Neuro Flashcards
1
Q
What are the two most common types of primary brain tumour?
A
Astrocytoma (95%) and oligodendroma (5%)
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
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)
4
Q
What is the presentation for primary brain tumour? (Describe the 4 cardinal symptoms)
A
- 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 - 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) - 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) - Lethargy/ tiredness caused by pressure on the brainstem
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
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)
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)
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
9
Q
How are secondary brain tumours managed?
A
- Surgery if aged <75y
- Radiotherapy
- Chemotherapy
- Palliative care
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
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
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
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
14
Q
What are the differential diagnoses of giant cell arthritis?
A
- Migraine
- Tension headache
- Trigeminal neuralgia
- Polyarthritis nodosa
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
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)
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
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
19
Q
What are the differential diagnoses of spinal-cord compression?
A
- Transverse myelitis
- Multiple sclerosis
- Cord vasculitis
- Trauma
- Dissecting aneurysm
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
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
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
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
What are the differential diagnoses of cauda equina?
- Conus medularis syndrome
- Vertebral fracture
- Peripheral neuropathy
- Mechanical back pain
26
How is cauda equina diagnosed?
- 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
How is cauda equina managed?
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
What are the causes of cranial nerve lesions?
- Tumour
- MS
- Trauma
- Aneurysm
- Vertebral artery dissection resulting in infarction
- Infection – cerebellar abscess from ear
29
What are the causes of the oculomotor nerve lesion?
- Raised ICP
- Diabetes
- Hypertension
- Giant cell arthritis
30
What is the presentation of an oculomotor nerve lesion?
- Ptosis (drooping eyelids)
- Fixed dilated pupil
- Eye moves down and out
31
What are the causes of a trochlear nerve lesion?
- Trauma to the orbit
32
What is the presentation of a trochlear nerve lesion?
- Head lilt to correct eye extorsion
| - Causes diplopia when looking down (e.g. when walking down stairs)
33
What are the causes of a combined cranial nerve 3, 4 and 6 lesion?
- Stroke
- Tumours
- Wernicke’s encephalopathy
34
What is the presentation of a combined cranial nerve 3, 4 and 6 lesion?
Non-functioning eye
35
What are the causes of a trigeminal nerve lesion?
- Trigeminal neuralgia
- Herpes zoster
- Nasopharyngeal cancer
36
What is the presentation of a trigeminal nerve lesion?
- Jaw deviated to side of lesion
| - Loss of corneal reflex
37
What are the causes of an abducens nerve lesion?
- MS
- Wernicke’s encephalopathy
- Pontine stroke
38
What is the presentation of an abducens nerve lesion?
Eye adducted
39
What are the causes of the facial nerve lesion?
- Bell’s palsy
- Fractures of petrous bones
- Middle ear infections
- Inflammation of the parotid gland (facial nerve passes through it)
40
What is the presentation of the facial nerve lesion?
Facial droop and weakness
41
What are the causes of vestibulocochlear nerve lesion?
- Surrounding tumours
- Skull fracture
- Toxic drug effects
- Ear infections
42
What is the presentation of vestibulocochlear nerve lesion?
- Hearing impairment
| - Vertigo and lack of balance
43
What are the causes of a combined glossopharyngeal in vagus nerve lesion?
Jugular foramen lesion
44
What is the presentation of a combined glossopharyngeal in vagus nerve lesion?
- Gag reflex and swallowing issues
| - Vocal issues
45
What is the aetiology of carpal tunnel syndrome?
- Median nerve compression
- Usually idiopathic
- Associated with hypothyroidism, diabetes mellitus, pregnancy, obesity, amyloidosis, RA, acromegaly
46
What is the risk factor for carpal tunnel syndrome?
Diabetes mellitus
47
What is the presentation of carpal tunnel syndrome?
- 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
What are the differential diagnoses of carpal tunnel syndrome?
- Peripheral neuropathy
- Motor neurone disease
- MS
49
How is carpal tunnel syndrome diagnosed?
- 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
How is carpal tunnel syndrome managed?
- Wrist splint at night
- Local steroid injection
- Decompression surgery (cut carpal tunnel ligament to reduce pressure)
51
What is the pathophysiology of myasthenia gravis?
- 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
What are the risk factors of myasthenia gravis?
- 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
What is the presentation of myasthenia gravis?
- 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
What are the differential diagnoses of myasthenia gravis?
- MS, hyperthyroidism, acute Guillain-Barre syndrome
| - Lambert-Eaton myasthenic syndrome
55
How is myasthenia gravis diagnosed?
- Raised serum anti-AChR
- EMG will detect it
- CT of thymus to detect hyperplasia, atrophy or tumour
- Tensilon test
56
How is myasthenia gravis managed?
- 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
