Neuro Paces Flashcards
How to test upper limb myotomes and peripheral nerve
C5- shoulder abduction
C6- elbow flexion and wrist extension
C7- elbow extension
C8- thumb extension
T1- finger abduction
Median - flexion and pronation
Ulnar- flexion of ring and little finger DIP, intrinsic muscles of the hand
Radial- extension
How to differentiate ulnar nerve palsy from C8/T1 pathology
Abductor pollicis brevis would be weak in a C8-T1 lesion, it is supplied by the median nerve
Normal sensation in T1 if ulnar lesion
What are the signs of an ulnar nerve palsy?
- Relevant scar
- ‘Ulnar claw’ Extension at 4th and 5th metacarpal phalangeal joint and flexion at distal joint
- Wasting of small muscles of the hand
- Weak abduction of fingers
- Normal strength in abductor pollicis brevis
- Altered sensation in ulnar distribution
Types of diabetic neuropathy
- Distal symmetric polyneuropathy - progressive distal sensory loss in a glove and stocking distribution results in axonal loss in nerve conduction studies, motor involvement in severe cases
- Autonomic neuropathy- postural hypotension, gastroparesis, gustatory sweating, resting tachycardia
- Diabetic amyotrophy- microvasculitis presents with asymmetric pain then weakness in the proximal leg along with weight loss
Causes of peripheral neuropathy
1) Metabolic
- Diabetes (chronic, sensory predominant, length dependent)
- B12, B1, B6 deficiency
- Uraemia
- Hypothyroidism
2) Infective
- HIV (distal sensory, often painful)
- Lyme disease
3) Immune
- CIDP (relapsing course, often not length dependent)
- Paraprotrinaemic (myeloma or MGUS)
- Connective tissue disease (RA, sjogren, SLE, sarcoidosis)
- paraneoplastic (most commonly lung ca
- GBS
4) Genetic
- Charcot Marie Tooth
- Acute intermittent porphyria
5) Toxic
- isoniazid
- pyridoxine
- lead
- chemotherapy
Investigating diabetic neuropathy
Nerve conduction studies show a sensory axonal loss with reduced or absent sensory nerve action potentials in a length- dependent manner with the legs being most affected
Management of diabetic neuropathy
Optimise diabetes control
Foot care
Pain management
Postural hypotension managed with fludrocortisone
GI symptoms with prokinetics and antiemetics
Clinic signs of hereditary sensory motor neuropathy (Charcot Marie Tooth)
Wasting of distal lower limb muscles with preservation of the thigh muscle bulk
Pes cavus
Stocking distribution sensory loss
High steppage gait due to foot drop and stamping due to loss of proprioception
Wasting of hand muscles
Palpable lateral popliteal nerve
What causes hereditary sensory motor neuropathy
Most common types are I (demyelinating) and II (axonal) therefore nerve conduction studies are useful
Autosomal dominant inheritance (test for PMP22 mutations in HSMN I)
Tests for HSMN
Nerve conduction studies
Genetic testing
Management of HSMN
Physiotherapist/ occupational therapist
Orthotics
Genetic counselling
Causes of predominantly sensory peripheral neuropathy
DM
Alcohol
Drugs eg. Isoniazid and vincristine
Vitamin deficiencies - b12 and b1
Causes of predominantly motor peripheral neuropathy
Guillain barre and botulism present acutely
Lead toxicity
Porphyria
HSMN
Causes of mononeuritis multiplex
DM
Connective tissue disease eg. SLE and RA
Vasculitis
HIV
Malignancy
What causes a central scotoma?
Optic nerve disease eg. Optic neuritis
Affects ipsilateral side
What causes a bitemporal haemianopia?
Chiasmal lesion
Upper fields worse affected in pituitary tumours
Lower fields worse affected in craniopharynhiomas
What causes a homonomous superior quadrantanopia?
Temporal lobe lesion
What causes a homonymous inferior quadrantanopia?
Parietal lobe lesion
What causes a homonymous hemianopia?
Post chiasmal lesion, the more congruous the more posterior the lesion is
A posterior cerebral stroke can cause macular sparing due to dual blood supply
What is the Pathophysiology of MS?
BBB is more permeable to immune cellls. T cells enter the CNS. T cells attack the myelin sheath leading to inflammation.
How does MS present?
Sensory- Parasthesia, hypoaesthesia, pain, MS hugs
Optic neuritis- diminished visual acuity, decreased colour perception, periorbital pain preceding vision loss
Weakness- exercised induced weakness is characteristic, UMN signs
Spasticity
Bladder dysfunction
Constipation
Sexual dysfunction
Uthoff’s phenomenon- symptoms worse after hot bath
Lhermitte’s sign- lightening pains down the spine on neck flexion due to cervical cord plaques
Disease course of MS
Relapsing remitting
Secondary progressive
Primary progressive
Differentials for MS
Inflammatory conditions- neuromyelitis optica, shortens, ADEM, CNS lupus/vasculitis
Infection - syphilis, Lyme disease, HIV
Metabolic- B12 deficiency, mitochondrial disease
Diagnosis and investigation of MS
Need to prove dissemination of disease activity in time and space.
1. Clinical history
2. MRI
3. Unpaired oligoclonal bands in the CSF (not specific for MS, occur in 85% of cases)