Neuro Flashcards
Horner’s syndrome criteria?
central lesions:
anhidrosis of face, arms and trunk
- stroke, syringomyelia, MS
pre-ganglionic:
anhidrosis of face
- pancoast tumour, thyroidectomy, cervical rib
post-ganglionic:
no anhidrosis
- carotid artery dissection, cavernous sinus thrombosis, cluster headache
What is mcdonald’s criteria?
So, if you visit your doctor with a neurological symptom that suggests a potential first MS event (CIS), you could therefore have an MRI scan and lumbar puncture. If these tests show lesions in the central nervous system and oligoclonal bands in your spinal fluid, a diagnosis of MS could be made immediately.
What evidence for MS does the patient already have? What additional data is needed for an MS diagnosis?
Two or more relapses AND EITHER objective clinical evidence of two or more lesions OR objective clinical evidence of one lesion together with reasonable historical evidence of a previous relapse None
Two or more relapses; objective clinical evidence of one lesion
(shows DIT)
Dissemination in space shown by:
One or more MRI detected lesions typical of MS OR A further relapse showing damage to another part of the CNS
One relapse; objective clinical evidence of two or more lesions
(shows DIS)
Dissemination in time shown by:
Oligoclonal bands OR MRI evidence of a new lesion since a previous scan OR A further relapse
One attack/relapse; objective clinical evidence of one lesion (known as ‘clinically isolated syndrome’)
Dissemination in space shown by:
One or more MRI detected lesions typical of MS OR A further relapse showing activity in another part of the CNS Dissemination in time shown by: Oligoclonal bands OR MRI showing new lesions since a previous scan OR A further relapse
Insidious neurological progression suggestive of multiple sclerosis (typical for primary progressive MS) Continued progression for one year (from previous symptoms or by ongoing observation) plus any two of: One or more MRI detected lesions in the brain typical of MS, Two or more MRI detected lesions in the spinal cord, Oligoclonal bands in the spinal fluid
What are the causes of peripheral neuropathy?
predominantly sensory PN:
ABCDEFGHI
A Alcohol (and liver dysfunction) LFTs
B B12, B1 deficiency FBC, B12
C Cancer, chemo, CKD, coeliac, connective tissue disease U+E, multiple myeloma
screen, paraneoplastic screen, CXR, mammogram, coeliac, ESR, ANA, ANCA, RF, Igs,
complement, etc.
D Diabetes, Drugs (and toxins) Hba1c
E Endocrine TFTs
F Folate deficiency Folate
G Granulomatous disease eg. sarcoid Calcium, serum ACE
H Hereditary eg. HSMN
I Infection eg. leprosy, idiopathic HIV, syphilis, lyme etc.
What are the upper limb mononeuropathies?
axillary (C5-C6):
- anterior shoulder dislocation, humeral neck fracture
- impaired shoulder abduction
radial nerve lesions (C5-T1):
- humeral fracture, sleeping with hand over back of chair (saturday night palsy)
- wrist and finger drop
- anatomical snuffbox numbness
median nerve lesions (C6-T1):
- carpal tunnel (gout, acromegaly, pregnancy, obesity, hypothyroidism, diabetes, amyloidosis)
- sensory loss of lateral 3 fingers
- analgesia and splint -> steroid injections -> nerve release
ulnar nerve lesions (C7-T1):
- compression at medial epinodyle (cubital tunnel syndrome)
- wasting of ulnar, claw hand which lessens if lesion closer to elbow as paralysis of flexor digitorum profundus, reduced sensation over little finger and ring
What investigations would you do for peripheral neuropathy?
FBC, U+E, LFT, TFT, ESR, CRP, B12, folate, glucose/hba1c, bone profile
urine dip
ANA, ANCA, Immunoglobulins, RF, complement, serum electrophoresis, urine bence jones proteins, serum ACE, paraneoplastic antibodies (eg. anti-mag, anti-hu, anti-yo), HIV, syphilis, lyme, coeliac serology
CXR
EMG
Nerve conduction studies (sensory vs. motor, low amplitude = axonal, low velocity = demyelinating)
Lumbar puncture
MRI spine
Nerve/muscle biopsy
Screen for cancer: mammogram, CT, skeletal survey if possible myeloma
Genetic testing
What nerves supply the rotator cuff muscles?
subscapularis, supraspinatous, infraspinatous -> subscapular nerve
teres minor -> axillary nerve
What is bulbar palsy
lower motor neuron palsy effecting brainstem cranial nerves 9-11
Tx:
sx to control sx e.g. SALT, physios, meds to control drooling
Whats drugs cause drug induced parkinsons?
metocelopramide
antipsychotics e.g. chlorpromazine
Visual field defects
inferior quadrantopia - parietal lobe
superior quadrantopia - temporal
craniopharyngioma - inferior bitemporal hemianopnia
pituitary tumour- superior bitemporal hemianopia
What are the causes and management of proximal myopathy?
foot drop causes?
CMN injury
peripheral nerve disorders: CMT
Muscle disorders, such as muscular dystrophy or myositis
Injury to the nerve roots, such as in spinal stenosis
Neurodegenerative disorders of the brain that cause muscular problems, such as multiple sclerosis, stroke, and cerebral palsy
Charcot Marie Tooth
Inherited peripheral neuropathy (motor>sensory)
Autosomal dominant mainly
CMT type 1. Chromosome 17. Mutation in PMP22 gene. Demyelination (reduced velocity on nerve conduction studies).
Causes distal wasting of legs (inverted champagne bottle appearance) and hands (clawed appearance) with weakness and mild sensory loss (can have sensory ataxia with positive Rhombergs) and areflexia. Bilateral foot drop with high-stepping gait. Bilateral pes cavus and toe clawing. Scoliosis. Occasionally palpable peripheral nerves.
Management: Multidisciplinary (physio, OT, geneticist, neurologist, orthopaedics, orthotics), analgesia, orthopaedic procedures
What problems do diabetics get with their feet and why might it be difficult to treat them?
neuropathy, ulcers, osteomyelitis
immunosuppressed, poor vascular supply so hard to reach abx
Parkinson’s disease ix:
postural BP
drug chart
eyes: psp, nystagmus in MSA
Hereditary haemorrhagic telangiectasia is a rare autosomal dominant condition where multiple small telangiectases occur on the skin and mucous membranes, most commonly on the lips and the tongue. Lesions are also often scattered over the pulps of fingers. The size and number of lesions increases with age.
Arteriovenous malformations may occur in the:
liver
lungs, causing:
clubbing
murmurs
paradoxical emboli
Aneurysm (popliteal)
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Peutz-Jegher’s syndrome
Last reviewed 1 Jan 2022
Authoring team
Peutz-Jegher’s syndrome is an autosomal dominant condition characterised by:
multiple hamartogenous polyps of the gastrointestinal tract - most often in the small bowel but may occur affect any portion of the GI tract
mucocutaneous pigmentation - mainly, of the lips, buccal mucosa, genitalia, hands and feet
so freckles, haemartomatous GI polyps, high cancer risk
Mx: upper and lower GI endoscopy, large polyp removal, breast/gynae/pancreatic surveillance
FAP: genetic testing for all 1st degree relatives, annual sigmoidoscopy if positive, prophylactic resection with ileal-anal anastamosis
