neuro middle tier Flashcards
are primary or secondary brain tumours more common
secondary
risk factors for primary brain tumours
Ionising radiation
Immunosuppression
Family history, genetics
Vinyl chloride
adults vs children. where are most primary brain tumours
Adults: majority = supratentorial
Children: majority = in posterior fossa
grading gliomas
1: pilocytic astrocytoma (paeds)
2: diffuse astrocytoma (benign)
3: anaplastic astrocytoma (malignant)
4: glioblastoma multiforme (GBM) - given enough time, all will progress to this except 1
types of brain tumour
- which is most common
- gliomas - astrocytomas (most common) and oligodendrogliomas
- Meningiomas
- Lymphomas
- Neurofibromas
- Ependymmomas
where do secondary brain tumours metastasise from
Lung, bronchus Breast Melanoma GI tract Kidney Thyroid Stomach Prostate
common and less common cause of astrocytomas
Common (esp under 50): genetic error in glycolysis due to isocitrate dehydrogenase enzyme mutation. This causes instability in glial cells causing inappropriate mitosis
Less common (more common over 60): different mutation (no isocitrate dehydrogenase). Catastrophic. Poor prognosis
differential diagnosis of brain tumours
Other causes of space occupying lesion Aneurysm Abscess Cyst Haemorrhage Idiopathic intracranial hypertension
presentation of brain tumour in frontal lobe
personality change, hemiparesis, broca’s dysphasia, loss of smell, decreased verbal fluency, lack of initiative, unable to plan
presentation of brain tumour in temporal lobe
dysphasia, amnesia, contralateral homonymous hemianopia,
presentation of brain tumour in parietal lobe
hemisensory loss, dysphasia (wernicke’s), sensory inattention
presentation of brain tumour in occipital lobe
contralateral visual field defects, palinopsia (image remains seen for longer than it is present), polyopia (multiple images either side of object at fixation)
presentation of brain tumour in cerebellum
dysdiadochokinesia (impaired ability to do rapid alternating movements), dysmetria (uncoordinated - problems judging distance), ataxia, nystagmus, intention tremor, slurred speech, hypotonia, gait
presentation of brain tumour as a result of raised ICP
Headaches - worse on walking, lying down, bending forward, coughing
Vomitting
Papilloedema (swelling of optic discs)
drowsiness
other features of brain tumours (not specific to location or raised ICP)
Seizures, epilepsy (focal or generalised)
General cancer symptoms :
Weight loss
Malaise
Anaemia
brain tumour investigation
and what in contraindicated
CT/MRI/ PET – to find masses
Biopsy (via skull bore) - confirm cancer and grade it
Bloods : FBC, LFTS, U/Es, B12
Contraindicated = lumbar puncture (may provoke immediate coning- brain stem compressed through foramen magnum)
brain tumour management
Surgery - Removal or debulk where possible
Radiotherapy - Good for gliomas and radiosensitive masses
Chemo - for glioma and post op
Cerebral oedema /inflammation reduced with corticosteroids
Epilepsy treated with anticonvulsants
Palliative therapy
complications of giant cell arteritis
blindness if untreated
stroke
giant cell arteritis treatment
High dose steroids immediately - oral prednisolone
- 2 years. Can be tapered eventually once disease is suppressed
- Reduced risk of complete blindness
- IV methylprednisolone if vision loss is progressing/occuring
- Low dose aspirin
- Bone protective drugs to prevent osteoperosis should be considered
- PPI (medications are associated with GI toxicity)
investigations for giant cell arteritis
- inc diagnosis criteria
Diagnosis = 3 of 5 :
- Age >50
- New headache
- Temporal artery =tender / decreased pulsation
- ESR elevated (50/50 rule – over 50 with ESR over 50)
- Biopsy of temporal artery abnormal. (Histology may be normal if it a ‘skip lesion’ is sampled – arteritis is patchy)
- CPR elevated
- High ALP (liver/ gallbladder)
- Platelets elevated
- Haemoglobin reduced
symptoms of giant cell arteritis
- Headache- Abrupt onset
- Tender temporal artery. May be palpable, firm, tender and pulseless
- Jaw / tongue claudication
- Visual symptoms- unilateral blindness (amaurosis fugax) in 25% of untreated
- Scalp tenderness (from skin ischemia)
- Systemic features
- –Weight loss
- –Malaise
- –Fever
- –Morning muscle stiffness - polymyalgia rheumatica (esp shoulders)
what condition is associated with giant cell arteritis
Associated with polymyalgia rheumatica (PMR) in 50%
- Muscle pain, stiffness, inflammation in the shoulder, neck, hips
- Morning stiffness worse
giant cell arteritis risk factors
Age (over 55)
Family history
Polymyalgia rheumatica (shoulder inflam muscle pain)
giant cell arteritis pathophysiology
- Large vessel vasculitis
- Granulomatous arteritis
- Chronic inflammation of the medium-large arteries( aorta, carotid and its extracranial branches)
- Blindness = inflammation and occlusion of the ciliary or central retinal artery
- Onset can be insidious or abrupt
complications of cauda equina/ spinal cord compression
persistent neurological deficit
management of cauda equina
Emergency lumbar decompression (surgical decompression) - remove causative agent
management of spinal cord compression
- Corticosteroids (dexamethasone) - if malignancy. Reduced oedema around the lesion
- Chemotherapy
- Radiotherapy
- Surgery : decompressive laminectomy
investigations into cauda equina / spinal cord compression
- MRI
- Biopsy / exploration of any masses
- Chest X ray - look for primary lung cancers (spinal cord compression)
- Also, in cauda equina - Anal tone reduced (PR exam) and anal wink reflex reduced
how to distinguish cauda equina and spinal cord compression
In cauda equina, leg weakness is flaccid and areflexic (LMN)
In spinal cord compression, leg weakness is spastic and hyperreflexic (UMN)
cauda equina presentation
Develops progressively : coming/going over weeks/months
- Loss of anal tone (on PR examination)
- Loss of sensation around the saddle region (groin, upper inner thighs, genitals, bum)- saddle anasthesia
- Loss of anal wink reflex (contraction)
- Urinary retention, overflow incontinence
- Bilateral muscular leg pain and loss of power (weakness), and sensory deficit (paraesthesia /numbness) - LMN
- Impotence - sexual dysfunction
- Nerve root pain - sharp, stabbing (Sciatica : this pain down both sciatic nerve in legs)
- Gait disturbance
- Lower back pain - severe , rapid
spinal cord compression presentation
Onset = hours to days
At level of lesion:
- Localised back pain
- Nerve root pain - typically shooting/sharp/ burning/ radiating
- Numbness
- Paraesthesia
- LMN signs
Below the level of the lesion: (this is the key part! )
- UMN signs!
- Sensory loss
- Progressive motor loss - BI lateral- legs/arms depending on where in spine → eventual paralysis
May also have sphincter disturbance- loss of bowel and bladder control. Manifests as hesitancy, frequency and later, as painless retention
causes of cauda equina compression
- Disk prolapse (herniation)
- Tumour
- Infection (osteomyelitis)
- Bleeding
- Trauma
- Inflammatory conditions - ankylosing spondylitis
causes of spinal cord compression
- Spondylosis (spine degeneration)
- Disc prolapse (herniation)
- Spondylolisthesis (one vertebra slips forward on another)
- Spinal tumours = main! Metastases from lung, breast, prostate, or myeloma
- Spinal stenosis
- Spinal abscess
- Spinal tuberculosis
age for cauda quina/ spinal cord compression
which is a medical emergency
can occur at any age
both
risk factors for spinal cord compression
Osteoporosis Trauma Tumour Rheumatoid arthritis Ankylosing spondylitis
risk factors for cauda equina
Obesity
Heavy lifting
nerve root lesion symptoms
Tingling in the affected dermatome
Pain
Paraesthesia
weakness
nerve root lesion management
Steroid injection in nerve root
Surgical decompression
carpals tunnel
- age
- gender
f>m
- Females have narrower wrists but similar sized tendon
Usually over 30y
risk factors for carpals tunnel
Usually idiopathic Associated with - Hypothyroidism - Diabetes - Pregnancy - Obesity - Rheumatoid arthritis - Amyloidosis - Acromegaly
tinnels sign
lightly tap over nerves. Patient feels tingling sensation
carpals tunnel
phalen’s test
flex wrist 90deg (prayer hands). Sensation on medial nerve region.
carpals tunnel
carpals tunnel presentation
- Intermittent and gradual onset of symptoms
- Pain
- Aching
- Loss of sensation of median nerve
- Paraesthesia - worse at night– Relieved by hand over side of bed
- Weakening and wasting of thenar eminence
- tinnels sign
- phalens sign
carpals tunnel investigation
Electromyography
Slower conduction velocity in median sensory nerves
Confirms site and severity
carpals tunnel management
Surgical decompression
Nocturnal splint - pain relief
Steroid injections - pain relief
myasthenia crisis =
treatment
= weakness of respiratory muscles
Treatment = Plasmaphereisis (antibody removal) + imunoglobulin
MG treatment
Anticholinesterase eg pyridostigmine
Relapses
– Immunosuppressant drugs eg azathioprine
If anticholinesterase fails
– Prednisolone
Thymectomy
- Young onset
- Anticholinesterase fails
MG investigation
Serum antibodies
- antiAChR
- anti-MuSK - this is less important, look when antiAChR is neg
Nerve stimulation test = electromyography
- Reduction in evoked potential following motor nerve stimulation, slower response
- Esp in repetitive stimulation
Ice test = ptosis improves with ice pack
CT thymus - look for tumour/hyperplasia /atrophy
Test fatigability
- Count to 50: as they continue, their voice becomes quieter
- Ask the patient to raise eyes, not head, to finger. They will eventually be unable to maintain this
MG symptoms
- Diurnal variability (in the day) – improves after rest
- Increasing Muscular weakness (fatiguing)
- Fatigability of ocular (ptosis, double vision), bulbar (swallowing - dysphagia, chewing, dysarthria, myasthenic snarl on smiling), and proximal limbs
- Myasthenia crisis= weakness of respiratory muscles
MG pathophysiology
Autoimmune - antibodies to nicotinic ACh receptors (anti-AChR antibodies)
- Immune complex deposition at postsynaptic membranes
- Depletion of working postsynaptic receptor sites
- B cells and T cells involved
- ACh less able to activate neuromuscular junction - excitatory effect blocked
Antibodies to Muscle specific tyrosine kinase (anti -MuSK) at the postsynaptic membrane of the neuromuscular junction – causing receptor blockade /loss
what conditions is MG associated with
Associated with other autoimmune conditions eg SLE, RA Associated with thymic hyperplasia (esp under 50) Thymic tumour (esp if over 50) Thymic atrophy (esp if over 50) (thymus)
MG age and gender
Overall f>m
- But m> f over 50
- F peak = 30y
- M peak = 60y
6 causes nerve malfunction
- Demyelination
- Due to Schwann cell damage
- Conduction slows
- Eg guillain barre - Axonal degeneration
- Axon damage causes nerve fibre to die
- Toxic neuropathies - Compression
- Focal demyelination at compression site
- Causes disruption of conduction
- Eg entrapment neuropathies (Carpals tunnel) - Infarction
- Micro-infarction of vasa nervorum
- Diabetes, polyarteritis nodosa - Infiltration
- By inflammatory cells (leprosy), neoplastic cells, and granulomas (sarcoid) - Wallerian degeneration
- Nerve fibre lesion causes axon distal to this degenerates (separated from neuron cell body)
list 5 causes of peripheral neuropathies
guillain barre syndrome (acute) diabetes (chronic) alcohol (chronic) leprosy RA renal failure syphillis sarcoidosis malignancy polyarteritis nodosa hypothyroidism hypoglycaemia HIV lyme disease lead arsenic drugs nutritional defects
Mononeuritis multiplex =
2 or more individual nerves are affected
causes tend to be systemic eg RA, diabetes, AIDs, leprosy, carcinoma, sarcoidosis, polyarteritis
polyneuropathy characteristics
eg
widespread, symmetrical disease, usually commencing peripherally/distally (glove and stocking).
eg leprosy, guillain barre
sensory neuropathy symptoms
- numbness
- paraesthesia eg pins and needles, burning
- Affects extremities/peripheral first - glove and stocking
- May have dexterity issues eg buttons
- May have signs of trauma that indicate sensory loss eg cuts, burns, joint deformation
- — Often presents as foot ulcers
- Pain
- — Esp alcoholic and diabetic neuropathies
motor neuropathy presentation
- Often progressive (May be rapidly so)
- Weakness, clumsiness
- Wasting
- walking/ gait issues eg stumbling, falling
- Breathing issues - reduced vital capacity
autonomic neuropathy presentation
incontinence
sexual dysfunction
treatment for neuropathic pain
amitriptyline
