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2a mid tier > Neuro > Flashcards

Neuro Flashcards

1
Q

What are the two most common types of primary brain tumour?

A

Astrocytoma (95%) and oligodendroma (5%)

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2
Q

What are the risk factors for primary brain tumours?

A
  • More common in affluent groups
  • Ionising radiation
  • Vinyl chloride
  • Immunosuppression
  • Family history - genetics
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3
Q

What are the four cardinal presenting symptoms of primary brain tumours?

A
  • Raised ICP
  • Progressive neurological deficit
  • Epilepsy/ seizures
  • Lethargy/ tiredness (from pressure on brainstem)
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4
Q

What is the presentation for primary brain tumour? (Describe the 4 cardinal symptoms)

A
  1. Symptoms of raised ICP:
    - Progressive headache (worse on waking and pain is increased by coughing, straining and bending forwards but can be sometimes relieved by vomiting)
    - Drowsiness
    - ± Vomiting
    - Papilloedema
  2. Progressive neurological deficit:
    - Depend on part of brain affected
    - Temporal lobe: dysphagia, amnesia
    - Frontal lobe: hemiparesis, personality change, Broca’s dysphagia, lack of initiative, unable to plan tasks
    - Parietal lobe: hemisensory loss, reduction in 2-point discrimination, dysphagia, astereognosis (can’t recognise objects from touch alone)
    - Occipital lobe: contralateral visual defects
    - Cerebellum: DASHING (dysdiadochokinesis, ataxia, slurred speech, hypotonia, intension tremor, nystagmus, gait abnormality)
  3. Epilepsy/ seizure:
    - Sinister when of recent onset
    - Partial/ focal seizures are more common with tumours (motor, sensory, temporal lobe pattern – olfactory aura or déjà vu or a funny feeling in the gut/stomach a few minutes before and/or during the seizure)
  4. Lethargy/ tiredness caused by pressure on the brainstem
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5
Q

What are the differential diagnoses of a primary brain tumour?

A

Other causes of a space-occupying lesion

  • Aneurysm
  • Abscess
  • Cyst
  • Haemorrhage
  • Idiopathic intracranial hypertension
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6
Q

How are primary brain tumours diagnosed?

A
  • Blood tests: FBC, U&E, LFTs, B12
  • CT and MRI: MRI is better for posterior fossa lesions to determine size and location of lesions
  • Biopsy to determine cancer grade and confirm
  • Lumbar puncture in contraindicated when there’s any possibility of a mass lesion (withdrawing CSF may cause immediate coning)
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7
Q

How are primary brain tumours managed?

A
  • Surgery to remove mass if possible
  • Chemotherapy for glioma (given at same time as surgery): temozolomide
  • Can give oral dexamethasone
  • Can give anticonvulsants for epilepsy (e.g. oral carbamazepine)
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8
Q

What are the most common primary sites for secondary brain tumours?

A

Non-small cell lung, small cell lung, breast, melanoma, renal cell, GI

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9
Q

How are secondary brain tumours managed?

A
  • Surgery if aged <75y
  • Radiotherapy
  • Chemotherapy
  • Palliative care
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10
Q

What is the aetiology of giant cell arthritis?

A
  • Unknown aetiology

- Systemic autoimmune vasculitis affecting medium to large size arteries of the aorta and its extra cranial branches

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11
Q

What is the pathophysiology of giant cell arthritis?

A
  • Arteries become inflamed and thickened and can obstruct blood flow
  • Cerebral arteries in particular are affected e.g. temporal artery
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12
Q

What are the risk factors of giant cell arthritis?

A
  • Caucasian
  • Elderly women (>60y)
  • Genetic
  • Age (incidence increases with age)
  • Associated with polymyalgia rheumatica
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13
Q

What is the presentation of giant cell arthritis?

A
  • Should be suspected in all adults >50y with a headache lasting a few weeks
  • Severe headache (temporal pulsing)
  • Tenderness of scalp or temple (combing hair can be painful)
  • Claudification of jaw when eating
  • Tenderness and swelling of one or more temporal or occipital arteries
  • Sudden painless vision loss (EMERGENCY)
  • Malaise, lethargy, fever
  • Associated symptoms of polymyalgia rheumatica
  • Dyspnoea, morning stiffness and unequal or weak pulses
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14
Q

What are the differential diagnoses of giant cell arthritis?

A
  • Migraine
  • Tension headache
  • Trigeminal neuralgia
  • Polyarthritis nodosa
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15
Q

How is giant cell arthritis diagnosed?

A
  • Diagnostic criteria = 3 or more of: over 50, new headache, temporal artery tenderness/ decreased pulsation, raised ESR, abnormal artery biopsy
  • Normochromic, normocytic anaemia
  • Raised ESR
  • ANCA negative
  • CRP very high
  • Serum alk phos may be raised
  • Temporal artery biopsy: definitive diagnostic test, taken before or within 7 days of starting treatment, need to take a big chunk as lesions are patchy
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16
Q

How is giant cell arthritis managed?

A
  • High dose corticosteroids rapidly (gradually reduce steroids over 12-18m)
  • IV methylprednisolone for 3 days if symptom persist
  • GI and bone protection e.g. lansoprazole and alendronate with Ca2+ and vitamin D
  • Monitor treatment progress by looking at ESR/CRP (should fall)
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17
Q

What is the aetiology of spinal-cord compression?

A
  • Vertebral body neoplasms (most common cause of acute compression): secondary malignancy commonly from lung, breast, prostate, myeloma, lymphoma
  • Spinal pathology: disc herniation, disc prolapse
  • Rare causes: infection, haematoma, primary spinal cord tumour
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18
Q

What is the presentation of spinal-cord compression?

A
  • Spinal or foot pain by precede leg weakness and sensory loss
  • Progressive weakness of the legs with upper motor neurone signs e.g. contralateral spasticity and hyperreflexia
  • Onset may be acute or chronic, depending on the cause
  • Arm weakness is often less severe
  • Bladder and sphincter involvement is late and manifests as hesitancy, frequency and later as painless retention
  • Sensory loss below the level of the lesion
  • Look for motor, reflex and sensory level with normal findings above the level of the lesion
  • LMN signs at the level and UMN signs below
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19
Q

What are the differential diagnoses of spinal-cord compression?

A
  • Transverse myelitis
  • Multiple sclerosis
  • Cord vasculitis
  • Trauma
  • Dissecting aneurysm
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20
Q

How is spinal-cord compression diagnosed?

A
  • DO NOT DELAY IMAGING (irreversible paraplegia may follow if the cord is not decompressed)
  • MRI is the cold standard as it identifies the cause and site of cord compression
  • Biopsy/ surgical exploration may be required if there’s a mass
  • Blood tests: FBC, ESR, B12, U&E, LFT, PSA, syphilis serology
  • CXR if TB or malignancy
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21
Q

How is spinal-cord compression managed?

A
  • IV dexamethasone if malignancy (reduces inflammation. Oedema around malignancy, improving outcome)
  • Epidural abscess must be surgically decompressed, and antibiotics given
  • Refer to neurosurgery: epidural steroid injection, surgical cord decompression, laminectomy, microdisectomy
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22
Q

What is the epidemiology of cauda equina syndrome?

A
  • Herniation of lumbar disc (usually L4/5 and L5/S1)
  • Tumours/metastases
  • Trauma
  • Infection
  • Spondylolisthesis
  • Post-op haematoma
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23
Q

What is the pathophysiology of cauda equina?

A
  • Nerve root compression caudal (=distal) to the termination of the spinal cord at L1/2
  • Usually large central disc herniation at L4/5 or L5/S1 levels
  • Generally S1-S5 nerve root compression
24
Q

What is the presentation of cauda equina?

A
  • 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
  • Bilateral sciatica
  • Saddle anaesthesia
  • Bladder/bowel dysfunction
  • Erectile dysfunction
  • Variable leg weakness that is flaccid and areflexic (main difference between this and other spinal lesions higher up)
25
Q

What are the differential diagnoses of cauda equina?

A
  • Conus medularis syndrome
  • Vertebral fracture
  • Peripheral neuropathy
  • Mechanical back pain
26
Q

How is cauda equina diagnosed?

A
  • MRI to localise lesion
  • Knee flexion – test L5-S1
  • Ankle plantar flexion (downwards) – test S1-S2
  • Straight leg rising (people with acute problem can’t lift leg off bed) – L5, S1, root problem
  • Femoral stretch test – L4 root problem
27
Q

How is cauda equina managed?

A

URGENT NEUROSURGERY REFERAL to relieve pressure (risks irreversible paralysis/ sensory loss/ incontinence)

  • Microdiscectomy (remove part of a disc, may tear dura)
  • Epidural steroid injection (more effective for pain)
  • Surgical spine fixation (if vertebra slipped)
  • Spinal fusion (reduces pain from motion and nerve root inflammation)
28
Q

What are the causes of cranial nerve lesions?

A
  • Tumour
  • MS
  • Trauma
  • Aneurysm
  • Vertebral artery dissection resulting in infarction
  • Infection – cerebellar abscess from ear
29
Q

What are the causes of the oculomotor nerve lesion?

A
  • Raised ICP
  • Diabetes
  • Hypertension
  • Giant cell arthritis
30
Q

What is the presentation of an oculomotor nerve lesion?

A
  • Ptosis (drooping eyelids)
  • Fixed dilated pupil
  • Eye moves down and out
31
Q

What are the causes of a trochlear nerve lesion?

A
  • Trauma to the orbit
32
Q

What is the presentation of a trochlear nerve lesion?

A
  • Head lilt to correct eye extorsion

- Causes diplopia when looking down (e.g. when walking down stairs)

33
Q

What are the causes of a combined cranial nerve 3, 4 and 6 lesion?

A
  • Stroke
  • Tumours
  • Wernicke’s encephalopathy
34
Q

What is the presentation of a combined cranial nerve 3, 4 and 6 lesion?

A

Non-functioning eye

35
Q

What are the causes of a trigeminal nerve lesion?

A
  • Trigeminal neuralgia
  • Herpes zoster
  • Nasopharyngeal cancer
36
Q

What is the presentation of a trigeminal nerve lesion?

A
  • Jaw deviated to side of lesion

- Loss of corneal reflex

37
Q

What are the causes of an abducens nerve lesion?

A
  • MS
  • Wernicke’s encephalopathy
  • Pontine stroke
38
Q

What is the presentation of an abducens nerve lesion?

A

Eye adducted

39
Q

What are the causes of the facial nerve lesion?

A
  • Bell’s palsy
  • Fractures of petrous bones
  • Middle ear infections
  • Inflammation of the parotid gland (facial nerve passes through it)
40
Q

What is the presentation of the facial nerve lesion?

A

Facial droop and weakness

41
Q

What are the causes of vestibulocochlear nerve lesion?

A
  • Surrounding tumours
  • Skull fracture
  • Toxic drug effects
  • Ear infections
42
Q

What is the presentation of vestibulocochlear nerve lesion?

A
  • Hearing impairment

- Vertigo and lack of balance

43
Q

What are the causes of a combined glossopharyngeal in vagus nerve lesion?

A

Jugular foramen lesion

44
Q

What is the presentation of a combined glossopharyngeal in vagus nerve lesion?

A
  • Gag reflex and swallowing issues

- Vocal issues

45
Q

What is the aetiology of carpal tunnel syndrome?

A
  • Median nerve compression
  • Usually idiopathic
  • Associated with hypothyroidism, diabetes mellitus, pregnancy, obesity, amyloidosis, RA, acromegaly
46
Q

What is the risk factor for carpal tunnel syndrome?

A

Diabetes mellitus

47
Q

What is the presentation of carpal tunnel syndrome?

A
  • Symptoms are intermittent and onset is gradual
  • Aching pain in the hand and arm (especially at night and can wake patient up)
  • Paraesthesia in thumb, index, middle and ½ ring finger and palm (median nerve)
  • Relieved by dangling hand over side of bed
  • May be sensory loss and weakness ± wasting of thenar eminence
  • Light touch, 2-point discrimination and sweating may be impaired
48
Q

What are the differential diagnoses of carpal tunnel syndrome?

A
  • Peripheral neuropathy
  • Motor neurone disease
  • MS
49
Q

How is carpal tunnel syndrome diagnosed?

A
  • EMG see slowing of conduction velocity in median sensory nerves
  • Phalen’s test (pt can only maximally flex wrist for 1 min)
  • Tinel’s test (tapping nerve at wrist induces non-specific tingling)
50
Q

How is carpal tunnel syndrome managed?

A
  • Wrist splint at night
  • Local steroid injection
  • Decompression surgery (cut carpal tunnel ligament to reduce pressure)
51
Q

What is the pathophysiology of myasthenia gravis?

A
  • Mediated by antibodies to nicotinic ACh receptors via depletion of working post-synaptic receptor sites
  • Block excitatory effect of ACh on nicotinic receptors, resulting in muscle weakness
52
Q

What are the risk factors of myasthenia gravis?

A
  • If <50y, more common in women and is associated with other autoimmune diseases
  • If >50y, more common in men and associated with thymic atrophy
53
Q

What is the presentation of myasthenia gravis?

A
  • Increasing muscular fatigue
  • Muscle groups affected in order: extra-ocular, bulbar (swallowing and chewing), face, neck, trunk
  • Look for ptosis, diplopia and myasthenic snarl on smiling
  • Respiratory difficulties in generalised myasthenia
  • Weakness worsened by pregnancy, hypokalaemia, infection, emotion, exercise and drugs (opiates, BB, gentamicin)
  • Progressive weakness shown by counting to 50 and voice getting quieter and unable to keep eyes raised for more than a few seconds
54
Q

What are the differential diagnoses of myasthenia gravis?

A
  • MS, hyperthyroidism, acute Guillain-Barre syndrome

- Lambert-Eaton myasthenic syndrome

55
Q

How is myasthenia gravis diagnosed?

A
  • Raised serum anti-AChR
  • EMG will detect it
  • CT of thymus to detect hyperplasia, atrophy or tumour
  • Tensilon test
56
Q

How is myasthenia gravis managed?

A
  • Symptom control: anti-cholinesterase
  • Immunosuppression to treat relapses
  • Thymectomy (removal of thymus if <50y and disease poorly controlled with anti-cholinesterase)
  • Myasthenic crisis: weakness of resp muscles during a relapse, treat with IV immunoglobulins

2a mid tier (10 decks)

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