness
    • andtonic (muscle tensing) THEN → clonic(muscle jerking) movements.
  • Myoclonic Seizures
    • present as sudden brief muscle contractions, like a sudden “jump” - short muscle twitches - sometimes many in a short amount of time

aka petit mal - typically happen in children

  • patient becomes blank, stares into space and then abruptly returns to normal
    • lose consciousness then quickly regain consciousness
62
Q

epilepsy: focal/partial seizures - further classfied into?

A

these are seizures where only one hemisphere or one part of the brain or one lobe is affected

  • Simple partial seizure:
    • when they remain conscious
    • Not affecting consciousness or memory
    • Awareness is unimpaired - usually knows something is happening -
  • Complex partial seizure:
    • impaired consciousness
    • Affecting awareness or memory before, during or immediately
      after the seizure
63
Q

epilepsy: focal/partial seizures - symptoms?

A

Focal seizures start in thetemporal lobes. They affect hearing, speech, memory and emotions. Can present:

  • Hallucinations
  • Memory flashbacks
  • Déjà vu
  • Doing strange things on autopilot
64
Q

epilepsy: Mx for each type of seizure?

A
  • Generalised tonic-clonic seizures (grand-mal):
    • First line:*sodium valproate
      S/E: weight gain, hair loss, liver failure
      NOT IN PREGNANCY WOMEN - teratogenic
    • Second line:lamotrigineorcarbamazepine
  • Focal Seizures* - First line:carbamazepineorlamotrigine- Second line:sodium valproateorlevetiracetam*
  • Absence seizure (petit mal):
    • First line:sodium valproateor**ethosuximide
      S/E: rashes, night terrors
  • Atonic Seizures:
    • First line:sodium valproate
    • Second line:lamotrigine
  • Myoclonic Seizures:
    • First line:sodium valproate
    • Other options:lamotrigine,levetiracetamortopiramate
65
Q

Status Epilepticus: define and Mx in hospital vs community?

A

Status epilepticus is an important condition you need to be aware of and how to treat. It is a medical emergency. Causes could be: Abruptly stopping anti epileptic treatment; Alcohol abuse; Poor compliance to therapy

It is defined as a seizure lastingmore than 5 minutesor2 or more seizures without regaining consciousnessin the interim.

take an ABCDE approach):
- Secure the airway
- Give high-concentration oxygen
……
IVlorazepam, repeated after 10 minutes if the seizure continues
If the seizures persist the final step is an infusion of IVphenobarbitalorphenytoin. At this point intubation and ventilation to secure the airway needs to be considered, along with transfer to the intensive care unit if appropriate.

Medical options in the community:

  • Buccal midazolam
  • Rectal diazepam (BENZODIAZAPINE) - enhance effect of inhibitory neurotransmitter GABA
66
Q

stages of a seizure?

A
  • Prodrome:
    • Lasting hours or days may rarely precede the seizure
    • Not part of the seizure, results in change of mood or behaviour
  • Aura:
    • Part of seizure where the patient is aware and may precede its
      other manifestations
    • Strange feeling in the gut, deja vu or strange smells or flashing
      lights
    • Implies a partial (focal) seizure often but not necessarily from the
      temporal lobe
  • Post-ictally (after seizure):
    • Headache, post-ictal confusion, myalgia and a sore tongue
    • Temporary weakness after a focal seizure in motor cortex - Todd’s
      palsyparalysis (usually limited to one side of body) - TODD’S PARALYSIS
      • lasts average -15hrs
      • subsides completely after 2 days
      • due to maybe temporary and severe suppression of area of brain
67
Q

MS: epidemiology?

A
  • More common in FEMALES than males
  • Presentation is typically between 20-40yrs
    More common the further from the equator you go - rare in tropical countries
68
Q

MS: symptoms/.

A

Diagnosis requires TWO or more attacks affecting DIFFERENT PARTS of
CNS; that is 2 CNS lesions disseminated in time and space i.e. cannot
diagnose MS after one potential relapse

  • Usually presents in young adults 20-40 yrs
  • worsens over weeks and can linger for mths wo treatment
  • CHARCOT’S NEUROLOGIC TRIAD
    dysarthria
    nystagmus
    intention tremors
  • Spacticity
    • Spasticity & weakness - can result in stiffness/tightness of muscles that can interfere with normal movement, speech and gait
  • Symptoms can be exacerbated by -
    • Heat - typically a warm shower.
    • Symptoms can be relieved by cool temperatures.
  • Visual problems eg blurred vision
    • Unilateral optic neuritis:
      • Pain in one eye on eye movement
      • Reduced central vision
  • Abnormal sensations
    • e.g. numbness or tingling in the limbs or paraesthesias
  • weakness eg
    • Leg weakness
  • plaques in autonomic systems
    • Bladder dysfunction e.g. urgency, frequency and INCONTINENCE
    • Sexual dysfunction
69
Q

MS: investigations?

A

Diagnosis requires TWO or more attacks affecting DIFFERENT PARTS of
CNS; that is 2 CNS lesions disseminated in time and space i.e. cannot
diagnose MS after one potential relapse

MRI scan brain & cord:
• DIAGNOSTIC

  • Lumbar puncture:
    • CSF examination shows oligoclonal IgG bands in over 90% cases - but
    these are not specific to MS
    • CSF - may be high levels of ab!!! - cell count may be raised - ELECTROPHORESIS OF CSF might show **oligoclonal IgG bands*
  • Electrophysiology (visual evoked potential studies): measures nervous system response to visual stimuli
70
Q

MS: pharmacological and non-pharmacological treatment?

A
  • non-pharmacological treatment for MS:
    1. Psychological therapies and counselling.
    2. Speech therapists.
    3. Physiotherapy and occupational therapy.

Acute relapse: short course steroids like
• IV METHYLPREDNISOLONE for less than 3 days can help shorten acute relapse - use steroid sparingly and aim to use less than twice a year

  • Relapsing Remitting MS (RRMS)
    • IMMUNOMODULATORS - like SC INTERFERON 1B or 1A

MONOCLONAL ANTIBODIES EG IV ALEMTUZUMAB or IV NATALIZUMAB!!!!

Symptomatic treatment FOR MORE PROGRESSIVE MS: eg for spasticity
- **muscle relaxants**
    - **Physiotherapy**
    - **BACLOFEN**
TIZANIDINE
BOTOX INJECTION
  • Incontinence -
    • anti-cholinergic alpha-blocker drugs e.g. DOXAZOSIN

Aggressive treatment is STEM CELL TRANSPLANT

71
Q

MNDs include which diseases?

A
  • Amyotrophic lateral sclerosis (ALS) is the most common and well-known specificmotor neurone disease. Stephen Hawking had amyotrophic lateral sclerosis.
  • Progressive bulbar palsyis the second most common form ofmotor neurone disease. It affects primarily the muscles of talking and swallowing.
  • Other types of motor neurone disease to be aware of areprogressive muscular atrophyandprimary lateral sclerosis.
72
Q

Progressive bulbar pasty (PBP): define and symptoms?

A

a type of MNd
Lower cranial nerves (CN 9,10,11,12) and nuclei initially ONLY
affected
LMN only

Dysarthria, dysphagia, nasal regurgitation of fluids and choking are the presenting symptoms
3. Wasting and fascitulations of the tongue.

73
Q

LMN disease signs?

UMN disease signs?

A
  • insidious, progressive weakness of the muscles throughout the body affecting the limbs, trunk, face and speech.
    • The weakness is often first noticed in the upper limbs.

Signs oflower motor neurone disease:

  • Muscle wasting
  • Reduced tone
  • Fasciculations (twitches in the muscles)
  • Reduced reflexes

Signs ofupper motor neurone disease:

  • Increased tone or spasticity
  • Brisk reflexes
  • Upgoing plantar responses
74
Q

MND: management?

A
  • Riluzole - inhibits glutamate release and slows disease progression.
  • Ventilatory support.
  • Feeding by a PEG.
75
Q

Upper and lower motor neuron lesions: - Give 4 potential sites of UMN damage.

A
  1. Motor cortex lesions.
    1. Internal capsule.
    2. Brainstem.
    3. Spinal cord.
76
Q

Upper and lower motor neuron lesions: UMN signs?

A

signs are CONTRALATERAL to lesion

  • Indicate that the lesion is above the anterior horn cell i.e. in the spinal cord, brainstem and motor cortex
  • HYPERREFLEXIA - Increased reflexes, they are brisk
  • Increased muscle tone - SPASTICITY:
    • Velocity dependent and non-uniform i.e. the faster you move the patients muscle, the greater the resistance, until it finally gives way
      in a clasp-knife manner
    • little or no muscle atrophy
  • Weakness:
    • Flexors are generally weaker than extensors in legs and reverse in arms
  • POSITIVE babinski’s sign
77
Q

Upper and lower motor neuron lesions: LMN signs?

A

signs are IPSILATERAL to lesion

Indicate that the lesion is either in the anterior horn cell or distal to the anterior horn cell i.e. in anterior horn cell, plexus or peripheral nerve

  • Decreased muscle tone
  • muscle WASTING (atrophy) +/- FASCICULATIONS (spontaneous involuntary muscle twitching/contraction)
  • Weakness that corresponds to those muscles supplied by the involved cord segment, nerve root, part of plexus or peripheral nerve
  • Reflexes are reduced or absent
    • inc plantatr reflex / negative babinski’s sign!!
    • diminished or absent tendon reflexes
78
Q

Myasthenia gravis: define and pp?

A

Autoimmune disease against (skeletal muscles) NICOTINIC ACETYLCHOLINE RECEPTORS (AChR) in the neuromuscular junction

baso NMJ DAMAGE

motor neurone release ACh which binds to nicotinic ACh receptors on muscle cell membranes → muscle contraction

type II hypersensitivity reaction-

cytotoxic injury and mediated by autoantibodies

baso body’s b cells make ab (anti-AChR antibodies) which bind to nicotinic recpetors on muscle cell membranes

79
Q

Myasthenia gravis: symptoms?

A
  • Increasing muscular fatigue AND WEAKNESS
    • might wake up feeling fine but end of day feel v weak - perhaps weakness w repetitive movements eg chopping veg
- **Muscle groups affected in order:**
• **Extra-ocular**
• Bulbar - swallowing & chewing
• Face
• Neck
• Trunk
  • affects extra-ocular muscles - controls movement of eye and eyelid
    • Look for ptosis (drooping of upper eyelid), diplopia (double vision) and myasthenic snarl on smiling
80
Q

Myasthenia gravis: investigations?

A

Serum anti-AChR: SERUM ANTI-ACh receptor antibodies
• Raised in 90%
• If negative then look for MuSK (muscle specific tyrosine kinase) antibodies (anti-MuSK) Antibodies against tyrosine kinase - anti-MuSK antibodies ,y be present .

81
Q

Myasthenia gravis: Mx?

A

Anti-cholinesterase - ACETYLCHOLINISTERASE INHIBITORS - baso stops the breakdown of ACh and increases concen of ACh - so more ACh remains in neuromuscular junction e.g. ORAL PYRIDOSTIGMINE OR NEOSTIGIMINE

82
Q

syncope: define

A

Syncope is the loss of consciousness due to hypoperfusion to brain

Insufficient blood or oxygen supply to the brain causes paroxysmal changes in behaviour, sensation and cognitive processes.

83
Q

syncope: aetiology?

A

Prolonged upright position e.g. long time standing, sweat prior to loss of consciousness, nausea, pre-syncopal symptoms

84
Q
  • Give 5 signs that a transient loss of consciousness is due to syncope.
A
  1. Situational.
    1. 5-30s in duration.
    2. Sweating
    3. Nausea.
    4. Pallor.
    5. Dehydration.
85
Q

Trigeminal neuralgia: aetiology?

A

neuralgia (facial pain) - a painful cranial neuropathy

Compression of the trigeminal nerve results in demyelination and excitation of the nerve resulting in erratic pain signalling

  • In most cases is due to compression of the trigeminal nerve by a loop of vein or artery
  • Can be due to local pathology such as aneurysms, meningeal inflammation, tumours

Trigeminal nerve (CN5) has both motor and sensory functions and enters the brainstem at the level of the pons

86
Q

Trigeminal neuralgia: symptoms?

A
  • ALMOST ALWAYS UNILATERAL
  • At least 3 attacks of unilateral facial pain - RECURRENT EPISODES freq increases over time
  • Facial pain MANDIBULAR zone affected most
  • few seconds
  • Severe intensity INTENSE AND EXCRICIATING!!
    • Electric shock like, shooting, stabbing
  1. Unilateral face pain.
  2. Pain commonly in V3 distributon.
  3. Very severe.
  4. Electric shock like/shooting/sharp.

can be triggered by: 1. Washing your face.2. Eating.3. Shaving.4. Talking.

87
Q

Trigeminal neuralgia: investigations?

A
  • Clinical diagnosis based on criteria above and based on history
  • MRI to exclude secondary causes or other pathologies
88
Q

Trigeminal neuralgia: Mx?

A

typical analgesics and opioids DO NOT WORK

  • Anticonvulsant e.g. ORAL CARBAMAZEPINE suppresses attacks in most patients or oxcarbazepine

2nd line:

  • baclofen or lamotrigine

severe cases: surgery

89
Q

sciatica: define and aetiolgoy?

A

Sciaticarefers to the symptoms associated with irritation of thesciatic nerve
Sciatica is pain, numbness and a tingling sensation that
radiates from lower back and travels down one of the legs to the foot and toes

The main causes of sciatica are lumbosacral nerve root compression by:

  • Herniated disc
  • Spondylolisthesis(anterior displacement of a vertebra out of line with the one below)
  • Spinal stenosis
90
Q

sciatica: symptoms?

A
  • unilateral pain from the buttock radiating down the back of the thigh to below the knee or feet.
  • “electric” or “shooting” pain
  • paraesthesia (pins and needles),
  • numbnessandmotor weakness
  • Reflexesmay be affected depending on the affected nerve root.
91
Q

sciatica: investigations?(1)

and Mx?
contraindications?

A

Thesciatic stretch testcan be used to help diagnose sciatica.

  • Treatment for sciatica WO NEUROLOGICAL SIGNS:
    • Conservative management e.g. physio and NSAIDs.- Self-management
  • Education
  • Reassurance- Analgesia
  • Staying active and continuing to mobilise as tolerated

They suggest considering a neuropathic medication if symptoms are persisting or worsening at follow up, butnotgabapentin or pregabalin, leaving at the main choices of:

  • Amitriptyline!!!
  • Duloxetine!!!

Specialist management options for chronic sciatica include:

  • Epidural corticosteroid injections
  • Local anaesthetic injections
  • Radiofrequency denervation
  • Spinal decompression
92
Q

what is bilateral sciatica a red flag for?

A

CAUDA EQUINA SYNDROME

93
Q

symptoms of all cranial nerve lesions?

A
  • CN3 PalsyCN 3 (Oculomotor) palsy:
    • Ptosis - dropping eyelids
    • Fixed dilated pupil - loss of PARASYMPATHETIC outflow from EDINGER WESTPHAL NUCLEUS which supply pupillary sphincter and ciliary bodies - lens accomadation
    • Eye down and out
  • CN4 PalsyCN 4 (Trochlear) palsy:
    • Innervate superior oblique muscle and results in a head tilt to correct the extortion that results in diplopia on looking down e.g. walking downstairs
  • CN6 PalsyInnervate the lateral rectus muscle thus eyes will be adducted
  • CN 3,4,6 palsy:
    • Non-functioning eye
  • CN 5 (Trigeminal) palsy:
    • Jaw deviates to side of lesion
    • Loss of corneal reflex
  • CN 7 (Facial) palsy:Facial droop and weakness
  • CN 8 (Vestibulocochlear) palsy:
    • Hearing impairment
    • Vertigo and lack of balance
  • CN 9 (Glossopharyngeal) & CN 10 (Vagus) palsy:
    • Gag reflex issues
    • Swallowing issues
    • Vocal issues

med 2a (13 decks)

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